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Shayista H, Prasad MN, Raj SN, Ranjini H, Manju K, Baker S. Mechanistic overview of gut microbiota and mucosal pathogens with respect to cardiovascular diseases. THE MICROBE 2024; 5:100160. [DOI: 10.1016/j.microb.2024.100160] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/05/2025]
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2
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Abdulrazzaq SB, Abu-Samak M, Omar A, Barakat M, Alzaghari LF, Mosleh I, Al-Najjar M, Al-Najjar MAA. The effect of vitamin D3 and omega-3 combination, taken orally, on triglycerides, lining of intestine, and the biodiversity of gut microbiota in healthy rats. J Appl Microbiol 2024; 135:lxae223. [PMID: 39223094 DOI: 10.1093/jambio/lxae223] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2023] [Revised: 07/31/2024] [Accepted: 09/01/2024] [Indexed: 09/04/2024]
Abstract
AIM The gut microbiota plays a key role in host health. An intake of omega-3 and vitamin D3 in a separate manner is vital for maintaining good health of gut microbiota and controlling some illness manifestations. The aim of this study is to investigate the potential change in biodiversity of the gut microbiome in healthy rats supplemented with vitamin D3, omega-3 alone and their combination and to reflect onto the triglyceride levels in serum and fecal samples. METHODS AND RESULTS Using the 16S rRNA gene Miseq Illumina NGS, and monitoring triglyceride levels in serum and fecal samples coupled with several clinical parameters, we examined the effect of orally taken combination of omega-3 and vitamin D3 alongside the separate intake of supplements on gut microbiota in 24 healthy white Wistar rats for six weeks. The study findings showed that combination treatment encouraged the growth of opportunistic Clostridia class during day 21 and 42 of treatment by 7.7 and 7.4 folds, respectively, exhibited incomplete absorption levels for both supplements when used concomitantly, demonstrated a damaging effect on the gut intestinal lining wall thickness (126 µm) when compared to control group (158 µm), increasing lumen diameter (400 µm), and showed higher triglyceride level in fecal samples. CONCLUSIONS These findings indicate that omega-3 and vitamin D3 supplements as combination intake reveal unfavorable effects, thus, it is advised to conduct further in-depth studies to clarify the presence or absence of any chemical interaction between both supplements' molecules and to investigate based on human model to attain a superior perspective.
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Affiliation(s)
- Shaymaa B Abdulrazzaq
- Department of Pharmaceutical Science and Pharmaceutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
| | - Mahmoud Abu-Samak
- Department of Clinical Pharmacy and Therapeutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
| | - Amin Omar
- Department of Pharmaceutical Science and Pharmaceutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
| | - Muna Barakat
- Department of Clinical Pharmacy and Therapeutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
| | - Lujain F Alzaghari
- Department of Clinical Pharmacy and Therapeutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
| | - Ibrahim Mosleh
- Department of Medical Laboratory Sciences, University of Jordan, Amman 11942, Jordan
| | - Moath Al-Najjar
- Department of Advanced Computing Sciences, Maastricht University, 6211LK, The Netherlands
| | - Mohammad A A Al-Najjar
- Department of Pharmaceutical Science and Pharmaceutics, Faculty of Pharmacy, Applied Science Private University, Amman 11937, Jordan
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Zhou Y, Jiang WD, Zhang JX, Feng L, Wu P, Liu Y, Jiang J, Kuang SY, Tang L, Peng Y, Zhou XQ. Cinnamaldehyde improves the growth performance and digestion and absorption capacity in grass carp (Ctenopharyngodon idella). FISH PHYSIOLOGY AND BIOCHEMISTRY 2020; 46:1589-1601. [PMID: 32440967 DOI: 10.1007/s10695-020-00813-9] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/17/2019] [Accepted: 04/23/2020] [Indexed: 06/11/2023]
Abstract
The present study evaluated the effect of cinnamaldehyde (CIN) on the growth performance and digestion and absorption capacity of grass carp (Ctenopharyngodon idella). Fish were fed five diets including graded levels of CIN for 60 days. The results indicated that (1) appropriate CIN supplementation increased the growth performance and promoted the intestine growth of grass carp; (2) dietary appropriate CIN supplementation increased the digestion and absorption capacity by increasing the activities of intestinal and hepatopancreas digestive enzymes (lipase, chymotrypsin, trypsin, and amylase) and intestinal brush border enzymes (creatine kinase (CK), Na+/K+-ATPase, γ-glutamyl transpeptidase (γ-GT), and alkaline phosphatase (AKP)); (3) dietary CIN increased the absorption capacity which may be associated with the upregulated messenger RNA (mRNA) abundances of their amino acid transporters (AATs) in the intestine, which might be associated with activating the target of rapamycin (TOR) signaling pathway. The best CIN supplementation in the diets of grass carp was estimated to be 76.40 mg kg-1 diet based on the best percent weight gain (PWG). In general, CIN increased the digestion and absorption capacity of grass carp and raised the mRNA abundances of AATs which may be partly related to activation of the TOR signaling pathway.
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Affiliation(s)
- Yang Zhou
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
| | - Wei-Dan Jiang
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
- Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China
- Key Laboratory of Animal Disease-resistant Nutrition, Ministry of Education, Chengdu, China
| | - Jin-Xiu Zhang
- Animal Nutrition Institute, Sichuan Animal Science Academy, Chengdu, 610066, China
| | - Lin Feng
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
- Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China
- Key Laboratory of Animal Disease-resistant Nutrition, Sichuan Province, Chengdu, China
| | - Pei Wu
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
- Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China
- Key Laboratory of Animal Disease-resistant Nutrition, Ministry of Education, Chengdu, China
| | - Yang Liu
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
- Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China
- Key Laboratory of Animal Disease-resistant Nutrition and Feed, Ministry of Agriculture and Rural Affairs, Chengdu, China
| | - Jun Jiang
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China
| | - Sheng-Yao Kuang
- Animal Nutrition Institute, Sichuan Animal Science Academy, Chengdu, 610066, China
| | - Ling Tang
- Animal Nutrition Institute, Sichuan Animal Science Academy, Chengdu, 610066, China
| | - Yan Peng
- Shanghai Menon Animal Nutrition Technology Co., Ltd., Shanghai, 201807, China
| | - Xiao-Qiu Zhou
- Animal Nutrition Institute, Sichuan Agricultural University, Chengdu, 611130, Sichuan, China.
- Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, 611130, China.
- Key Laboratory of Animal Disease-resistant Nutrition, Sichuan Province, Chengdu, China.
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Retinoid-Related Orphan Receptor RORγt in CD4 + T-Cell-Mediated Intestinal Homeostasis and Inflammation. THE AMERICAN JOURNAL OF PATHOLOGY 2020; 190:1984-1999. [PMID: 32735890 DOI: 10.1016/j.ajpath.2020.07.010] [Citation(s) in RCA: 21] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/10/2019] [Revised: 07/13/2020] [Accepted: 07/17/2020] [Indexed: 02/07/2023]
Abstract
Retinoic acid-related orphan receptor (ROR)-γt, the master transcription factor of the Th17 subset of CD4+ Th cells, is a promising target for treating a host of autoimmune diseases. RORγt plays a vital role in the pathogenesis of inflammatory bowel diseases-Crohn disease and ulcerative colitis-caused by untoward reactivity of the immune system to the components of the intestinal microbiome. The mammalian intestinal tract is a highly complex and compartmentalized organ with specialized functions, and is a privileged site for the generation of both peripherally induced regulatory CD4+ T cells (Tregs) and effector Th17 cells. As Th17 cells can be proinflammatory in nature, the equilibrium between effector Th17 and Treg cells is crucial for balancing intestinal homeostasis and inflammation. Recent findings suggest that RORγt, in addition to Th17 cells, is also expressed in peripherally induced, colonic regulatory CD4+ T cells. Therefore, RORγt is expressed in both effector and regulatory subsets of CD4+ T cells in the intestine. The present review discusses the role of RORγt in cellular and molecular differentiation of Th17 and Treg, and examines how targeting RORγt in inflammatory bowel disease therapy could influence the development of these two diverse subsets of immune cells with opposing functions.
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Hurley E, Mullins D, Barrett MP, O'Shea CA, Kinirons M, Ryan CA, Stanton C, Whelton H, Harris HMB, O'Toole PW. The microbiota of the mother at birth and its influence on the emerging infant oral microbiota from birth to 1 year of age: a cohort study. J Oral Microbiol 2019; 11:1599652. [PMID: 32128038 PMCID: PMC7034431 DOI: 10.1080/20002297.2019.1599652] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/24/2018] [Revised: 03/12/2019] [Accepted: 03/22/2019] [Indexed: 01/11/2023] Open
Abstract
Background: The acquisition of microbial communities and the influence of delivery mode on the oral microbiota of the newborn infant remains poorly characterised. Methods: A cohort of pregnant women were enrolled in the study (n = 84). All infants were born full term, by Spontaneous vaginal delivery (SVD) or by Caesarean section (CS). At delivery a saliva sample along with a vaginal/skin sample from the mother. Saliva samples were the taken from the infant within one week of birth, and at week 4, week 8, 6 months and 1 year of age. We used high-throughput sequencing of V4-V5 region 16S rRNA amplicons to compare the microbiota of all samples. Results: The vaginal microbiota had a lower alpha diversity than the skin microbiota of the mother, while the infant oral microbiota diversity remained relatively stable from birth to 8 weeks of age. The oral microbiota of the neonate differed by birth modality up to 1 week of age (p < 0.05), but birth modality did not have any influence on the infant oral microbiota beyond this age. Conclusions: We conclude thatbirth mode does not have an effect on the infant oral microbiota beyond 4 weeks of age, and the oral microbiota of infants continues to develop until 1 year of age.
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Affiliation(s)
- Eimear Hurley
- School of Microbiology, University College Cork, Cork, Ireland.,Cork University Dental School & Hospital, Cork University Hospital, Wilton, Cork, Ireland
| | - David Mullins
- School of Microbiology, University College Cork, Cork, Ireland.,APC Microbiome Ireland, University College Cork, Cork, Ireland
| | - Maurice P Barrett
- School of Microbiology, University College Cork, Cork, Ireland.,APC Microbiome Ireland, University College Cork, Cork, Ireland
| | - Carol Anne O'Shea
- APC Microbiome Ireland, University College Cork, Cork, Ireland.,Department of Neonatology, Cork University Maternity Hospital, Wilton, Cork, Ireland
| | - Martin Kinirons
- Cork University Dental School & Hospital, Cork University Hospital, Wilton, Cork, Ireland
| | - C Anthony Ryan
- Department of Neonatology, Cork University Maternity Hospital, Wilton, Cork, Ireland
| | | | - Helen Whelton
- Cork University Dental School & Hospital, Cork University Hospital, Wilton, Cork, Ireland.,College of Medicine and Health, UCC, Cork, Ireland
| | - Hugh M B Harris
- School of Microbiology, University College Cork, Cork, Ireland.,APC Microbiome Ireland, University College Cork, Cork, Ireland
| | - Paul W O'Toole
- School of Microbiology, University College Cork, Cork, Ireland.,APC Microbiome Ireland, University College Cork, Cork, Ireland
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6
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Belorkar SA, Gupta AK. Oligosaccharides: a boon from nature's desk. AMB Express 2016; 6:82. [PMID: 27699701 PMCID: PMC5047869 DOI: 10.1186/s13568-016-0253-5] [Citation(s) in RCA: 72] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2016] [Accepted: 09/15/2016] [Indexed: 11/10/2022] Open
Abstract
This article reviews the varied sources of oligosaccharides available in nature as silent health promoting, integral ingredients of plants as well as animal products like honey and milk. The article focuses on exotic and unfamiliar oligosaccharides like Galactooligosaccharides, Lactulose derived Galactooligosaccharides, Xylooligosaccharides, Arabinooligosaccharides and algae derived Marine oligosaccharides along with the most acknowledged prebiotic fructooligosaccharides. The oligosaccharides are named as on the grounds of the monomeric units forming oligomers with functional properties. The chemical structures, natural sources, microbial enzyme mediated synthesis and physiological effects are discussed. An elaborate account of the different types of oligosaccharides with special reference to fructooligosaccharides are presented. Finally, the profound health benefits of oligosaccharides are rigourously discussed limelighting its positive physiological sequel.
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Affiliation(s)
- Seema A. Belorkar
- Department of Microbiology and Bioinformatics, Bilaspur University, 206, Budhiya complex, Sarkanda, Bilaspur, Chhattisgarh 495004 India
| | - A. K. Gupta
- Pt. Ravishankar Shukla University, Raipur, CG 492010 India
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New Role of Nod Proteins in Regulation of Intestinal Goblet Cell Response in the Context of Innate Host Defense in an Enteric Parasite Infection. Infect Immun 2015; 84:275-85. [PMID: 26527214 DOI: 10.1128/iai.01187-15] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/15/2015] [Accepted: 10/24/2015] [Indexed: 12/12/2022] Open
Abstract
Mucins secreted by intestinal goblet cells are considered an important component of innate defense in a number of enteric infections, including many parasitic infections, but also likely provide protection against the gut microbiota. Nod proteins are intracellular receptors that play key roles in innate immune response and inflammation. Here, we investigated the role of Nod proteins in regulation of intestinal goblet cell response in naive mice and mice infected with the enteric parasite Trichuris muris. We observed significantly fewer periodic acid-Schiff (PAS)-stained intestinal goblet cells and less mucin (Muc2) in Nod1 and Nod2 double-knockout (Nod DKO) mice after T. muris infection than in wild-type (WT) mice. Expulsion of parasites from the intestine was significantly delayed in Nod DKO mice. Treatment of naive WT mice with Nod1 and Nod2 agonists simultaneously increased numbers of PAS-stained goblet cells and Muc2-expressing cells, whereas treatment with Nod1 or Nod2 separately had no significant effect. Stimulation of mucin-secreting LS174T cells with Nod1 and Nod2 agonists upregulated core 3 β1,3-N-acetylglucosaminyltransferase (C3GnT; an important enzyme in mucin synthesis) and MUC2. We also observed lower numbers of PAS-stained goblet cells and less Muc2 in germfree mice. Treatment with Nod1 and Nod2 agonists enhanced the production of PAS-stained goblet cells and Muc2 in germfree mice. These data provide novel information on the role of Nod proteins in goblet cell response and Muc2 production in relation to intestinal innate defense.
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8
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Chichlowski M, Rudolph C. Visceral pain and gastrointestinal microbiome. J Neurogastroenterol Motil 2015; 21:172-81. [PMID: 25829337 PMCID: PMC4398233 DOI: 10.5056/jnm15025] [Citation(s) in RCA: 40] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/16/2014] [Revised: 03/10/2015] [Accepted: 03/11/2015] [Indexed: 12/20/2022] Open
Abstract
A complex set of interactions between the microbiome, gut and brain modulate responses to visceral pain. These interactions occur at the level of the gastrointestinal mucosa, and via local neural, endocrine or immune activity; as well as by the production of factors transported through the circulatory system, like bacterial metabolites or hormones. Various psychological, infectious and other stressors can disrupt this harmonious relationship and alter both the microbiome and visceral pain responses. There are critical sensitive periods that can impact visceral pain responses in adulthood. In this review we provide a brief background of the intestinal microbiome and emerging concepts of the bidirectional interactions between the microbiome, gut and brain. We also discuss recent work in animal models, and human clinical trials using prebiotics and probiotics that alter the microbiome with resultant alterations in visceral pain responses.
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Affiliation(s)
| | - Colin Rudolph
- Mead Johnson Nutrition, Evansville, IN, USA.,Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of California, San Francisco, CA, USA
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9
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Hernández N, Escudero JA, San Millán Á, González-Zorn B, Lobo JM, Verdú JR, Suárez M. Culturable aerobic and facultative bacteria from the gut of the polyphagic dung beetle Thorectes lusitanicus. INSECT SCIENCE 2015; 22:178-190. [PMID: 24339348 DOI: 10.1111/1744-7917.12094] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Accepted: 12/03/2013] [Indexed: 06/03/2023]
Abstract
Unlike other dung beetles, the Iberian geotrupid, Thorectes lusitanicus, exhibits polyphagous behavior; for example, it is able to eat acorns, fungi, fruits, and carrion in addition to the dung of different mammals. This adaptation to digest a wider diet has physiological and developmental advantages and requires key changes in the composition and diversity of the beetle's gut microbiota. In this study, we isolated aerobic, facultative anaerobic, and aerotolerant microbiota amenable to grow in culture from the gut contents of T. lusitanicus and resolved isolate identity to the species level by sequencing 16S rRNA gene fragments. Using BLAST similarity searches and maximum likelihood phylogenetic analyses, we were able to reveal that the analyzed fraction (culturable, aerobic, facultative anaerobic, and aerotolerant) of beetle gut microbiota is dominated by the phyla Proteobacteria, Firmicutes, and Actinobacteria. Among Proteobacteria, members of the order Enterobacteriales (Gammaproteobacteria) were the most abundant. The main functions associated with the bacteria found in the gut of T. lusitanicus would likely include nitrogen fixation, denitrification, detoxification, and diverse defensive roles against pathogens.
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Affiliation(s)
- Noemi Hernández
- Department Sanidad Animal, Facultad de Veterinaria, Universidad Complutense de Madrid, Avenida Puerta de Hierro s/n, Madrid, CP, 28040
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10
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Lee KN, Lee OY. Intestinal microbiota in pathophysiology and management of irritable bowel syndrome. World J Gastroenterol 2014; 20:8886-8897. [PMID: 25083061 PMCID: PMC4112865 DOI: 10.3748/wjg.v20.i27.8886] [Citation(s) in RCA: 41] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/09/2014] [Revised: 04/02/2014] [Accepted: 06/17/2014] [Indexed: 02/07/2023] Open
Abstract
Irritable bowel syndrome (IBS) is a functional bowel disorder without any structural or metabolic abnormalities that sufficiently explain the symptoms, which include abdominal pain and discomfort, and bowel habit changes such as diarrhea and constipation. Its pathogenesis is multifactorial: visceral hypersensitivity, dysmotility, psychosocial factors, genetic or environmental factors, dysregulation of the brain-gut axis, and altered intestinal microbiota have all been proposed as possible causes. The human intestinal microbiota are composed of more than 1000 different bacterial species and 1014 cells, and are essential for the development, function, and homeostasis of the intestine, and for individual health. The putative mechanisms that explain the role of microbiota in the development of IBS include altered composition or metabolic activity of the microbiota, mucosal immune activation and inflammation, increased intestinal permeability and impaired mucosal barrier function, sensory-motor disturbances provoked by the microbiota, and a disturbed gut-microbiota-brain axis. Therefore, modulation of the intestinal microbiota through dietary changes, and use of antibiotics, probiotics, and anti-inflammatory agents has been suggested as strategies for managing IBS symptoms. This review summarizes and discusses the accumulating evidence that intestinal microbiota play a role in the pathophysiology and management of IBS.
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Abstract
The human intestine is colonised by 10¹³ to 10¹⁴ micro-organisms, the vast majority of which belong to the phyla Firmicutes and Bacteroidetes. Although highly stable over time, the composition and activities of the microbiota may be influenced by a number of factors including age, diet and antibiotic treatment. Although perturbations in the composition or functions of the microbiota are linked to inflammatory and metabolic disorders (e.g. inflammatory bowel diseases, irritable bowel syndrome and obesity), it is unclear at this point whether these changes are a symptom of the disease or a contributing factor. A better knowledge of the mechanisms through which changes in microbiota composition (dysbiosis) promote disease states is needed to improve our understanding of the causal relationship between the gut microbiota and disease. While evidence of the preventive and therapeutic effects of probiotic strains on diarrhoeal illness and other intestinal conditions is promising, the exact mechanisms of the beneficial effects are not fully understood. Recent studies have raised the question of whether non-viable probiotic strains can confer health benefits on the host by influencing the immune system. As the potential health effect of these non-viable bacteria depends on whether the mechanism of this effect is dependent on viability, future research needs to consider each probiotic strain on a case-by-case basis. The present review provides a comprehensive, updated overview of the human gut microbiota, the factors influencing its composition and the role of probiotics as a therapeutic modality in the treatment and prevention of diseases and/or restoration of human health.
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12
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Xie YR, Liu SL, Liu X, Luo ZB, Zhu B, Li ZF, Li LJ, He Y, Jiang L, Li H, Ruan B. Intestinal microbiota and innate immunity-related gene alteration in cirrhotic rats with liver transplantation. Transplant Proc 2012; 43:3973-9. [PMID: 22172882 DOI: 10.1016/j.transproceed.2011.08.113] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/01/2011] [Revised: 06/17/2011] [Accepted: 08/29/2011] [Indexed: 02/07/2023]
Abstract
BACKGROUND The present study investigated the alteration of intestinal microbiota, innate immunity-related genes, and bacterial translocation in rats with cirrhosis and liver transplantation. METHODS Specific pathogen-free Sprague-Dawley rats were randomized into 4 groups: (1) normal controls (N); (2) liver cirrhosis (LC); (3) normal control groups with liver transplantation (LTN); and (4) liver cirrhosis with liver transplantation (LTC). We examined plasma endotoxin, bacterial tacslocation, denaturing gradient gel electrophoresis (DGGE) profile of intestinal mucosa-associated bacteria, abundance of key bacterial populations, and expression of innate immunity-related gene. RESULTS The LTC and LC group, showed higher endotoxin levels (1.08±0.73 EU/mL and 0.74±0.70 EU/mL, respectively) than the N group (0.27±0.13 EU/mL; P<.05). the incidence of bacterial translocation (BT) to liver and mesenteric lymph nodes (MLN), and the number of total bacteria were increased significantly in the LTC and LC groups compared with the N group (P<.05). The counts of Lactobacilli and Bacteroides were lower, whereas Enterobacteria were higher in the LC than the N group (P<.05). Mucins (MUC2, MUC3) and Toll-like receptors (TLR2, TLR4) messenger RNA (mRNA) expression were significantly higher in the LC and LTC groups than the N group (P<.05). The marked difference between the groups in the overall structure of the bacterial community was also generated by DGGE profiles. CONCLUSION Liver cirrhosis disturbs intestinal microbiota and innate immunity-related genes, which contributes to endotoxemia and bacterial translocation. These had not completely recovered in cirrhotic rats until 1 month after orthotopic liver transplantation.
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Affiliation(s)
- Y R Xie
- State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Infectious Disease Center, the First Affiliated Hospital of Medical School, Zhejiang University, Hangzhou, China
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13
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Fitch PM, Henderson P, Schwarze J. Respiratory and gastrointestinal epithelial modulation of the immune response during viral infection. Innate Immun 2012; 18:179-189. [PMID: 21239454 DOI: 10.1177/1753425910391826] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023] Open
Abstract
Respiratory and enteric viral infections cause significant morbidity and mortality world-wide and represent a major socio-economic burden. Many of these viruses have received unprecedented public and media interest in recent years. A popular public misconception is that viruses are a threat to which the human body has only limited defences. However, the majority of primary and secondary exposures to virus are asymptomatic or induce only minor symptoms. The mucosal epithelial surfaces are the main portal of entry for viral pathogens and are centrally involved in the initiation, maintenance and polarisation of the innate and adaptive immune response to infection. This review describes the defences employed by the epithelium of the respiratory and gastrointestinal tracts during viral infections with focus on epithelial modulation of the immune response at the innate/adaptive interface.
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Affiliation(s)
- Paul M Fitch
- Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, UK.
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14
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Mori K, Ito T, Miyamoto H, Ozawa M, Wada S, Kumagai Y, Matsumoto J, Naito R, Nakamura S, Kodama H, Kurihara Y. Oral administration of multispecies microbial supplements to sows influences the composition of gut microbiota and fecal organic acids in their post-weaned piglets. J Biosci Bioeng 2011; 112:145-50. [DOI: 10.1016/j.jbiosc.2011.04.009] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/15/2011] [Revised: 04/01/2011] [Accepted: 04/21/2011] [Indexed: 12/24/2022]
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15
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Torres DP, Gonçalves MDPF, Teixeira JA, Rodrigues LR. Galacto-Oligosaccharides: Production, Properties, Applications, and Significance as Prebiotics. Compr Rev Food Sci Food Saf 2010; 9:438-454. [DOI: 10.1111/j.1541-4337.2010.00119.x] [Citation(s) in RCA: 407] [Impact Index Per Article: 27.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]
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16
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Evans EA, Chen WC, Tan MW. The DAF-2 insulin-like signaling pathway independently regulates aging and immunity in C. elegans. Aging Cell 2008; 7:879-93. [PMID: 18782349 DOI: 10.1111/j.1474-9726.2008.00435.x] [Citation(s) in RCA: 108] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023] Open
Abstract
The Caenorhabditis elegans DAF-2 insulin-like signaling pathway, which regulates lifespan and stress resistance, has also been implicated in resistance to bacterial pathogens. Loss-of-function daf-2 and age-1 mutants have increased lifespans and are resistant to a variety of bacterial pathogens. This raises the possibility that the increased longevity and the pathogen resistance of insulin-like signaling pathway mutants are reflections of the same underlying mechanism. Here we report that regulation of lifespan and resistance to the bacterial pathogen Pseudomonas aeruginosa is mediated by both shared and genetically distinguishable mechanisms. We find that loss of germline proliferation enhances pathogen resistance and this effect requires daf-16, similar to the regulation of lifespan. In contrast, the regulation of pathogen resistance and lifespan is decoupled within the DAF-2 pathway. Long-lived mutants of genes downstream of daf-2, such as pdk-1 and sgk-1, show wildtype resistance to pathogens. However, mutants of akt-1 and akt-2, which we find to individually have modest effects on lifespan, show enhanced resistance to pathogens. We also demonstrate that pathogen resistance of daf-2, akt-1, and akt-2 mutants is associated with restricted bacterial colonization, and that daf-2 mutants are better able to clear an infection after challenge with P. aeruginosa. Moreover, we find that pathogen resistance among insulin-like signaling mutants is associated with increased expression of immunity genes during infection. Other processes that affect organismal longevity, including Jun kinase signaling and caloric restriction, do not affect resistance to bacterial pathogens, further establishing that aging and innate immunity are regulated by genetically distinct mechanisms.
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Affiliation(s)
- Eric A Evans
- Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305-5120, USA
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McGuire AL, Colgrove J, Whitney SN, Diaz CM, Bustillos D, Versalovic J. Ethical, legal, and social considerations in conducting the Human Microbiome Project. Genome Res 2008; 18:1861-4. [PMID: 18971311 DOI: 10.1101/gr.081653.108] [Citation(s) in RCA: 58] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/24/2022]
Affiliation(s)
- Amy L McGuire
- Center for Medical Ethics and Health Policy, Baylor College of Medicine, Houston, Texas 77030, USA.
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Flanagan JL, Lynch SV, Wiener-Kronish J. Molecular Approaches to Detection of Bacteria in Critical Care Patients. Intensive Care Med 2007. [DOI: 10.1007/978-0-387-49518-7_5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/22/2022]
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Caballero-Franco C, Keller K, De Simone C, Chadee K. The VSL#3 probiotic formula induces mucin gene expression and secretion in colonic epithelial cells. Am J Physiol Gastrointest Liver Physiol 2007; 292:G315-22. [PMID: 16973917 DOI: 10.1152/ajpgi.00265.2006] [Citation(s) in RCA: 289] [Impact Index Per Article: 16.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/31/2023]
Abstract
Several studies have stressed the importance of the microbiota in the maintenance of the gastrointestinal epithelium. Administration of probiotic bacteria, supplements composed of microbiota constituents, was previously shown to diminish symptoms in patients suffering from inflammatory bowel diseases. This raises the possibility that probiotics may play an active role in enhancing the intestinal barrier at the mucosal surface. In this study, we investigated whether the clinically tested VSL#3 probiotic formula and/or its secreted components can augment the protective mucus layer in vivo and in vitro. For in vivo studies, Wistar rats were orally administered the probiotic mixture VSL#3 on a daily basis for seven days. After treatment, basal luminal mucin content increased by 60%. In addition, we exposed isolated rat colonic loops to the VSL#3 probiotic formula, which significantly stimulated colonic mucin (MUC) secretion and MUC2 gene expression; however, MUC1 and MUC3 gene expression were only slightly elevated. The effect of the VSL#3 mucin secretagogue was also tested in vitro by use of LS 174T colonic epithelial cells. In contrast to the animal studies, cultured cells incubated with VSL#3 bacteria did not exhibit increased mucin secretion. However, the bacterial secreted products contained in the conditioned media stimulated a remarkable mucin secretion effect. Among the three bacterial groups (Lactobacilli, Bifidobacteria, and Streptococci) contained in VSL#3, the Lactobacillus species were the strongest potentiator of mucin secretion in vitro. A preliminary characterization of the putative mucin secretagogue suggested that it was a heat-resistant soluble compound, which is not sensitive to protease and DNase treatment. These findings contribute to a better understanding of the complex and beneficial interaction between colonic epithelial cells and intestinal bacteria.
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Affiliation(s)
- C Caballero-Franco
- Institute of Parasitology, McGill University, Saint Anne de Bellevue, Quebec, Canada
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Troemel ER, Chu SW, Reinke V, Lee SS, Ausubel FM, Kim DH. p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. PLoS Genet 2006; 2:e183. [PMID: 17096597 PMCID: PMC1635533 DOI: 10.1371/journal.pgen.0020183] [Citation(s) in RCA: 500] [Impact Index Per Article: 26.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/13/2006] [Accepted: 09/11/2006] [Indexed: 11/26/2022] Open
Abstract
The PMK-1 p38 mitogen-activated protein kinase pathway and the DAF-2–DAF-16 insulin signaling pathway control Caenorhabditis elegans intestinal innate immunity. pmk-1 loss-of-function mutants have enhanced sensitivity to pathogens, while daf-2 loss-of-function mutants have enhanced resistance to pathogens that requires upregulation of the DAF-16 transcription factor. We used genetic analysis to show that the pathogen resistance of daf-2 mutants also requires PMK-1. However, genome-wide microarray analysis indicated that there was essentially no overlap between genes positively regulated by PMK-1 and DAF-16, suggesting that they form parallel pathways to promote immunity. We found that PMK-1 controls expression of candidate secreted antimicrobials, including C-type lectins, ShK toxins, and CUB-like genes. Microarray analysis demonstrated that 25% of PMK-1 positively regulated genes are induced by Pseudomonas aeruginosa infection. Using quantitative PCR, we showed that PMK-1 regulates both basal and infection-induced expression of pathogen response genes, while DAF-16 does not. Finally, we used genetic analysis to show that PMK-1 contributes to the enhanced longevity of daf-2 mutants. We propose that the PMK-1 pathway is a specific, indispensable immunity pathway that mediates expression of secreted immune response genes, while the DAF-2–DAF-16 pathway appears to regulate immunity as part of a more general stress response. The contribution of the PMK-1 pathway to the enhanced lifespan of daf-2 mutants suggests that innate immunity is an important determinant of longevity. The innate immune system provides the first line of defense against pathogen infection and relies upon pathways conserved across mammals, insects, and nematodes. Here, the authors have analyzed the transcriptional response of the nematode Caenorhabditis elegans to infection by the human pathogen Pseudomonas aeruginosa. They investigated this transcriptional response in the context of two conserved pathways involved in pathogen defense: the PMK-1 p38 mitogen-activated protein kinase (p38 MAPK) pathway and the DAF-2–DAF-16 insulin-signaling pathway. Specifically, the authors found that the p38 MAPK pathway plays a critical role in the infection-induced expression of secreted immune response genes. These genes include C-type lectins, lysozymes, and antimicrobial peptides that fight off infection in many species. In contrast, they found that the DAF-16 pathway is not required for immune response gene expression and may regulate immunity as part of a general stress response that functions in parallel to p38 MAPK. In addition, the authors observed that p38 MAPK contributes to the enhanced longevity of daf-2 mutants, implicating p38 MAPK signaling in the regulation of longevity, possibly through its role in immunity.
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Affiliation(s)
- Emily R Troemel
- Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America
- Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America
| | - Stephanie W Chu
- Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America
| | - Valerie Reinke
- Department of Genetics, Yale University School of Medicine, New Haven, Connecticut, United States of America
| | - Siu Sylvia Lee
- Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York, United States of America
| | - Frederick M Ausubel
- Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America
- Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts, United States of America
| | - Dennis H Kim
- Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America
- * To whom correspondence should be addressed. E-mail:
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Liévin-Le Moal V, Servin AL. The front line of enteric host defense against unwelcome intrusion of harmful microorganisms: mucins, antimicrobial peptides, and microbiota. Clin Microbiol Rev 2006; 19:315-37. [PMID: 16614252 PMCID: PMC1471992 DOI: 10.1128/cmr.19.2.315-337.2006] [Citation(s) in RCA: 367] [Impact Index Per Article: 19.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
Abstract
The intestinal tract is a complex ecosystem that combines resident microbiota and the cells of various phenotypes with complex metabolic activities that line the epithelial wall. The intestinal cells that make up the epithelium provide physical and chemical barriers that protect the host against the unwanted intrusion of microorganisms that hijack the cellular molecules and signaling pathways of the host and become pathogenic. Some of the organisms making up the intestinal microbiota also have microbicidal effects that contribute to the barrier against enteric pathogens. This review describes the two cell lineages present in the intestinal epithelium: the goblet cells and the Paneth cells, both of which play a pivotal role in the first line of enteric defense by producing mucus and antimicrobial peptides, respectively. We also analyze recent insights into the intestinal microbiota and the mechanisms by which some resident species act as a barrier to enteric pathogens. Moreover, this review examines whether the cells producing mucins or antimicrobial peptides and the resident microbiota act in partnership and whether they function individually and/or synergistically to provide the host with an effective front line of defense against harmful enteric pathogens.
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Affiliation(s)
- Vanessa Liévin-Le Moal
- Unité 756 INSERM, Faculté de Pharmacie Paris XI, Signalisation et Physiopathologie des Cellules Epithéliales, Institut National de la Santé et de la Recherche Médicale, F-92296 Chātenay-Malabry, France
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