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Expansion of the humoral effector cell compartment of both systemic and mucosal immune systemsin a weanling murine model which duplicates critical features of human protein-energy malnutrition

Published online by Cambridge University Press:  09 March 2007

C.-L. Ha
Affiliation:
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, ON NIG 2 W1, Canada
L.E. Paulino
Affiliation:
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, ON NIG 2 W1, Canada
B.D. Woodward
Affiliation:
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, ON NIG 2 W1, Canada
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Abstract

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A direct comparison of systemic (spleen) and mucosal (intestine) antibody-producing systems was made in weanling male C57BL/6J mice subjected to wasting protein-energy malnutrition (PEM) by means of a low-protein protocol known to duplicate immunological and physiological features of human malnutrition. ELISA revealed low concentrations of biliary and gut lumen immunoglobulin (Ig) A in malnourished mice concomitantly with a high concentration of blood IgA. The low-protein model, therefore, exhibited fidelity to human protein-energy malnutrition in its influence on the concentrations of the mucosal Ig, IgA, in critical biological fluids. The number of IgA-, IgM- and IgG-containing cells was estimated morphometrically on a per organ basis. The low-protein protocol supported expansion in numbers of mucosal IgA-containing cells (18 x relative to a zero-time control group) and of splenic IgG- containing cells (135 x ), albeit an attenuated expansion in comparison with that of well-nourished control animals (132x and 571x respectively relative to zero-time controls). Up to terminal differentiation of Ig-containing cells, systemic and mucosal antibody-producing systems exhibited similarly remarkable resistance to wasting malnutrition. Epithelial transport of IgA may be an aspect of the mucosal antibody response which is particularly sensitive to PEM.

Type
immune response in malnutrition
Copyright
Copyright © The Nutrition Society 1996

References

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