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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Intestinal Lymph-Borne Factors Induce Lung Release of Inflammatory Mediators and Expression of Adhesion Molecules After an Intestinal Ischemic Insult

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Author(s):
Breithaupt-Faloppa, Ana Cristina ; Vitoretti, Luana Beatriz ; Cavriani, Gabriela ; Lino-dos-Santos-Franco, Adriana ; Sudo-Hayashi, Lia Siguemi ; Oliveira-Filho, Ricardo Martins ; Boris Vargaftig, B. ; Tavares-de-Lima, Wothan [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Inst Ciencias Biomed, Lab Fisiopatol Inflamacao Expt, Dept Pharmacol, BR-05508900 Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: JOURNAL OF SURGICAL RESEARCH; v. 176, n. 1, p. 195-201, JUL 2012.
Web of Science Citations: 9
Abstract

Background. Intestinal ischemia and reperfusion (I/R) is a documented cause of acute lung injury (ALI) and systemic inflammation. We previously reported that obstruction of thoracic lymphatic flow during intestinal I/R blunts pulmonary neutrophil recruitment and microvascular injury and decreases the systemic levels of tumor necrosis factor. Here, we consider the existence of a gut-lung axis promoting the induction of systemic inflammation, whereby drained intestinal lymph stimulates lung expression of adhesion molecules and matrix components and generation of inflammatory mediators. Material and Methods. Upon administration of anesthesia, male Wistar rats were subjected to occlusion of the superior mesenteric artery for 45 min, followed by 2 h of intestinal reperfusion (I/R); groups of rats were subjected to I/R with or without thoracic lymphatic duct ligation immediately before the procedure. The non-manipulated rats were used to investigate basal parameters. Results. Obstruction of thoracic lymphatic flow before intestinal I/R decreased the ability of cultured lung tissue explants to release IL-1 beta, IL-10, and VEGF. In contrast, lymphatic obstruction normalized the elevated lung expression of PECAM-1 caused by intestinal I/R. On the other hand, lung E-selectin expression was significantly reduced, whereas fibronectin expression and collagen synthesis were not affected. Lymph levels of LTB4 and TXB2 were found to be significantly increased. Conclusions. These data suggest that lymph factors drained from the intestine during ischemic trauma stimulate the lung to generate inflammatory mediators and alter the expression of adhesion molecules. Disturbances in lung homeostasis mediated by lymph might contribute to the spread of inflammatory processes, thereby accounting for the systemic inflammation induced by intestinal I/R. (C) 2012 Elsevier Inc. All rights reserved. (AU)

FAPESP's process: 07/07139-3 - The role of heme oxygenase 1 in different renal inflammatory process in experimental animal models
Grantee:Niels Olsen Saraiva Câmara
Support type: Research Projects - Thematic Grants
FAPESP's process: 05/02271-5 - Mechanisms underlying endothelial-leukocyte interaction after gut trauma and their relevance to acute lung injury: regulatory role of the lymphatic system
Grantee:Wothan Tavares de Lima
Support type: Regular Research Grants