Inflammation intestinal

Read S, Malmstrom V, Powrie F Cytotoxic T lym- l23 phocyte-associated antigen 4 plays an essential role in the function of CD25+CD4+ regulatory cells that control intestinal inflammation. J Exp Med 2000 192 295-302. 

The mechanisms whereby mast cells enhance host protection to H. polygyms and T. spiralis (and whether these are related to the leak-lesion hypothesis) have not yet been fully defined. Certainly, mast cells contribute to intestinal inflammation during infection through the secretion of a range of cytokines (Gordon et al., 1990) and vasoactive substances (see above). In addition, the release of mast cell proteases are known to increase enterocyte permeability to macromolecules in the rat intestine (Scudamore et al., 1995) and regulate epithelial cell functions at other mucosal sites (Cairns and Walls, 1996). 

Whilst eosinophils appear unimportant in the induction of protective responses to GI helminths, they are present in large numbers in the inflamed gut and it has therefore been suggested that they play a part in the induction of enteropathy. Moreover, eosinophils have been implicated in the induction of intestinal inflammation eosinophilic gastroenteritis, ulcerative colitis and Crohn s disease. However, IL-5-deficient mice, or GM-CSF transgenic mice (which typically have a blood eosinophilia of approximately 25%) infected with T. spiralis did not show a significant exacerbation or amelioration of either protective or pathological responses (C.E. Lawrence, unpublished observation). 

Increased numbers of goblet cells (GCs) and qualitative changes in mucus secretions are coincident with infection with a number of nematode parasites and it has been proposed that mucin proteins mediate this response by enveloping the parasites and/or interrupting attachment (Nawa et al., 1994). However, the role of GCs and mucus in the generation of a protective response versus its role in resolving intestinal inflammation following infection with GI nematode parasites remains unresolved. 

Steiner TS, Lima AAM, Nataro JP, Guerrant RL Enteroaggregative Escherichia coli produce intestinal inflammation and growth impairment and cause interleukin-8 release from intestinal epithelial cells. J Infect Dis 1998 177 88-96. 

Table 13. Reduction of intestinal inflammation and blood loss by metronidazole in patients on NSAIDs (from Bjarnason et al. [242])... 

Intestinal inflammation was assessed by fecal excretion of " In-labeled neutrophils while blood loss was quantitated via fecal excretion of 51Cr4abeled red cells. The urinary excretion ratio or51 Cr-EDTA//.-rhamnose was used as an index of intestinal permeability. ... 

Bjamason I, Hayllar J, Smethurst P, Price A, Gumpel MJ Metronidazole reduces intestinal inflammation and blood loss in non-steroidal anti-inflammatory drug induced enteropathy. Gut 1992,33 1204-1208. 

Recent experimental data, coming particularly from animal models of IBD, are consistent with the hypothesis that gut flora and bacterial products are implicated in the initiation and/or perpetuation of chronic intestinal inflammation. Purified bacterial products can initiate and perpetuate experimental colitis [1,2]. 

The leading hypothesis for the development of chronic intestinal inflammation is that an abnormal immune response to normal flora might be crucial. This loss of tolerance might be due to a lack of regulatory mediators or cells, or a breakdown in barrier function which makes possible the access of inflammatory bacterial products to the local immune system, thereby overwhelming the normal regulation [3], These possibilities were supported by... 

All these data, taken together suggest that this antibiotic is clinically useful in most cases of active intestinal inflammation. 

Sartor RB, Rath HC, Sellon RK Microbial factors in chronic intestinal inflammation. Curr Opin Gastoenterol 1996 12 327-333. 

Postmortem findings include small hemorrhages present in the internal organs, carcasses may be jaundiced, fluid in body cavities that frequently is blood-stained, intestinal inflammation, edematous and hemorrhagic gall bladder, and the liver may be necrotic. 

Sydora, B. C., Tavemini, M. M., Wessler, A., Jewell, L. D., and Fedorak, R. N. (2003). Lack of interleukin-10 leads to intestinal inflammation, independent of the time at which luminal microbial colonization occurs. Inflamm. Bowel Dis. 9, 87-97. 

Iran. The grain is taken orally for intestinal inflammation and administered rectally for diarrhea. The grain flour is used externally to reduce topical inflammation, to remove rash and erythema, and to treat genital irritation in children resulting from contact with urine, and it is mixed with talc powder to prevent dryness of the skin . ... 

Collins, S.M. 2001. Stress and the gastrointestinal tract IV. Modulation of intestinal inflammation by stress basic mechanisms and clinical relevance. Am J Physiol 280 G315-G318. 

Modification of intestinal flora for increasing the predominance of specific nonpathogenic bacteria, and thereby alter the milieu in intestine, can have alternative therapeutic effects in intestinal inflammation and infections (Isolauri et al. 2002). 

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