• Aspergillus awamori
• Anti-oxidant
• Apoptosis
• Colitis
• Inflammatory mediators
• Oxidative stress

• Animals
• Colitis, Ulcerative/chemically induced
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/metabolism
• Acetic Acid
• Male
• Rats
• Antioxidants/pharmacology
• Anti-Inflammatory Agents/pharmacology
• Aspergillus
• Apoptosis/drug effects
• Oxidative Stress/drug effects
• Rats, Wistar
• Colon/drug effects
• Colon/pathology
• Colon/metabolism

• Damanhour University

• drug development
• drug discovery
• medicine
• protein engineering
• therapeutic antibodies

• Humans
• Medicine
• Antibodies, Monoclonal/therapeutic use
• Autoimmune Diseases/drug therapy
• Biological Products
• Clinical Relevance

• CXC motif chemokine ligand 1
• Th1 cytokine interferon-γ
• electroacupuncture
• immune infiltrating cells
• macrophages
• transcriptome
• ulcerative colitis

• Humans
• Animals
• Colitis, Ulcerative/genetics
• Colitis, Ulcerative/therapy
• Transcriptome
• Electroacupuncture
• Cytokines
• Body Weight
• Chemokine CXCL1

• Anti-inflammatory
• GLP-2
• Glepaglutide
• Inflammatory bowel disease
• Mucosal healing

Olmesartan medoxomil (OM) is an angiotensin receptor blocker. This study aimed to investigate the effects of OM self-microemulsifying drug delivery system (OMS) in trinitrobenzene sulfonic acid (TNBS)-induced acute colitis in rats. Besides two control groups, five TNBS-colitic-treated groups (n = 8) were given orally sulfasalazine (100 mg/kg/day), low and high doses of OM (3.0 and 10.0 mg/kg/day) (OML and OMH) and of OMS (OMSL and OMSH) for seven days. A colitis activity score was calculated. The colon was examined macroscopically. Colonic levels of myeloperoxidase, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde, and reduced glutathione were measured. Plasma and colonic olmesartan levels were measured. Colonic sections were subjected to hematoxylin and eosin staining and immunohistochemical staining for E-cadherin, caspase-3, and matrix metalloproteinase-9 (MMP-9). Protein expression of E-cadherin, Bcl-2 associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2), and cleaved caspase-3 by Western blot was done. TNBS-colitic rats showed increased colonic myeloperoxidase, TNF-α, IL-6, and malondialdehyde, decreased colonic glutathione, histopathological, immunohistochemical, and protein expression alterations. OMS, compared with OM, dose-dependently achieved higher colonic free olmesartan concentration, showed better anti-inflammatory, antioxidant, and anti-apoptotic effects, improved intestinal barrier, and decreased mucolytic activity. OMS more effectively up-regulated the reduced Bcl-2, Bcl-2/Bax ratio, and E-cadherin expression, and down-regulated the overexpressed Bax, cleaved caspase-3, and MMP-9. OMSL exerted effects comparable to OMH. Sulfasalazine exerted maximal colonic protective effects and almost completely reversed colonic damage, and OMSH showed nearly similar effects with non-significant differences in-between or compared with the normal control group. In conclusion, OMS could be a potential additive treatment for Crohn's disease colitis.

• Bcl-2
• Caspase
• Crohn's disease
• E-cadherin
• MMP-9
• colitis
• drug delivery
• olmesartan medoxomil

Our previous study found that deletion of Sorting nexin 10 (SNX10) can protect against colonic inflammation and pathological damage induced by dextran sulfate sodium (DSS). This inspired us that modulation of SNX10 expression in colonic epithelial cells might represent a promising therapeutic strategy for inflammatory bowel disease (IBD).

Effective delivery of siRNA/shRNA to silence genes is a highly sought-after means in the treatment of multiple diseases. Here, we encapsulated SNX10-shRNA plasmids (SRP) with polylactide-polyglycolide (PLGA) to make oral nanoparticles (NPs), and then applied them to acute and chronic IBD mice model, respectively. The characteristics of the nanoparticles were assayed and the effects of SRP-NPs on mouse IBD were evaluated.

High-efficiency SNX10-shRNA plasmids were successfully constructed and coated with PLGA to obtain nanoparticles, with a particle size of 275.2 ± 11.4mm, uniform PDI distribution, entrapment efficiency of 87.6 ± 2.5%, and drug loading of 13.11 ± 1.38%, displayed dominant efficiency of SNX10 RNA interference in the colon. In both acute and chronic IBD models, SRP-NPs could effectively reduce the loss of mice body weight, relieve the intestinal mucosal damage and inflammatory infiltration, inhibit the expression of inflammatory cytokines IL-1β, IL-23, TNF-α, and down-regulate the expression of toll-like receptors (TLRs) 2 and 4.

Oral nanoparticles of SNX10-shRNA plasmid displayed dominant efficiency of SNX10 RNA interference in the colon and ameliorate mouse colitis via TLR signaling pathway. SNX10 is a new target for IBD treatment and nanoparticles of SNX10-shRNA plasmid might be a promising treatment option for IBD.

• IBD
• SNX10
• SRP-NPs
• TLR
• shRNA

Ulcerative colitis is a gut inflammatory disorder due to altered immune response to gut microbiome, with interplay of environmental and genetic factors. TNF-α activates inflammatory response through a cascade of immune responses, augmenting pro-inflammatory mediators and proteases, activating chemotaxis, and infiltration of inflammatory cells, leading to ulceration and haemorrhage through cytotoxic reactive oxygen species. 6-Paradol, a dietary component in several plants belonging to the Zingiberaceae family, has shown anti-inflammatory and antioxidant activities. Current study evaluates the effect of 6-paradol in amelioration of ulcerative colitis in rats for the first time.

6-Paradol (95% purity) was obtained from seeds of Aframomum melegueta. Rats were divided randomly into six groups (n = 8). Group one was administered normal saline; group two was treated with the vehicle only; group three, sulfasalazine 500 mg/kg; and groups four, five, and six, were given 6-paradol (50, 100, 200, respectively) mg/kg orally through gastric gavage for 7 days. Colitis was induced on 4th day by intrarectal administration of 2 ml acetic acid (3%), approximately 3 cm from anal verge. On 8th day, rats were sacrificed, and distal one-third of the colon extending proximally up to 4 cm from anal orifice was taken for biochemical and gross examination. Two centimetres of injured mucosal portion was taken for histopathological investigations. SPSS (ver.26) was used for statistical analysis.

Colonic and serum glutathione (GSH) levels decreased, while colonic and serum malondialdehyde (MDA), colonic myeloperoxidase (MPO) activity, serum interleukin-6 (IL-6), serum tumour necrosis factor-α (TNF-α) levels, and colon weight to length ratio were increased significantly in the colitis untreated group compared to normal control. Treatment with 6-paradol considerably improved all these parameters, especially at a dose of 200 mg/kg (p < 0.001), revealing non-significant differences with sulfasalazine 500 mg/kg and normal control (p = 0.998). Sulfasalazine and 6-paradol in a dose dependent manner also markedly reversed mucosal oedema, atrophy and inflammation, cryptic damage, haemorrhage, and ulceration. There were non-significant differences between low and medium doses and between medium and high doses of 6-paradol for IL-6 and serum MDA levels.

6-Paradol demonstrated protection against acetic acid-induced ulcerative colitis, probably by anti-inflammatory and antioxidant actions.

The online version contains supplementary material available at 10.1186/s12906-021-03203-7.

• 6-paradol
• Antioxidant
• Ginger
• Grain of paradise
• Gut
• IBD
• Spices

• Inflammation
• Melittin
• TLR4
• TRAF6
• Ulcerative colitis
• sPLA2

• CAMP
• Glabridin
• INOS
• Myleoperoxidase
• TNF-α
• Ulcerative colitis

• Animals
• Anti-Inflammatory Agents/pharmacology
• Antioxidants/metabolism
• Colitis, Ulcerative/chemically induced
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/metabolism
• Cyclic AMP/metabolism
• Dextran Sulfate/pharmacology
• Down-Regulation/drug effects
• Inflammation Mediators/metabolism
• Isoflavones/pharmacology
• Male
• Nitric Oxide/metabolism
• Nitric Oxide Synthase Type II/metabolism
• Peroxidase/metabolism
• Phenols/pharmacology
• Rats
• Rats, Wistar
• Tumor Necrosis Factor-alpha/metabolism

• Antioxidants
• Averrhoa bilimbi L.
• Cytokines
• Inflammatory markers
• Ulcerative colitis
• Wistar rats

To examine the role of A20 in the regulation of intestinal epithelial cells (IECs) inflammation.

Using gene transfection, both stable overexpression and knockdown A20-expressed HT-29 cell lines were established. Accordingly, the cells were divided into the following groups: The control group, the A20 overexpression group, the A20 knockdown group and the respective controls. A20 was stimulated with lipopolysaccharide (LPS) in a dose- and time-dependent manner and was detected using western blotting and real-time polymerase chain reaction (PCR) analyses. Immunofluorescence and western blotting analyses were performed to investigate the role of A20 in the regulation of nuclear factor (NF)-κB activation and translocation into the nucleus. ELISA and real-time PCR were performed to examine A20 in regulating the release of the following inflammatory cytokines: Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IL-8.

The expression of A20 in IECs was inducible. When intestinal epithelial cells were subjected to the stimulation of LPS, the expression of A20 was increased, and the expression of A20 was induced in a dose- and time-dependent manner. The expression of A20 was very low in HT-29 cells without LPS stimulation but rapidly increased and was maintained at a high level 2-4 h after stimulation with LPS. These levels gradually declined with a change in time-course, and the expression of A20 increased with increasing LPS stimulation. Western blotting and immunofluorescence revealed that overexpression of A20 can inhibit NF-κB activation and its translocation to the nucleus. The overexpression of A20 can reduce the levels of proinflammatory cytokines involved in the pathophysiology of inflammatory bowel disease. There was no significant difference in the expression of IL-8 mRNA in the control group, A20 overexpression group or A20 knockdown group without LPS stimulation (P > 0.05); however, while after 2 h, 4 h and 8 h stimulation with LPS, the expression of IL-8 in the A20 overexpression group was lower than the control group and the A20 knockdown group (P < 0.05 or P < 0.01). The expression of TNF-α was different at different time points after 8 h of LPS stimulation (F = 31.33, DF = 5, P < 0.001), and the expression of TNF-α increased as the LPS stimulation time increased. Upon LPS stimulation, lower levels of TNF-α were detected in the A20 overexpression cell lines (P < 0.05). There were no significant differences in the induction of IL-6 and IL-1β among the control group, A20 overexpression group and A20 knockdown group (P > 0.05).

A20 plays an important role in limiting inflammation by inhibiting LPS-induced NF-κB responses in the gut luminal. A20 may be a potential therapeutic tool for inflammatory diseases.

• A20 (TNFAIP3)
• Lipopolysaccharide
• Nuclear factor-κB
• Inflammatory bowel disease

• Biologics
• Crohn's disease
• Inflammatory bowel disease
• Treatment
• Ulcerative colitis

• DSS
• Experimental colitis
• Intestinal anti-inflammation
• Raphanus sativus L.
• TNBS

• Animals
• Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
• Body Weight/drug effects
• Colitis, Ulcerative/chemically induced
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/pathology
• Colon/pathology
• Cytokines/metabolism
• Dextran Sulfate
• Dose-Response Relationship, Drug
• Inflammation Mediators/metabolism
• Male
• Mesalamine/therapeutic use
• Plant Extracts/therapeutic use
• Raphanus/chemistry
• Rats
• Rats, Sprague-Dawley
• Seeds/chemistry
• Trinitrobenzenesulfonic Acid
• Water

• 2,4,6-trinitrobenzene sulfonic acid-induced colitis
• Astragalus polysaccharides
• Chinese medicine
• GATA-3
• T-bet
• rats

We examined the modulatory activity of β-caryophyllene (CA) and gene expression in colitic colon tissues in a dextran sulfate sodium (DSS)-induced colitis model. Experimental colitis was induced by exposing male BALB/c mice to 5% DSS in drinking water for 7 days. CA (30 or 300 mg/kg) was administered orally once a day together with DSS. CA administration attenuated the increases in the disease activity index, colon weight/length ratio, inflammation score, and myeloperoxidase activity in DSS-treated mice. Microarray analysis showed that CA administration regulated the expression in colon tissue of inflammation-related genes including those for cytokines and chemokines (Ccl2, Ccl7, Ccl11, Ifitm3, IL-1β, IL-28, Tnfrsf1b, Tnfrsf12a); acute-phase proteins (S100a8, Saa3, Hp); adhesion molecules (Cd14, Cd55, Cd68, Mmp3, Mmp10, Sema6b, Sema7a, Anax13); and signal regulatory proteins induced by DSS. CA significantly suppressed NF-κB activity, which mediates the expression of a different set of genes. These results suggest that CA attenuates DSS-induced colitis, possibly by modulating the expression of genes associated mainly with colon inflammation through inhibition of DSS-induced NF-κB activity.

• CA, β-caryophyllene
• CD, crohn disease
• Cebpb, CCAAT/enhancer-binding protein &beta
• Colitis
• DSS, dextran sulfate sodium
• Dextran sulfate sodium
• Gene expression
• Hp, haptoglobin
• IBD, inflammatory bowel disease
• IL, interleukin
• Inflammation
• IκB, inhibitor κB
• MPO, myeloperoxidase
• NF-κB, nuclear factor-kappa B
• S100a8, S100 calcium binding protein a8
• SAL, sulfasalazine
• Saa3, serum amyloid A3
• TNF-α, tumor necrosis factor-α
• UC, ulcerative colitis
• β-Caryophyllene (PubChem CID5281515)

• Crohn’s Disease
• Drug Development
• Immune Regulation
• Ulcerative Colitis

• Anti-inflammatory
• Functional food
• Glucosamine oligomers
• Inflammatory bowel disease
• Nuclear factor-kappa B

• Biologic therapy
• Crohn disease
• IBD
• Inflammatory bowel disease
• Ulcerative colitis

• Animals
• Antibodies/pharmacology
• CD146 Antigen/metabolism
• Carcinogenesis/pathology
• Cell Communication/drug effects
• Colitis/pathology
• Colitis/prevention & control
• Colorectal Neoplasms/pathology
• Colorectal Neoplasms/prevention & control
• Dextran Sulfate
• Disease Models, Animal
• Endothelial Cells/drug effects
• Endothelial Cells/metabolism
• Human Umbilical Vein Endothelial Cells
• Humans
• Inflammation/pathology
• Interleukin-1beta/metabolism
• Leukocytes/drug effects
• Leukocytes/pathology
• Mice, Inbred C57BL
• Mice, Knockout
• NF-kappa B/metabolism
• Neovascularization, Pathologic/pathology
• Transcriptional Activation/drug effects
• Tumor Necrosis Factor-alpha/metabolism
• Up-Regulation/drug effects

To elucidate the effects of a solution containing interleukin-10 and anti-IL-1 antibody in modulating experimental intestinal inflammation.

Colitis was induced in BALB/c mice by oral administration of dextran sodium sulphate; mice were then treated with interleukin-10 plus anti-IL-1 antibody at low dosage. Transepithelial electrical resistance of isolated mouse colon and colon lengths were evaluated. Cytokines concentrations in organocultures supernatants and plasma samples were evaluated by Enzyme-Linked Immuno Sorbent Assay. Tight junction proteins were evaluated by immunofluorescence, respectively.

Oral administration of tested products restores intestinal barrier function during experimental intestinal inflammation in association with reduced levels of proinflammatory cytokines, increased interleukin-10 plasma concentrations and a tight junction architecture restoration.

Obtained results may contribute to modelling an interesting strategy for the treatment of patients with inflammatory bowel diseases.

• Anti-interleukin-1 alpha antibody
• Interleukin-10
• Intestinal bowel disease
• Low doses
• Tight-junctions

Background. Free radicals and proinflammatory cytokines have been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Picroliv, a Picrorhiza kurroa derivative, has been demonstrated to have antioxidant and anti-inflammatory effect. The purpose of the study was to investigate the effects of picroliv on experimental model of UC in mice. Materials and Methods. Picroliv was administrated orally by gavage to mice with colitis induced by dextran sulfate sodium (DSS). Disease activity index (DAI), colon length, and histology score were observed. Myeloperoxidase (MPO) activity, and SOD, MDA concentrations were measured by enzyme-linked immunosorbent assay (ELISA) while the expression of cytokine mRNAs was studied by real-time-quantitative polymerase chain reaction and also ELISA. The expression of NF-κB p65 was observed by immunohistochemistry staining and western blotting. Results. A significant improvement was observed in DAI and histological score in mice treated with picroliv, and incerased MPO activity, MDA concentrations, and the expression of IL-1β, TNF-α, and NF-κB p65 in mice with DSS-induced colitis were significantly reduced while decreased SOD level increased following administration of picroliv. Conclusion. The administration of picroliv leads to an amelioration of DSS-induced colitis, suggesting administration of picroliv may provide a therapeutic approach for UC.

• Acetic Acid/toxicity
• Animals
• Citrus sinensis/chemistry
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/physiopathology
• Disease Models, Animal
• Dose-Response Relationship, Drug
• Drug Therapy, Combination
• Fruit
• Male
• Malondialdehyde/metabolism
• Mice
• Moringa oleifera/chemistry
• Peroxidase/metabolism
• Plant Extracts/administration & dosage
• Plant Extracts/pharmacology
• Plant Roots
• Prednisolone/pharmacology
• Solvents/chemistry

Enteropathic arthritis is one of the recognized extraintestinal manifestations of inflammatory bowel disease and affects up to 25% of patients. The treatment options for refractory disease were rather limited and ineffective until the arrival of biologic therapy in the last few years. The use of etanercept was unique for this disease.

In this case report, a 58-year-old Malay woman with a 17-year history of ulcerative colitis had persistent left knee effusion and synovitis for seven years, despite remission of the primary disease. She had had multiple courses of systemic and intra-articular steroid that caused significant systemic side effects such as impaired fasting glucose, hypertension, cataract, and weight gain. She also had a total left knee replacement for secondary osteoarthritis. But the left knee synovitis and effusion recurred a month after the total knee replacement, and she was subjected to a total synovectomy the following year. In view of failure of remission despite multiple immunosuppressants (100 mg of azathioprine daily, 1 g of sulfasalazine twice a day, 10 mg of prednisolone daily, and 10 mg of methotrexate weekly), 25 mg of subcutaneous etanercept twice weekly was started. After 5 weeks of treatment, complete resolution of left knee effusion and normalization of the inflammatory markers were shown. This continued up to 12 months of follow-up while our patient was on etanercept and 10 mg of methotrexate weekly. No relapse or serious side effects were noted.

This case demonstrates the efficacy of etanercept in recalcitrant enteropathic arthritis with no relapse of the underlying colitis while on treatment. The usage of this tumor necrosis factor inhibitor was unique in this case of rheumatology and gastroenterology.

• Animals
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/metabolism
• Colitis, Ulcerative/pathology
• Colitis, Ulcerative/prevention & control
• Colon/drug effects
• Colon/pathology
• Dose-Response Relationship, Drug
• India
• Male
• Malondialdehyde/blood
• Malondialdehyde/metabolism
• Mice
• Peroxidase/blood
• Peroxidase/drug effects
• Phytotherapy
• Plant Extracts/pharmacology
• Plant Extracts/therapeutic use
• Plant Roots/chemistry
• Prednisolone/pharmacology
• Prednisolone/therapeutic use
• Protective Agents/pharmacology
• Protective Agents/therapeutic use
• Vitex

• Animals
• Antioxidants/metabolism
• Antioxidants/pharmacology
• Antioxidants/therapeutic use
• Benzothiazoles/metabolism
• Biphenyl Compounds/metabolism
• Colitis, Ulcerative/chemically induced
• Colitis, Ulcerative/drug therapy
• Colitis, Ulcerative/pathology
• Colon/pathology
• Cordia
• Free Radical Scavengers/metabolism
• Free Radical Scavengers/pharmacology
• Male
• Malondialdehyde/blood
• Malondialdehyde/metabolism
• Medicine, Ayurvedic
• Mice
• Peroxidase/blood
• Peroxidase/metabolism
• Phenols/analysis
• Phytotherapy
• Picrates/metabolism
• Plant Bark/chemistry
• Plant Extracts/metabolism
• Plant Extracts/pharmacology
• Plant Extracts/therapeutic use
• Sulfonic Acids/metabolism

Tumor Necrosis Factor-α (TNF-α), a secreted cytokine, plays an important role in inflammatory diseases and immune disorders, and is a potential target for drug development. The traditional assays for detecting TNF-α, enzyme linked immunosorbent assay (ELISA) and radioimmunoassay, are not suitable for the large size compound screens. Both assays suffer from a complicated protocol, multiple plate wash steps and/or excessive radioactive waste. A simple and quick measurement of TNF-α production in a cell based assay is needed for high throughput screening to identify the lead compounds from the compound library. We have developed and optimized two homogeneous TNF-α assays using the HTRF (homogeneous time resolved fluorescence) and AlphaLISA assay formats. We have validated the HTRF based TNF-α assay in a 1536-well plate format by screening a library of 1280 pharmacologically active compounds. The active compounds identified from the screen were confirmed in the AlphaLISA TNF-α assay using a bead-based technology. These compounds were also confirmed in a traditional ELISA assay. From this study, several beta adrenergic agonists have been identified as TNF-α inhibitors. We also identified several novel inhibitors of TNF-α, such as BTO-1, CCG-2046, ellipticine, and PD 169316. The results demonstrated that both homogeneous TNF-α assays are robust and suitable for high throughput screening.

• 1536-well plate.
• AlphaLISA technology
• HTRF technology
• TNF-α
• inhibition of TNF-α production
• qHTS

RNA silencing utilizing short interfering RNA (siRNA) offers a new and exciting means to overcome the limitations of current treatment options of many diseases. However, delivery of these molecules still poses a great challenge to date.

In the present study, a multicompartmental biodegradable polymer-based nanoparticles-in-microsphere oral system (NiMOS) using gelatin nanoparticles encapsulating a combination of siRNA duplexes specifically targeted against tumor necrosis factor-α (TNF-α) and cyclin D1 (Ccnd1) was employed to study its effects on a dextran sulfate sodium (DSS)-induced acute colitis mouse model mimicking inflammatory bowel disease (IBD). DSS colitis-bearing animals were divided into several control and treatment groups and received either no treatment, blank NiMOS, NiMOS-encapsulating inactive (scrambled), active TNF-α silencing, CyD1 silencing siRNA, or a combination of both active siRNAs by repeated oral administration of three NiMOS doses.

Successful gene silencing with the aid of dual siRNA treatment led to decreased colonic levels of TNF-α or CyD1, suppressed expression of certain pro-inflammatory cytokines (interleukin-1α and -β, interferon-γ), an increase in body weight, and reduced tissue myeloperoxidase activity, while the silencing effect of CyD1 siRNA or the dual treatment was more potent than that of TNF-α siRNA alone.

Results of this study demonstrate the therapeutic potential of a NiMOS-based oral combined TNF-α and CyD1 gene silencing system for the treatment of IBD as shown in an acute colitis model.

AIM: To assess the efficacy and tolerability of thalidomide in pediatric Crohn’s disease (CD).

METHODS: Six patients with refractory CD received thalidomide at an initial dose of 2 mg/kg per day for one month, then increased to 3 mg/kg per day or decreased to 1 mg/kg per day, and again further reduced to 0.5 mg/kg per day, according to the individual patient’s response to the drug.

RESULTS: Remission was achieved within three months. Dramatic clinical improvement was demonstrated after thalidomide treatment. Endoscopic and pathological improvements were also observed after thalidomide treatment, which was well tolerated by all patients.

CONCLUSION: Thalidomide is a useful drug for pediatric refractory CD.

• Inflammatory bowel disease
• Thalidomide
• Tumor necrosis factor-α
• Children

• trefoil factor family 3

• Animals
• Chemotaxis, Leukocyte
• Colitis/chemically induced
• Colitis/enzymology
• Colitis/genetics
• Colitis/immunology
• Colitis/pathology
• Colitis/prevention & control
• Dextran Sulfate
• Diarrhea/enzymology
• Diarrhea/genetics
• Diarrhea/immunology
• Disease Models, Animal
• Fucosyltransferases/deficiency
• Fucosyltransferases/genetics
• Fucosyltransferases/metabolism
• Immunity, Innate
• Interleukin-2/deficiency
• Interleukin-2/genetics
• Intestinal Mucosa/enzymology
• Intestinal Mucosa/immunology
• Intestinal Mucosa/pathology
• Leukocytes/enzymology
• Leukocytes/immunology
• Leukocytes/pathology
• Melena/enzymology
• Melena/genetics
• Melena/immunology
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Mucins/deficiency
• Mucins/genetics
• Mucins/metabolism
• Peroxidase/metabolism
• Severity of Illness Index
• Time Factors
• Trefoil Factor-3
• Weight Loss
• beta 2-Microglobulin/deficiency
• beta 2-Microglobulin/genetics

• DK043351 NIDDK NIH HHS
• P30 DK040561 NIDDK NIH HHS
• R01 DK060049 NIDDK NIH HHS
• CIHR
• HD12437 NICHD NIH HHS
• HD059126 NICHD NIH HHS
• R01 HD059126 NICHD NIH HHS
• DK83756 NIDDK NIH HHS
• DK70260 NIDDK NIH HHS

• Acute Disease
• Animals
• CX3C Chemokine Receptor 1
• Chemokine CX3CL1/physiology
• Colitis/chemically induced
• Cytokines/physiology
• Dextran Sulfate
• Macrophages/enzymology
• Mice
• Mice, Inbred BALB C
• Nitric Oxide Synthase Type II/genetics
• Receptors, Chemokine/physiology
• Tyrosine/analogs & derivatives
• Tyrosine/biosynthesis