Accelerated Inflammatory Bowel Disease of TCR-a-Deficient Mice Persistently Infected with Cryptosporidium parvum

1997 ◽  
Vol 83 (3) ◽  
pp. 460 ◽  
Author(s):  
W. Ray Waters ◽  
Mitchell V. Palmer ◽  
Mark R. Ackermann ◽  
James A. Harp
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cryptosporidium Parvum ◽  
Bowel Disease ◽  
Persistently Infected ◽  
Inflammatory Bowel ◽  
Deficient Mice

scholarly journals Cryptosporidium parvum Initiates Inflammatory Bowel Disease in Germfree T Cell Receptor-α-Deficient Mice

1998 ◽  
Vol 153 (6) ◽  
pp. 1717-1722 ◽  
Author(s):  
Randy E. Sacco ◽  
Joseph S. Haynes ◽  
James A. Harp ◽  
W. Ray Waters ◽  
Michael J. Wannemuehler
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
T Cell Receptor ◽  
Cryptosporidium Parvum ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Inflammatory Bowel ◽  
Deficient Mice

scholarly journals Cryptosporidium Parvum-Induced Inflammatory Bowel Disease of TCR-b- x TCR-d-Deficient Mice

1999 ◽  
Vol 85 (6) ◽  
pp. 1100 ◽  
Author(s):  
W. Ray Waters ◽  
Michael J. Wannemuehler ◽  
Randy E. Sacco ◽  
Mitchell V. Palmer ◽  
Joseph S. Haynes ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Cryptosporidium Parvum ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Deficient Mice

Characterization of Helicobacter-induced inflammatory bowel disease in IL-10 -/- and T cell deficient mice

2001 ◽  
Vol 120 (5) ◽  
pp. A523-A523
Author(s):  
A BURICH ◽  
R HERSHBERG ◽  
K WAGGIE ◽  
W ZENG ◽  
J VINEY ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Deficient Mice

Inflammatory bowel disease in IL-2 deficient mice requires T, but not B lymphocytes

1995 ◽  
Vol 108 (4) ◽  
pp. A867
Author(s):  
A. Ma ◽  
M.W. Datta ◽  
E. Margosian ◽  
E. Horak ◽  
F.W. Alt
Keyword(s):  
Inflammatory Bowel Disease ◽  
B Lymphocytes ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Deficient Mice

scholarly journals Dietary grape seed extract ameliorates symptoms of inflammatory bowel disease in IL10-deficient mice

2013 ◽  
Vol 57 (12) ◽  
pp. 2253-2257 ◽  
Author(s):  
Hui Wang ◽  
Yansong Xue ◽  
Hanying Zhang ◽  
Yan Huang ◽  
Guan Yang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Grape Seed Extract ◽  
Grape Seed ◽  
Seed Extract ◽  
Inflammatory Bowel ◽  
Deficient Mice

scholarly journals Studies on the Interleukin-10 Gene in Animal Models of Colitis

2001 ◽  
Vol 15 (8) ◽  
pp. 557-558
Author(s):  
Hugh J Freeman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Bowel Disease ◽  
Inflammatory Process ◽  
Intestinal Inflammation ◽  
Therapeutic Potential ◽  
Interleukin 10 ◽  
Necrosis Factor Alpha ◽  
Inflammatory Bowel ◽  
Deficient Mice

Cytokines play a role in the inflammatory process in colitis and may have therapeutic potential. Interleukin-10 (IL-10) has both immunomodulatory and anti-inflammatory properties. IL-10-deficient mice develop intestinal inflammation with increased tissue levels of other cytokines, including tumour necrosis factor-alpha. In patients with inflammatory bowel disease, impaired IL-10 production by lamina propria T cells occurs and human recombinant IL-10 improves clinical parameters in inflammatory bowel disease (eg, Crohn's disease). There seem to be conflicting results in differing animal models, and the timing of administration of IL-10 relative to onset of colitis may be critical, possibly due to rapid clearance of IL-10. Interestingly, in IL-10 gene-deficient mice raised in germ-free conditions, the intestinal inflammatory changes normally observed in conventional nongerm-free conditions are not detected, suggesting a role for luminal bacteria in the pathogenesis of the inflammatory process.

Inflammatory bowel disease in A20-deficient mice

2001 ◽  
Vol 120 (5) ◽  
pp. A122-A123 ◽  
Author(s):  
D BOONE ◽  
E LEE ◽  
S CHAI ◽  
J LODOLCE ◽  
S LIBBY ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Deficient Mice

scholarly journals Probiotic Lactobacillus spp. Diminish Helicobacter hepaticus-Induced Inflammatory Bowel Disease in Interleukin-10-Deficient Mice

2005 ◽  
Vol 73 (2) ◽  
pp. 912-920 ◽  
Author(s):  
Jeremy A. Peña ◽  
Arlin B. Rogers ◽  
Zhongming Ge ◽  
Vivian Ng ◽  
Sandra Y. Li ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Real Time ◽  
Bowel Disease ◽  
Interleukin 10 ◽  
Helicobacter Hepaticus ◽  
Murine Colitis ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Deficient Mice ◽  
Colitis Model

ABSTRACT Clinical and experimental evidence has demonstrated the potential role of probiotics in the prevention or treatment of inflammatory bowel disease. Probiotic clones with direct immunomodulatory activity may have anti-inflammatory effects in the intestine. We investigated the roles of tumor necrosis factor alpha (TNF-α)-inhibitory Lactobacillus clones with a pathogen-induced murine colitis model. Murine-derived probiotic lactobacilli were selected in vitro for their ability to inhibit TNF-α secretion by Helicobacter hepaticus-stimulated macrophages. Interleukin-10 (IL-10)-deficient mice were treated with probiotic Lactobacillus reuteri in combination with Lactobacillus paracasei and then challenged with H. hepaticus. Ten weeks postinoculation, the severity of typhlocolitis was assessed by histologic examination of the cecocolic region. Intestinal proinflammatory cytokine responses were evaluated by real-time quantitative reverse transcriptase PCR and immunoassays, and the quantities of intestinal H. hepaticus were evaluated by real-time PCR. Intestinal colonization by TNF-α-inhibitory lactobacilli reduced intestinal inflammation in H. hepaticus-challenged IL-10-deficient mice despite similar quantities of H. hepaticus in cocolonized animals. Proinflammatory colonic cytokine (TNF-α and IL-12) levels were lowered in Lactobacillus-treated animals. In this H. hepaticus-challenged IL-10-deficient murine colitis model, lactobacilli demonstrated probiotic effects by direct modulation of mucosal inflammatory responses.

scholarly journals An Abundance of Escherichia coli Is Harbored by the Mucosa- Associated Bacterial Flora of Interleukin-2-Deficient Mice

2004 ◽  
Vol 72 (4) ◽  
pp. 1983-1990 ◽  
Author(s):  
M. Schuppler ◽  
K. Lötzsch ◽  
M. Waidmann ◽  
I. B. Autenrieth
Keyword(s):  
Inflammatory Bowel Disease ◽  
16S Rdna ◽  
Bowel Disease ◽  
Bacterial Flora ◽  
Interleukin 2 ◽  
Healthy Controls ◽  
E Coli ◽  
Inflammatory Bowel ◽  
Deficient Mice

ABSTRACT Mice deficient in interleukin-2 are well suited for use as an animal model for inflammatory bowel disease. Raised under specific-pathogen-free conditions, interleukin-2-deficient mice develop an inflammatory bowel disease resembling ulcerative colitis in humans. The finding that colitis was attenuated when the mice were kept under germfree conditions implies that the resident intestinal flora is involved in the pathogenesis of colitis. The present study addresses the composition of the mucosa-associated bacterial flora in colon samples from interleukin-2-deficient mice that developed colitis. This was investigated by comparative 16S ribosomal DNA (rDNA) sequence analysis and fluorescence in situ hybridization using rRNA-targeted fluorescent probes to quantify the bacterial populations of the mucosa-associated flora. The investigations revealed distinct differences in the bacterial composition of the mucosa-associated flora between interleukin-2-deficient mice and healthy controls. Fluorescence in situ hybridization identified up to 10% of the mucosa-associated flora in interleukin-2-deficient mice as Escherichia coli, whereas no E. coli was detected in the mucosa from healthy wild-type mice. This finding was consistent with the results from comparative 16S rDNA analysis. About one-third of the clones analyzed from 16S rDNA libraries of interleukin-2-deficient mice represented Enterobacteriaceae, whereas none of the clones analyzed from the healthy controls harbored 16S rDNA from Enterobacteriaceae. The abundance of E. coli in the colonic mucosa of interleukin-2-deficient mice strongly suggests a participation in the pathogenesis of colitis in the interleukin-2-deficient mouse model for inflammatory bowel disease.

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