# Tachykinin NK1 receptors are involved in proteinase-activated receptor (PAR)-2-mediated colonic inflammation in mice

Nicolas Cenac, Bruno Guiard, Rafael Garcia Villar, Jean Fioramonti, Lionel

Bueno

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Nicolas Cenac, Bruno Guiard, Rafael Garcia Villar, Jean Fioramonti, Lionel Bueno. Tachykinin NK1 receptors are involved in proteinase-activated receptor (PAR)-2-mediated colonic inflammation in mice. 9th United European Gastroenterology Week (UEGW 2001), Oct 2001, Amsterdam, Netherlands. 2001, Gut 49 (5 Suppl.3). hal-01600602

HAL Id: hal-01600602

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Submitted on 4 Jun 2020

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GASTROENTERO-
GY

Gut

An International Journal of

Gastroenterology and Hepatology

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HEPATOLOGY

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See inside back cover for the UEGW abstract CD-ROM

Abstracts.

9th. United European Gastroenterology week

UEGW 2001

240 pp.

in: Gut 49 (5 Suppl. 3)
Submitted Abstract Data

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abstract nr.: 2834

TACHYKININ NK1 RECEPTORS ARE INVOLVED IN PROTEINASE-ACTIVATED RECEPTOR (PAR)-2-MEDIATED COLONIC INFLAMMATION IN MICE

**Author:** CENAC, N, INRA, TOULOUSE, France

**Co-author(s):** GUIARD, B
GARCIA-VILLAR, R
FIORAMONTI, J
BUENO, L

**Keyword:** (S69, S64) IBD pathogenesis / diagnosis

We showed that intracolonic infusion to mice of PAR-2 activating peptide SLIGRL provoked colonic inflammation probably by a neurogenic mechanism. This study characterizes PAR-2-induced inflammation by investigating: (i) response kinetics; (ii) mucosal permeability changes; (iii) involvement of NK1-receptors.

Groups of 6-8 male Swiss mice (26-31g) were infused (50µl) intracolonically with SLIGRL (100µg/mouse) or saline (controls): (i) Five groups received SLIGRL: colons collected at 0, 2, 4, 10, 24h, for histology and myeloperoxidase assay (U/g-protein); (ii) Four received SLIGRL (or saline) followed by 51Cr-EDTA (2x106cpm-75µL/h) between 0-2h or 2-4h: blood collected at 2 or 4h for radioactivity counting; (iii) Four received SLIGRL (or saline), and NK1-antagonist SR140333 (60µg/mouse, IP) or vehicle; colons collected at 4h for myeloperoxidase assay.

At 4h after SLIGRL infusion, there is a significant increase in microscopic dammage and myeloperoxidase activity compared with controls (334.4±70.3 vs 42,4±10.1), for other time (2, 10, 24h after SLIGRL infusion) no significant difference.

Permeability was enhanced from 2 to 4h by 94.6% after SLIGRL
the NK1 antagonist SR140333 prevented SLIGRL-induced myeloperoxidase increase
(236.3±21.9 vs 1030.0±147.5; p<0.01)

We conclude that activation of colonic PAR-2 induces NK1-receptor-mediated
inflammation after 2h which resolved at 10h, with subsequent alteration of mucosal
permeability.

**Presentation Preference:** Oral Presentation

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