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Closed Access item Caloric restriction reduces IgA levels and modifies cytokine mRNA expression in mouse small intestine
Berral de la Rosa, Francisco J.
|Keywords:||Caloric restriction, Secretory IgA, Polymeric immunoglobulin receptor, Cytokines, Mucosal immune response|
|Citation:||Journal of Nutritional Biochemistry 22(6): 560-566 (2010)|
|Abstract:||The aim of this study was to determine the effect of caloric restriction (CR) in mouse small intestine on the production and secretion of immunoglobulin (Ig) A, the population of lymphocytes in the lamina propria, and the expression of cytokines that mediate and regulate innate and adaptive immunity. One group of young Balb/c mice was fed ad libitum, while the CR group was fed ad libitum and fasted on alternate days. When mice were six months old, IgA levels in the proximal small intestine were quantified by enzyme-linked immunosorbent assay, while the number of IgA containing cells, CD4+ T cells and CD8+ T cells in the duodenal mucosa was determined by immunohistochemistry. Furthermore, the expression of several intestinal cytokines, the genes for α-chain IgA, and the polymeric Ig receptor (pIgR) were analyzed by real-time polymerase chain reaction. CR decreased the levels of IgA in the intestine, apparently a consequence of a reduced number of IgA+ cells in the lamina propria that decrease the production and secretion of this Ig, and a reduced secretion of S-IgA into the bile, which in turn discharges into the proximal intestine. Contrarily, CR increased the expression of genes for α-chain IgA, and the pIgR, indicating that transport of IgA was not a key factor in the decrease of this Ig. Additionally, CR modified the expression of genes for tumor necrosis factor-α, interferon-γ, tumor growth factor-β, interleukin (IL)-2 and IL-10, all of which regulate the synthesis of IgA and pIgR, the inflammatory response, and the immune response in the intestine.|
|Description:||7 páginas, 7 figuras, 2 tablas.|
|Publisher version (URL):||http://dx.doi.org/10.1016/j.jnutbio.2010.04.012|
|E-ISSNmetadata.dc.identifier.doi = DOI:||1873-4847|
|Appears in Collections:||(CABD) Artículos|
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