Effect of Bacterial Chemotactic Peptides on Intestinal Inflammation in Animal Models of Acute and Chronic “Relapsed” Colitis

2005 ◽  
Vol 50 (8) ◽  
pp. 1444-1453 ◽  
Author(s):  
Gerardo A. HernÁndez ◽  
Melanie R. ValentÍn ◽  
Caroline B. Appleyard
2008 ◽  
Vol 101 (5) ◽  
pp. 633-658 ◽  
Author(s):  
Amy R. Lomax ◽  
Philip C. Calder

β2-1 Fructans are carbohydrate molecules with prebiotic properties. Through resistance to digestion in the upper gastrointestinal tract, they reach the colon intact, where they selectively stimulate the growth and/or activity of beneficial members of the gut microbiota. Through this modification of the intestinal microbiota, and by additional mechanisms, β2-1 fructans may have beneficial effects upon immune function, ability to combat infection, and inflammatory processes and conditions. In this paper, we have collated, summarised and evaluated studies investigating these areas. Twenty-one studies in laboratory animals suggest that some aspects of innate and adaptive immunity of the gut and the systemic immune systems are modified by β2-1 fructans. In man, two studies in children and nine studies in adults indicate that the adaptive immune system may be modified by β2-1 fructans. Thirteen studies in animal models of intestinal infections conclude a beneficial effect of β2-1 fructans. Ten trials involving infants and children have mostly reported benefits on infectious outcomes; in fifteen adult trials, little effect was generally seen, although in specific situations, certain β2-1 fructans may be beneficial. Ten studies in animal models show benefit of β2-1 fructans with regard to intestinal inflammation. Human studies report some benefits regarding inflammatory bowel disease (four positive studies) and atopic dermatitis (one positive study), but findings in irritable bowel syndrome are inconsistent. Therefore, overall the results indicate that β2-1 fructans are able to modulate some aspects of immune function, to improve the host's ability to respond successfully to certain intestinal infections, and to modify some inflammatory conditions.


2001 ◽  
Vol 15 (8) ◽  
pp. 557-558
Author(s):  
Hugh J Freeman

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.


Gut Pathogens ◽  
2015 ◽  
Vol 7 (1) ◽  
Author(s):  
Janelle A. Jiminez ◽  
Trina C. Uwiera ◽  
G. Douglas Inglis ◽  
Richard R. E. Uwiera

2012 ◽  
Vol 6 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Stephanie Verschuere ◽  
Rebecca De Smet ◽  
Liesbeth Allais ◽  
Claude A. Cuvelier

2021 ◽  
Vol 11 (1) ◽  
pp. 80-87
Author(s):  
Nadja Maria da Costa Melo ◽  
Marília Virgo Silva Almeida ◽  
Daniel Melo de Oliveira Campos ◽  
Claudio Bruno Silva de Oliveira ◽  
Jonas Ivan Nobre Oliveira

Objective: To identify and describe comparatively the chemical models of the induction of inflammatory bowel diseases (IBD) in rodents most used and that best mimic the pathogenesis in humans. Methods: Based on an integrative review in the MEDLINE and LILACS databases, it was investigated which experimental induction models were most cited in articles published from 2004 to 2020, with the descriptors "Colitis/CI", "Colitis model ulcerative" and "Intestinal inflammation model." All empirical articles that addressed one or more inflammation models in rats or mice were included. Results: 239 articles were identified; of these, only ten empirical articles were selected. The most used models were colitis induced by TNBS acid, DSS, and colitis induced by acetic acid (AA). Conclusion: It was possible to identify the most used models to promote the induction of intestinal inflammation in rats, and both models proved to be effective according to the limitations observed in the models described, suggesting the need for new works that use more well-defined protocols and that more fully represent the pathophysiological complexity of the disease.


2016 ◽  
Vol 8 (7) ◽  
pp. 1
Author(s):  
Richard R. E. Uwiera ◽  
Trina C. Uwiera ◽  
Janelle A. Jiminez ◽  
G. Douglas Inglis

<p>This article examines several animal models used to investigate mechanisms involved in the induction and progression of inflammatory bowel disease in people. The use of appropriate animal models to study intestinal inflammation requires careful consideration as each model has strengths and limitations for investigating disease, and no single model provides a complete understanding of the disease process. In as such, it compels researchers to carefully contemplate the advantages and disadvantages of each animal model, and to consider the process of choosing the best animal model(s) as an essential component of the experimental design.</p>


2020 ◽  
Vol 8 (2) ◽  
pp. e001584
Author(s):  
David Bauché ◽  
Smita Mauze ◽  
Christina Kochel ◽  
Jeff Grein ◽  
Anandi Sawant ◽  
...  

BackgroundProgrammed cell death protein 1 (PD-1) and CTLA4 combination blockade enhances clinical efficacy in melanoma compared with targeting either checkpoint alone; however, clinical response improvement is coupled with increased risk of developing immune-related adverse events (irAE). Delineating the mechanisms of checkpoint blockade-mediated irAE has been hampered by the lack of animal models that replicate these clinical events.MethodsWe have developed a mouse model of checkpoint blockade-mediated enterocolitis via prolonged administration of an Fc-competent anti-CTLA4 antibody.ResultsSustained treatment with Fc-effector, but not Fc-mutant or Fc-null, anti-CTLA4 antagonist for 7 weeks resulted in enterocolitis. Moreover, combining Fc-null or Fc-mutant CTLA4 antagonists with PD-1 blockade results in potent antitumor combination efficacy indicating that Fc-effector function is not required for combination benefit.ConclusionThese data suggest that using CTLA4 antagonists with no Fc-effector function can mitigate gut inflammation associated with anti-CTLA4 antibody therapy yet retain potent antitumor activity in combination with PD-1 blockade.


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