Crypt hyperplasia

In those infections that are associated with enteropathy (exemplified by T. spiralis), no experimental manipulation has, until recently, been able to separate enteropathy and immune expulsion - if one is abrogated, so is the other. This chapter illustrates how the two processes can be separated, and discusses implications of this for understanding immune expulsion of gut nematodes and the prospects for anti-nematode vaccines that cause no ill effects at either the initial induction of immunity or the expression of protective responses. The definition of that which consitututes enteropathy may vary between authors, but we take as our primary definition the most destructive and quantifiable changes in intestinal tissue that are associated with expulsion, villus atrophy and crypt hyperplasia. 

The morbidity and mortality that are often associated with human GI helminth infections reflect in part the nutritional consequences of diarrhoea and malabsorption, and the resulting malnutrition that can accentuate the effects of infection by suppressing the protective immune response as well as compromising intestinal repair (Ferguson et al., 1980 Keymer and Tarlton, 1991 Cooper et al, 1992). In experimental rodents the pathology associated with infection is characterized by villus atrophy, crypt hyperplasia, goblet cell hyperplasia and infiltration of the mucosa by a variety of... 

In contrast with other enteropathies, there is no evidence that IFN-y plays an important role in either protection or pathology in T. spiralis infections. Infections in mice treated with anti-IFN-y antibody or in IFN-yR-deficient mice (Rose et al., 1994 Lawrence et al., 1998) were comparable in time course and pathology to those in controls. However, crypt hyperplasia was reduced following immunodepletion of IFN-y in SCID mice infected... 

T. spiralis-infected control, showing crypt hyperplasia and villus atrophy (C) day 13 p.i. T. spiralis-infected TNF-R1, mice, showing normal appearance, similar to (A) (D) day 13 p.i. T. sp/ra//s-infected IL-4, mice, again showing a normal appearance. Bar represents 100 pm. Reproduced from Lawrence etal. (1998), with permission. 

Celiac disease is a genetically dependent disease. In people who are genetically predisposed, the consumption of cereal products containing gluten leads to atrophy of villi structure with compensational crypts hyperplasia and massive lymphocytic infiltration around the lamina propria of the mucosa. The consecutive introduction of gluten into the diet results in the recurrence of histopathological changes (Kaukinen et al., 2002). 

Altmann GG, Lala PK. 1991. Control of 1,2-dimethylhydrazine-induccd crypt hyperplasia by natural-killer cells and its relevance to carcinogenics. In Chemically induced cell proliferation Implications for risk assessment. New York, NY Wiley-Liss, Inc. 417-428. 

Rotaviruses are double-stranded wheel-shaped RNA viruses. These strains cause diarrhea by infecting the enterocyts of the villi in the small intestine. Changes to the villi include shortening of villus height, crypt hyperplasia, and mononuclear cell infiltration of the lamina propria. Diarrhea results from decreased absorption across intestinal mucosal surface. ... 

Coeliac disease. Also known as gluten-sensitive enteropathy (GSE). A lifelong intolerance to a protein fraction of grain (e.g. gluten of wheat), leading to intestinal villous atrophy and crypt hyperplasia and characterized by specific autoimmune responses against tissue transglutaminase. 

Patients with coeliac disease show the symptoms associated with malabsorption, often characterized by steatorrhoea (pale stools that float because of their high fat content) (22a). Malabsorption may have any number of causes, one of which is coeliac disease, a gluten-sensitive enteropathy. This disorder results in loss of villi, crypt hyperplasia and chronic inflammation of the small bowel mucosa. The immature cells of the small intestine are unable to absorb nutrients or to produce G1 hormones. This reduces pancreatic and bile secretion, which impedes fat absorption in the gut. Anaemia is caused by the folate and B12 deficiency due to impaired absorption (22b). Treatment of coeliac disease is by a gluten-free diet, steroids (to treat inflammation) and immunosuppressants (22c). People with unrecognized and untreated coeliac disease may have an increased risk of small bowel carcinoma. 

The B-lymphocytes may represent one of the preferential targets of ricin toxicity in vivo. Lymphatic tissues from animals exposed to ricin show extensive hyperplasia and cellular necrosis with edema, hyperemia, and hemorrhage (Waller et al., 1966). Rats injected (i.m.) with ricin or abrin develop numerous apoptotic-like bodies in ileal crypts, para-aortic lymph nodes, and Peyer s patches (Griffiths et al., 1987). The finding of apoptosis in whole animals may be due to a direct effect of ricin on cells of the lymphatic tissue, as is observed with isolated cells in vitro, or it may partly reflect the numerous pathological sequelae of toxin exposure, including severe shock (Griffiths et al., 1988 Howat, 1988). 

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