• Anti-diabetic polysaccharides
• Bibliometric analysis
• Diabetes mellitus
• Gut microbiota modulation
• Oxidative and inflammatory regulation

• Animals
• Humans
• Bibliometrics
• Biomedical Research/trends
• Diabetes Mellitus/drug therapy
• Gastrointestinal Microbiome/drug effects
• Hypoglycemic Agents/therapeutic use
• Hypoglycemic Agents/pharmacology
• Polysaccharides/therapeutic use
• Polysaccharides/pharmacology
• Review Literature as Topic

• allergic rhinitis
• epithelial barrier
• fecal microbiota transplantation
• gut microbiota
• t cell

• Animals
• Fecal Microbiota Transplantation
• Gastrointestinal Microbiome/immunology
• Rhinitis, Allergic/therapy
• Rhinitis, Allergic/immunology
• Rhinitis, Allergic/microbiology
• Mice
• CD4-Positive T-Lymphocytes/immunology
• CD4-Positive T-Lymphocytes/metabolism
• Cytokines/metabolism
• Nasal Mucosa/immunology
• Nasal Mucosa/microbiology
• Nasal Mucosa/metabolism
• Ovalbumin/immunology
• Signal Transduction
• Mice, Inbred BALB C
• TOR Serine-Threonine Kinases/metabolism

• 81970860 National Natural Science Foundation of China

• Acne
• Diet
• Inflammation
• Ketogenic diet
• Nutrition
• Obesity
• Oxidative stress
• VLCKD
• Very low-calorie ketogenic diet

• Humans
• Female
• Diet, Ketogenic/adverse effects
• Obesity/complications
• Inflammation/complications
• Acne Vulgaris
• Anti-Inflammatory Agents
• Methylamines

• Histopathology
• Oxidative stress
• Parenteral nutrition
• Small intestine
• Starvation

• acute lung injury
• enteral nutrition
• length of stay
• respiratory distress syndrome
• retrospective studies

• Diabetes mellitus
• Intestinal flora
• Natural medicines
• Pathogenesis
• Treatment

• acute kidney injury
• fluid balance
• fluid overload
• pediatric
• pediatric acute respiratory distress syndrome
• pediatric intensive care unit

Intermittent hypoxia and sleep fragmentation are pathophysiological processes involved in obstructive sleep apnea (OSA) which affect gut microbiota, sleep architecture, and mTOR signaling pathway. However, the involvement of these elements in the pathogenesis mechanism of OSA-associated hypertension remains unclear. Therefore, this study investigated whether the OSA-associated hypertension mechanism is regulated by the gut microbiota and mTOR signaling pathway. Patients were diagnosed by polysomnography; their fecal samples were obtained and analyzed for their microbiome composition by 16S ribosomal RNA pyrosequencing and bioinformatics analysis. Transcript genes on fasting peripheral blood mononuclear cells (PBMCs) were examined using Illumina RNA-sequencing analysis. Totally, we enrolled 60 patients with severe OSA [without hypertension (n = 27) and with hypertension (n = 33)] and 12 controls (neither OSA nor hypertension). Results revealed that severe-OSA patients with hypertension had an altered gut microbiome, decreased short-chain fatty acid-producing bacteria (P < 0.05), and reduced arginine and proline metabolism pathways (P=0.001), compared with controls; also, they had increased stage N1 sleep and reduced stages N2 and N3 sleep accompanied by repeated arousals (P < 0.05). Analysis of PBMCs using the Kyoto Encyclopedia of Genes and Genomes database showed that the mTOR signaling pathway (P=0.006) was the most important differential gene-enriched pathway in severe-OSA patients with hypertension. Our findings extend prior work and suggest a possibility that the regulation of the mTOR signaling pathway is involved in developing OSA-associated hypertension through its interaction with the disturbance of the gut microbiome and sleep architecture.

The aim of the study was to analyse the relationship between nutritional disorders and the expression of innate antibacterial response genes in patients admitted to the intensive care unit (ICU). In 46 patients with severe malnutrition and life-threatening surgical complications, nutritional status tests were performed on the basis of the NRS 2002 (Nutritional Risk Screening) scale, cytokine, albumin, C-reactive protein concentrations, anthropometric tests, and body composition analysis. Concurrently, the expression of Toll-like receptor 2, NOD1, TRAF6, and HMGB1 genes was determined in peripheral blood leukocytes at the mRNA level using real-time polymerase chain reaction. It was found that both the nutritional status and the gene expression changed depending on the group of patients studied (including the group of survivors vs. non-survivors). Significant correlations were found between the results of routine tests used in the diagnostics of malnutrition (including NRS 2002, resistance, reactance, phase angle, excess of extracellular water) and the expression of the studied genes. Moreover, the expression of TRAF6 and HMGB1 genes correlated with the Acute Physiology and Chronic Health Evaluation II scale and the age of the patients. The results of the research suggest that the expression of innate antibacterial response genes may be a new diagnostic tool complementing the assessment of nutritional disorders in surgical patients admitted to the ICU. These tests may be helpful in providing more accurate diagnostics of the genetic effects of malnutrition and in the monitoring of patients for whom nutritional treatment is planned to support the functions of the immune system, thereby increasing the effectiveness of this type of treatment in the ICU.

• gene expression
• innate immunity
• malnutrition

Percutaneous endoscopic gastrostomy is an established method to provide nutrition to patients with restricted oral uptake of fluids and calories. Here, we review the methods, indications and complications of this procedure. While gastrostomy can be safely and easily performed during gastroscopy, the right patients and timing for this intervention are not always chosen. Especially in patients with dementia, the indication for and timing of gastrostomies are often improper. In this patient group, clear data for enteral nutrition are lacking; however, some evidence suggests that patients with advanced dementia do not benefit, whereas patients with mild to moderate dementia might benefit from early enteral nutrition. Additionally, other patient groups with temporary or permanent restriction of oral uptake might be a useful target population for early enteral nutrition to maintain mobilization and muscle strength. We plead for a coordinated study program for these patient groups to identify suitable patients and the best timing for tube implantation.

• Gastrostomy
• Nutrition
• Dementia
• Percutaneous endoscopic gastrostomy
• Oncologic diseases
• Endoscopy
• Neurodegenerative disorders

• Enteral Nutrition/methods
• Gastroscopy/standards
• Gastrostomy/methods
• Gastrostomy/standards
• Humans
• Patient Selection
• Practice Guidelines as Topic
• Time Factors
• Time-to-Treatment/standards

• liver diseases
• microbiome
• nutrition support
• parenteral nutrition
• sepsis
• short bowel syndrome

Acne is a highly prevalent inflammatory skin condition involving sebaceous sties. Although it clearly develops from an interplay of multiple factors, the exact cause of acne remains elusive. It is increasingly believed that the interaction between skin microbes and host immunity plays an important role in this disease, with perturbed microbial composition and activity found in acne patients. Cutibacterium acnes (C. acnes; formerly called Propionibacterium acnes) is commonly found in sebum-rich areas and its over-proliferation has long been thought to contribute to the disease. However, information provided by advanced metagenomic sequencing has indicated that the cutaneous microbiota in acne patients and acne-free individuals differ at the virulent-specific lineage level. Acne also has close connections with the gastrointestinal tract, and many argue that the gut microbiota could be involved in the pathogenic process of acne. The emotions of stress (e.g., depression and anxiety), for instance, have been hypothesized to aggravate acne by altering the gut microbiota and increasing intestinal permeability, potentially contributing to skin inflammation. Over the years, an expanding body of research has highlighted the presence of a gut–brain–skin axis that connects gut microbes, oral probiotics, and diet, currently an area of intense scrutiny, to acne severity. This review concentrates on the skin and gut microbes in acne, the role that the gut–brain–skin axis plays in the immunobiology of acne, and newly emerging microbiome-based therapies that can be applied to treat acne.

• acne
• brain
• gut
• microbiome
• microbiota
• skin
• therapeutic implications

• 2017R1C1B5016144 National Research Foundation of Korea

Sepsis is the leading cause of acute kidney injury (AKI) in the intensive care unit (ICU). Septic AKI is a complex and multifactorial process that is incompletely understood. During sepsis, the disruption of the mucus membrane barrier, a shift in intestinal microbial flora, and microbial translocation may lead to systemic inflammation, which further alters host immune and metabolic homeostasis. This altered homeostasis may promote and potentiate the development of AKI. As part of this vicious cycle, when AKI develops, the clearance of inflammatory mediators and metabolic products is decreased. This will lead to further gut injury and breakdown in mucous membrane barriers. Thus, changes in the gut during sepsis can initiate and propagate septic AKI. This deleterious gut–kidney crosstalk may be a potential target for therapeutic maneuvers. This review analyses the underlying mechanisms in gut–kidney crosstalk in septic AKI.

• Sepsis, AKI, Septic AKI, Gut–kidney crosstalk, Inflammation

• Butyrate
• Colon cancer
• Diabetes
• Gut microbiota
• Obesity
• mTOR

• Bacterial virulence
• Gut integrity
• Gut permeability
• Intestinal mucosal barrier
• Microbiome
• Pathobiome

• Epithelium
• Gut
• Immune system
• Intestine
• Microbiome
• Sepsis

• Animals
• Gastrointestinal Microbiome/immunology
• Humans
• Intestinal Mucosa/immunology
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/microbiology
• Intestinal Mucosa/pathology
• Lymphocytes/immunology
• Lymphocytes/metabolism
• Lymphocytes/pathology
• Multiple Organ Failure/immunology
• Multiple Organ Failure/metabolism
• Multiple Organ Failure/microbiology
• Multiple Organ Failure/pathology
• Sepsis/immunology
• Sepsis/metabolism
• Sepsis/pathology

• R01 GM113228 NIGMS NIH HHS
• R01 GM072808 NIGMS NIH HHS
• R01 GM104323 NIGMS NIH HHS
• T32 GM095442 NIGMS NIH HHS
• R01 GM109779 NIGMS NIH HHS

• Feeding strategy
• Mucositis
• Pediatric cancer patients

Impaired gastric emptying is common in critically ill patients. Intestinal dysmotility, a major cause of feed intolerance, may foster infectious complications due to mucosal barrier disruption. However, little is known about gut-directed immune activation, intestinal barrier function and its association with impaired gastric emptying in critically ill patients at ICU admission.

We conducted a prospective observational study at two tertiary care medical ICUs. Fifty consecutive patients needing invasive mechanical ventilation were recruited within 24 h of ICU admission, prior to any nutritional support. The acute physiology and chronic health evaluation (APACHE) II score, the sequential organ failure assessment (SOFA) score and the multiple organ dysfunction score (MODS) were used to assess illness severity and multiple organ dysfunction. Gastric emptying was assessed by paracetamol absorption test. Peripheral blood mononuclear cells were freshly isolated and cultured for 24 h, and TNF-α, IL-1β and IL-10 measured in cell culture supernatants and in serum by ELISA. The intestinal epithelial barrier was assessed, quantifying serum concentrations of intestinal fatty acid binding protein (I-FABP), ileal bile-acid binding protein (I-BABP) and zonulin-1 by ELISA. Small bowel homing T lymphocytes (CD4+ α4β7 + CCR9+) were analyzed by flow cytometry. The Mann-Whitney test and Spearman correlation were used in statistical evaluation.

CD4 + α4β7 + CCR9+ T lymphocytes were inversely correlated with gastric emptying. Patients with delayed gastric emptying at ICU admission (n = 35) had significantly higher serum and PBMC-induced TNF-α and IL-1β and increased intestinal barrier disruption reflected by higher I-FABP, I-BABP and zonulin-1. Patients who died in the ICU had significantly impaired gastric empting at admission compared to ICU survivors. No differences were observed in APACHE II, SOFA or MODS in patients with delayed gastric emptying compared to patients with normal gastric emptying.

Exaggerated CD4 + α4β7 + CCR9+ T lymphocyte homing with increased pro-inflammatory cytokine release and intestinal epithelial barrier disruption are associated with delayed gastric emptying. This is not simply due to differences in overall severity of illness at ICU admission and may represent a pathophysiological mechanism of gut-directed immune activation leading to impaired barrier function in the critically ill.

• Critically ill
• Gastric emptying
• Gut homing
• Intensive care
• Mucosal barrier
• T lymphocytes

• multiple organ dysfunction syndrome
• pediatrics
• nutrition
• bacterial translocation
• microbiome
• extracorporeal membrane oxygenation
• therapeutic plasma exchange
• continuous renal replacement therapy
• hemophagocytic lymphohistiocytosis
• macrophage activation syndrome
• anti-cytokine therapy
• bacterial toxin-mediated disease
• anti-toxin therapy
• corticosteroids
• hydrocortisone
• mineralocorticoids
• aldosterone
• gonadocorticoids
• oxandrolone
• tight glucose control
• anti-oxidant therapy

• Anti-Inflammatory Agents/therapeutic use
• Antioxidants/therapeutic use
• Antitoxins/therapeutic use
• Child
• Combined Modality Therapy
• Critical Care/methods
• Extracorporeal Circulation
• Humans
• Hypoglycemic Agents/therapeutic use
• Multiple Organ Failure/therapy
• Nutrition Therapy/methods
• Pediatrics
• Steroids/therapeutic use
• Treatment Outcome

• K23 DK106462 NIDDK NIH HHS
• R01 AI097434 NIAID NIH HHS
• R01 GM113838 NIGMS NIH HHS

Failure of gut homeostasis is an important factor in the pathogenesis and progression of systemic inflammation, which can culminate in multiple organ failure and fatality. Pathogenic events in critically ill patients include mesenteric hypoperfusion, dysregulation of gut motility, and failure of the gut barrier with resultant translocation of luminal substrates. This is followed by the exacerbation of local and systemic immune responses. All these events can contribute to pathogenic crosstalk between the gut, circulating cells, and other organs like the liver, pancreas, and lungs. Here we review recent insights into the identity of the cellular and biochemical players from the gut that have key roles in the pathogenic turn of events in these organ systems that derange the systemic inflammatory homeostasis. In particular, we discuss the dangers from within the gastrointestinal tract, including metabolic products from the liver (bile acids), digestive enzymes produced by the pancreas, and inflammatory components of the mesenteric lymph.

• Acute inflammation
• Gastrointestinal failure
• Gut-liver crosstalk
• Pancreatitis

• Sepsis
• T cell
• apoptosis
• gut microbiome
• immune suppression
• infection

• Bacterial translocation
• CD4+ and CD8+
• Early enteral nutrition
• Endotoxin
• MAdCAM-1
• Several acute pancreatitis

Alterations in the gut microbiota play a crucial role in host physiology and metabolism; however, the molecular pathways underlying these changes in diet-induced obesity are unclear. Mechanistic target of rapamycin (mTOR) signaling pathway is associated with metabolic disorders such as obesity and type 2 diabetes (T2D). Therefore, we examined whether changes in the regulation of mTOR signaling induced by diet (a high-fat diet [HFD] or normal-chow diet) and/or therapeutics (resveratrol [a specific inhibitor of mTOR complex 1] or rapamycin [an inhibitor of both mTOR complex 1 and 2]) altered the composition of the gut microbiota in mice. Oral administration of resveratrol prevented glucose intolerance and fat accumulation in HFD-fed mice, whereas rapamycin significantly impaired glucose tolerance and exacerbated intestinal inflammation. The abundance of Lactococcus, Clostridium XI, Oscillibacter, and Hydrogenoanaerobacterium increased under the HFD condition; however, the abundance of these species declined after resveratrol treatment. Conversely, the abundance of unclassified Marinilabiliaceae and Turicibacter decreased in response to a HFD or rapamycin. Taken together, these results demonstrated that changes in the composition of intestinal microbiota induced by changes in mTOR activity correlate with obese and diabetic phenotypes.

• Delayed gastric emptying
• Enteral nutrition
• Pancreaticoduodenectomy
• Parenteral nutrition
• Postoperative complications

• China
• Enteral Nutrition/adverse effects
• Female
• Humans
• Male
• Middle Aged
• Pancreaticoduodenectomy/adverse effects
• Parenteral Nutrition, Total/adverse effects
• Patient Selection
• Postoperative Complications/etiology
• Recovery of Function
• Retrospective Studies
• Risk Factors
• Time Factors
• Treatment Outcome

We investigated the effects of exogenous glucagon-like peptide-2 (GLP-2) on mucosal atrophy and intestinal antioxidant capacity in a mouse model of total parenteral nutrition (TPN). Male mice (6–8 weeks old) were divided into three groups (n = 8 for each group): a control group fed a standard laboratory chow diet, and experimental TPN (received standard TPN solution) and TPN + GLP-2 groups (received TPN supplemented with 60 µg/day of GLP-2 for 5 days). Mice in the TPN group had lower body weight and reduced intestinal length, villus height, and crypt depth compared to the control group (all p < 0.05). GLP-2 supplementation increased all parameters compared to TPN only (all p < 0.05). Intestinal total superoxide dismutase activity and reduced-glutathione level in the TPN + GLP-2 group were also higher relative to the TPN group (all p < 0.05). GLP-2 administration significantly upregulated proliferating cell nuclear antigen expression and increased glucose-regulated protein (GRP78) abundance. Compared with the control and TPN + GLP-2 groups, intestinal cleaved caspase-3 was increased in the TPN group (all p < 0.05). This study shows GLP-2 reduces TPN-associated intestinal atrophy and improves tissue antioxidant capacity. This effect may be dependent on enhanced epithelial cell proliferation, reduced apoptosis, and upregulated GRP78 expression.

• GRP78
• antioxidant capacity
• apoptosis
• glucagon-like peptide-2
• proliferation

• ARDS
• intensive care
• nutrition
• pediatric

• bacterial translocation
• enteral nutrition
• inflammation
• liver disease
• microbiome
• microbiota
• nutritional support
• parenteral nutrition
• surgery

• Chemotherapy
• Citrulline
• Gastrointestinal mucositis
• Methotrexate
• Minimal enteral feeding
• Nutrition
• Rat

• Animals
• Antimetabolites, Antineoplastic/adverse effects
• Citrulline/blood
• Disease Models, Animal
• Enteral Nutrition
• Humans
• Intestinal Mucosa/drug effects
• Male
• Methotrexate/adverse effects
• Mucositis/chemically induced
• Rats
• Rats, Wistar

• Absorption
• Bioavailability
• Intestinal atrophy
• Parenteral nutrition
• Pharmacokinetics
• Vancomycin

• Adherens junction
• Alcohol
• Cadherin
• Claudin
• Occludin
• Oxidative stress
• Tight junction

• bombesin
• enteric nervous system
• goblet cells
• innate immunity
• mucin 2
• parenteral nutrition
• resistin-like molecule β
• small intestine
• trefoil factor 3

• c-Kit
• choline
• interstitial cells of Cajal
• parenteral nutrition
• stem cell factor

• Critical Illness/therapy
• Enteral Nutrition/methods
• Hospitalization
• Humans
• Intensive Care Units
• Parenteral Nutrition
• Randomized Controlled Trials as Topic
• Standard of Care
• Time Factors
• Treatment Outcome

• Arginine/administration & dosage
• Burns/complications
• Burns/therapy
• Cachexia/etiology
• Cachexia/therapy
• Critical Illness/therapy
• Enteral Nutrition/methods
• Enteral Nutrition/statistics & numerical data
• Fish Oils/administration & dosage
• Gastrointestinal Tract/microbiology
• Glutamine/administration & dosage
• Humans
• Infusions, Intravenous
• Lipids/administration & dosage
• Microbiota
• Multiple Organ Failure/complications
• Multiple Organ Failure/metabolism
• Muscle, Skeletal/metabolism
• Neoplasms/complications
• Parenteral Nutrition/methods
• Parenteral Nutrition/statistics & numerical data
• Perioperative Care/methods
• Protein-Energy Malnutrition/etiology
• Protein-Energy Malnutrition/metabolism
• Protein-Energy Malnutrition/therapy
• Stress, Physiological

• cardiac intensive care
• intestinal epithelial barrier function
• vasopressin
• epinephrine
• congenital heart disease
• post-operative

• Cancer
• Children
• Diagnosis
• Gastrointestinal mucositis
• Nutrition
• Risk analysis

• Amino Acid Transport Systems/genetics
• Amino Acid Transport Systems/metabolism
• Amino Acids/blood
• Animals
• Body Weight
• Case-Control Studies
• Dietary Supplements
• Glutamic Acid/administration & dosage
• Glutamic Acid/pharmacology
• Intestinal Mucosa/metabolism
• Intestines/drug effects
• Intestines/pathology
• Mycotoxicosis/drug therapy
• Mycotoxicosis/veterinary
• Mycotoxins/toxicity
• Swine