PMID- 19925828 OWN - NLM STAT- MEDLINE DCOM- 20100611 LR - 20220317 IS - 1879-0542 (Electronic) IS - 0165-2478 (Linking) VI - 128 IP - 1 DP - 2010 Jan 18 TI - Regionalization of pIgR expression in the mucosa of mouse small intestine. PG - 59-67 LID - 10.1016/j.imlet.2009.11.005 [doi] AB - Few reports exist on the differences in cell populations or immunological functions between the proximal and distal segments of the small intestine (SI). In the current contribution we analyzed the expression of the polymeric immunoglobulin receptor (pIgR) and alpha chains as well as the density of IgA-producing cells from the proximal and distal intestinal segments from Balb/c mice. Furthermore, by using real-time RT-PCR we quantified the expression of cytokines (TNF-alpha, IFN-gamma, IL-4 and TGF-beta), Toll-like receptor-4 (TLR-4), and the glucocorticoid receptor (GR) involved in pIgR expression in intestinal epithelial cells (IEC). In this study, for the first time it has been demonstrated that the expression of the pIgR as well as alpha chain was greater in the proximal than the distal segment of the small intestine of normal mice. Moreover, we found striking differences in the expression of cytokines at the different intestinal compartments. Whereas the expression of TNF-alpha, IFN-gamma and TGF-beta was higher in lamina propria lymphocytes (LPL) of the distal than proximal segment, it was higher in IEC of the proximal than distal segment. In contrast, the expression of the gene for IL-4 was higher in the LPL of the proximal segment and the IEC of the distal segment. Although the overall expression of TNF-alpha, IL-4, IFN-gamma and TGF-beta was higher in the whole mucosa of the distal than proximal segment, we propose that cytokines produced by epithelial cells (TNF-alpha, IFN-gamma and TGF-beta) autocrinally up-regulate the expression of mRNA for the pIgR. Finally the expression of the GR was higher in the proximal segment, while the expression of the gene for TLR-4 was significantly higher in the IEC of the distal than proximal segment. The higher expression of pIgR found in the proximal segment is probably related to the effect on epithelial cells of the higher production of TNF-alpha, IFN-gamma and TGF-beta, as well as the higher expression of the glucocorticoid receptors. The increased expression of pIgR in the proximal segment appears primarily responsible for the increased secretory IgA levels in the small intestine of mice. These results confirm and extend previous findings supporting the compartmentalization of the intestinal immune system. FAU - Resendiz-Albor, Aldo A AU - Resendiz-Albor AA AD - Seccion de Estudios de Postgrado e Investigacion, Laboratorio de Inmunidad de Mucosas, Escuela Superior de Medicina, Instituto Politecnico Nacional, Plan de San Luis y Diaz Miron, Mexico, D.F., Mexico. FAU - Reina-Garfias, Humberto AU - Reina-Garfias H FAU - Rojas-Hernandez, Saul AU - Rojas-Hernandez S FAU - Jarillo-Luna, Adriana AU - Jarillo-Luna A FAU - Rivera-Aguilar, Victor AU - Rivera-Aguilar V FAU - Miliar-Garcia, Angel AU - Miliar-Garcia A FAU - Campos-Rodriguez, Rafael AU - Campos-Rodriguez R LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091117 PL - Netherlands TA - Immunol Lett JT - Immunology letters JID - 7910006 RN - 0 (Antibodies) RN - 0 (Cytokines) RN - 0 (Immunoglobulin A) RN - 0 (Receptors, Glucocorticoid) RN - 0 (Receptors, Polymeric Immunoglobulin) SB - IM MH - Animals MH - Antibodies MH - Apoptosis MH - B-Lymphocytes/immunology/metabolism/pathology MH - Cells, Cultured MH - Cytokines/metabolism MH - Immunization, Passive MH - Immunoglobulin A/immunology/*metabolism MH - Intestinal Mucosa/immunology/*metabolism/pathology MH - Intestine, Small/immunology/*metabolism MH - Mice MH - Mice, Inbred BALB C MH - Organ Specificity MH - Protein Structure, Tertiary/genetics MH - Rabbits MH - Receptors, Glucocorticoid/metabolism MH - Receptors, Polymeric Immunoglobulin/genetics/immunology/*metabolism MH - Signal Transduction MH - Spleen/immunology/metabolism/pathology EDAT- 2009/11/21 06:00 MHDA- 2010/06/12 06:00 CRDT- 2009/11/21 06:00 PHST- 2009/03/31 00:00 [received] PHST- 2009/10/20 00:00 [revised] PHST- 2009/11/10 00:00 [accepted] PHST- 2009/11/21 06:00 [entrez] PHST- 2009/11/21 06:00 [pubmed] PHST- 2010/06/12 06:00 [medline] AID - S0165-2478(09)00274-0 [pii] AID - 10.1016/j.imlet.2009.11.005 [doi] PST - ppublish SO - Immunol Lett. 2010 Jan 18;128(1):59-67. doi: 10.1016/j.imlet.2009.11.005. Epub 2009 Nov 17.