RGD Reference Report - Lymphatic-borne IL-1beta and the inducible isoform of nitric oxide synthase trigger the bronchial hyporesponsiveness after intestinal ischema/reperfusion in rats.

General

Lymphatic-borne IL-1beta and the inducible isoform of nitric oxide synthase trigger the bronchial hyporesponsiveness after intestinal ischema/reperfusion in rats.
Authors:	Coelho, FR Cavriani, G Soares, AL Teixeira, SA Almeida, PC Sudo-Hayashi, LS Muscara, MN Oliveira-Filho, RM Vargaftig, BB Tavares-de-Lima, W
Citation:	Coelho FR, etal., Shock. 2007 Dec;28(6):694-9.
RGD ID:	4891947
Pubmed:	PMID:17607157 (View Abstract at PubMed)
DOI:	DOI:10.1097/shk.0b013e318053621d (Journal Full-text)
Intestinal I/R (i-I/R) is an insult associated to further adult respiratory distress syndrome and multiple organ failure. This study was designed to evaluate the repercussions of i-I/R on bronchial reactivity to the cholinergic agent methacholine. Anesthetized rats were subjected to superior mesenteric artery occlusion (45 min) and killed after clamp release and defined intestinal reperfusion periods (30 min, 2, 4, or 24 h). Intestinal I/R caused a progressive bronchial hyporesponsiveness (BHR) that was maximal upon 2 h but reverted within 24 h of intestinal reperfusion. The BHR observed at 2-h i-I/R was prevented by NOS inhibitors (N-L-nitroarginine methyl ester and aminoguanidine) or the KATP channel blocker glibenclamide. Moreover, 2-h i-I/R increased the pulmonary iNOS mRNA expression, a fact prevented by lymphatic thoracic duct ligation. The methacholine reactivity of 2-h i-I/R bronchial segments incubated with NOS inhibitors or glibenclamide was similar to that of naive tissues. In vivo blockade of IL-1beta receptors or lymphatic duct ligation before 2-h i-I/R both abolished BHR. Incubation of naive bronchial segments with lymph collected from 2-h i-I/R rats determined BHR, an effect fully preventable by ex vivo blockade of IL-1beta receptors. Incubation of naive bronchial segments with IL-1beta, but not with IL-10 or TNF-alpha, significantly induced BHR that was prevented by N-L-nitroarginine methyl ester. Our data suggest that a gut ischemic insult generates IL-1beta that, upon reperfusion, travels through the lymph into the lungs. In this tissue, IL-1beta would stimulate the generation of NO that orchestrates the ensuing BHR for which the opening of KATP channels seems to play a pivotal role.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
Bronchial Hyperreactivity		ISO	Nos2 (Rattus norvegicus)	4891947; 4891947	associated with Reperfusion Injury	RGD
Bronchial Hyperreactivity		IMP		4891947	associated with Reperfusion Injury	RGD

Objects Annotated

Genes (Rattus norvegicus)

Nos2 (nitric oxide synthase 2)

Genes (Mus musculus)

Nos2 (nitric oxide synthase 2, inducible)

Genes (Homo sapiens)

NOS2 (nitric oxide synthase 2)

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Lymphatic-borne IL-1beta and the inducible isoform of nitric oxide synthase trigger the bronchial hyporesponsiveness after intestinal ischema/reperfusion in rats.