Volume 11, Issue 7 pp. 674-684
Original Article

cDNA array analysis of cytokines, chemokines, and receptors involved in the development of tnbs-induced colitis: Homeostatic role of VIP

Catalina Abad PhD

Catalina Abad PhD

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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Yasmina Juarranz

Yasmina Juarranz

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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Carmen Martinez

Carmen Martinez

Department of Cell Biology, Faculty of Medicine, Complutense University, Madrid, Spain

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Alicia Arranz

Alicia Arranz

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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Florencia Rosignoli PhD

Florencia Rosignoli PhD

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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María García-Gómez

María García-Gómez

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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Javier Leceta

Javier Leceta

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

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Rosa P Gomariz

Corresponding Author

Rosa P Gomariz

Department of Cell Biology, Faculty of Biology, Complutense University, Madrid, Spain

Department of Cell Biology, Faculty of Biology, Complutense University, 28040 Madrid, SpainSearch for more papers by this author
First published: 14 December 2006
Citations: 9

Abstract

Crohn's disease (CD) is a chronic inflammatory pathology of the intestine, characterized by diarrhea and weight loss. A healing effect of vasoactive intestinal peptide (VIP) in the murine model of CD based on 2,4,6-trinitrobencene sulfonic acid (TNBS) administration has been previously shown. The aim of this work was to analyze the expression of several mediators related to the inflammatory cascade in colitic and VIP-treated animals. With this aim, mice received either only TNBS or TNBS and VIP treatment on alternate days. cDNA microarray analysis and real-time polymerase chain reaction were performed on total mRNA from colon to study the expression of a battery of proinflammatory molecules such as the enzyme COX-2, the chemokines CX3CL1, CXCL12, CXCL13, CXCL14, CCR5, and CXCR2, and the cytokines interleukin (IL)-1β, IL-12, IL-18, IL-10, interferon-γ, and IL-4. TNBS administration induced the expression of all the proinflammatory mediators studied, whereas VIP treatment reduced their levels, increasing the anti-inflammatory IL-10 and the TH2 cytokine IL-4, explaining its beneficial action through inhibition of the inflammatory/TH1 response. These data describe not only the relation of several proinflammatory mediators to the development of TNBS colitis, reporting their time-course, but also show the beneficial action of VIP in this model through complete blockage of the inflammatory cascade and recovery of the colon homeostasis, providing a potential new alternative for CD therapy.

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