Infection goblet cells

It is the quality rather than the quantity of the goblet cell response that is important in resistance to nematode infection, as even strains that are susceptible to I. muris (harbouring chronic infections) have a dramatic increase in the number of goblet cells and amount of mucus secreted during infection. Indeed, detailed analysis of the biochemical nature of... 

Ishikawa, N., Horii, Y. and Nawa, Y. (1993) Immune mediated alteration of the terminal sugars of goblet cell mucins in the small intestine of Nippostrongylus brasiliensis infected rats. Immunology 78, 303-307. 

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... 

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. 

Muc2 and Muc3, and mucin mRNA are coordinately upregulated in response to T. spiralis infection and may form the basis of an innate mucosal response independent of specific IFN-y, TNF and IL-4 cytokines. Importandy, this study also demonstrated that goblet cell hyperplasia and upregulated mucin secretion are not essential components of the protective immune response to GI helminths. 

Retinoic acid is required for the development of goblet mucous cells. A deficiency results in basal cell proliferation with increased keratini-zation of the epithelial structures. Mucus is one of the essential physical barriers (part of innate immunity) that prevents pathogens from entering the body. Therefore, a retinol deficiency increases the risk of infection. 

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