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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Depression in the quantity of intestinal secretory IgA and in the expression of the polymeric immunoglobulin receptor in caloric deficiency of the weanling mouse.

The objective of this investigation was to determine the influence of weanling caloric restriction on the expression of the polymeric immunoglobulin receptor ( pIgR) in the liver and intestine and on the levels of IgA in the blood and intestinal secretions. Male C57BL/6J mice were allocated to a zero-time control group (19 days of age) or to groups fed for 14 days as follows: ad libitum intake of a complete purified diet (19% crude protein, 17 kJ/g gross energy) or restricted intake of a complete diet. Enzyme-linked immunosorbent assays revealed a low concentration of gut luminal immunoglobulin A (IgA) despite a normal concentration of serum IgA in the malnourished mice. The concentration and total quantity per organ of the pIgR were assessed in the liver and intestine by means of Western immunoblotting using an antiserum raised against the secretory component portion of rat pIgR. Malnourished animals exhibited low quantities of hepatic and intestinal pIgR relative to well-nourished controls (8% and 40% of control, respectively) and also exhibited a low concentration (soluble protein basis) of hepatic pIgR (39% of control). The concentration of biliary secretory component was also low in the malnourished animals (20% of well nourished). Despite the low quantity of hepatic pIgR, Western blotting revealed no change in the concentration of monomeric, dimeric, and polymeric forms of serum IgA in the malnourished group relative to well-nourished animals. Caloric deficiency in an experimental system that closely resembles human marasmus results in a decrease in the quantity of the pIgR that is sufficient to account for the low concentration of IgA in the mucous secretions of the intestine. Considered together with recent evidence pertaining to weanling protein deficiency, these results permit the conclusion that the pIgR is a focal point of the impact exerted by metabolically diverse forms of protein-energy malnutrition on mucosal humoral immunocompetence.[1]


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