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Effect of VIP on TLR2 and TLR4 Expression in Lymph Node Immune Cells During TNBS‐Induced Colitis
Author(s) -
ARRANZ ALICIA,
ABAD CATALINA,
JUARRANZ YASMINA,
TORROBA MARTA,
ROSIGNOLI FLORENCIA,
LECETA JAVIER,
GOMARIZ ROSA PÉREZ,
MARTÍNEZ CARMEN
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1317.001
Subject(s) - tlr2 , immune system , downregulation and upregulation , tlr4 , receptor , innate immune system , immunology , homeostasis , toll like receptor , intestinal mucosa , colitis , pattern recognition receptor , biology , cd8 , microbiology and biotechnology , inflammation , inflammatory bowel disease , medicine , disease , biochemistry , gene
Toll‐like receptors (TLRs) are a family of pattern recognition receptors (PRRs), which recognize numerous molecules collectively named pathogen‐associated molecular patterns, with an essential role in inflammatory conditions and connecting innate and acquired immune responses. Moreover, a new function of TLRs in the intestinal mucosa has been described. Under homeostatic conditions, TLRs act to protect the intestinal epithelium; but when homeostasis is disrupted, TLRs appear deregulated. Disruption of intestinal homeostasis occurs in disorders, such as Crohn's disease (CD). Trinitrobenzene sulfonic acid (TNBS)‐induced colitis is a murine model of human CD and vasoactive intestinal polypeptide (VIP) exerts a beneficial effect, by decreasing both inflammatory and autoimmune components of the disease. Recently, we have demonstrated the constitutive expression of TLR2 and TLR4 at mRNA and protein levels in colon extracts and their upregulation in TNBS‐treated mice as well as the effect of VIP treatment, approaching control levels. However, the systemic effect is little known. The present results demonstrate a beneficial role of VIP, restoring homeostatic conditions through the regulation of both lymphoid cell traffic and TLR2/4 expression on macrophages (MØ), dendritic cells (DCs), and CD4 and CD8 T lymphocytes.
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