Cells goblet

Mucus Viscous glycoprotein, proteoglycan secretion of goblet cells and... 

Sibley, D.A., Grisham, M.B. and Specian, KD. (1991). The generation of bactericidal and cytotoxic oxidants by goblet cell intestinal peroxidase. Gastroenterology 100, A841. 

Precellular solute ionization dictates membrane permeability dependence on mucosal pH. Therefore, lumenal or cellular events that affect mucosal microclimate pH may alter the membrane transport of ionizable solutes. The mucosal microclimate pH is defined by a region in the neighborhood of the mucosal membrane in which pH is lower than in the lumenal fluid. This is the result of proton secretion by the enterocytes, for which outward diffusion is slowed by intestinal mucus. (In fact, mucosal secretion of any ion coupled with mucus-restricted diffusion will provide an ionic microclimate.) Important differences in solute transport between experimental systems may be due to differences in intestinal ions and mucus secretion. It might be anticipated that microclimate pH effects would be less pronounced in epithelial cell culture (devoid of goblet cells) transport studies than in whole intestinal tissue. 

Figure 2 Comparison of intestinal epithelial cells in culture and in situ. (A) Human colon Caco-2 cells grown in culture for 16 days on a semiporous filter. (B) Epithelial layer of rat jejunum. AP, apical or luminal membrane B, basal or abluminal membrane BM, basement membrane G, goblet cell LS, lateral space mv, microvilli Nu, nucleus TJ, tight junction. Bars equal 10 pm. 

FIGURE 24.3 Distribution of CBP. (a) Analysis of tissue distribution by Western blotting, (b) Immunohistochemistry of the midgut epithelium. CBP was not detected in the goblet cells (G) of the midgut epithelium, which are thought to be involved in ion transport. 

The goblet cells produce mucus. The absorptive cells, found in a single layer covering the villi, are far more abundant. Taken together, the villi increase the absorptive surface area another 10-fold. 

Phillips, T.E., Phillips, T.H. and Neutra, M.H. (1984) Regulation of intestinal goblet cell secretion. IV. Electrical field stimulation in vitro. American Journal of Physiology 247, G682—G687. 

Specian, R.D. and Neutra, M.R. (1980) Mechanism of rapid mucus secretion in goblet cells stimulated by acetylcholine. Journal of Cell Biology 85, 626-640. 

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. 

Leblond, C.P. and Messier, B. (1958) Renewal of chief cells and goblet cells in the small intestine as shown by radioautography after injection of thymidine-H3 into mice. Anatomical Record 132, 49—58. 

Paulus, U., Loeffler, M., Zeidler, J., Owen, G. and Potten, C.S. (1993) The differentiation and lineage development of goblet cells in the murine small intestinal crypt experimental and modelling studies. Journal of Cell Science 106, 473-484. 

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. 

Tomita, M., Itoh, H., Ishikawa, N., Higa, A., Ide, H., Murakumo, Y., Maruyama, H., Koga, Y. and Nawa, Y. (1995) Molecular cloning of mouse intestinal trefoil factor and its expression during goblet cell changes. Biochemistry Journal 311, 293-297. 

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