Immune receptors and adhesion molecules in human pulmonary leptospirosis


Autoria(s): Bernardi, Fabiola Del Carlo; Ctenas, Bruno; Ferraz da Silva, Luiz Fernando; Nicodemo, Antonio Carlos; Nascimento Saldiva, Paulo Hilario; Dolhnikoff, Marisa; Mauad, Thais
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

19/09/2013

19/09/2013

2012

Resumo

Pulmonary involvement in leptospirosis has been increasingly reported in the last 20 years, being related to the severity and mortality of the disease. The pathogenesis of pulmonary hemorrhage in leptospirosis is not understood. Lung endothelial cells have been proposed as targets in the pathogenesis of lung involvement in leptospirosis through the activation of Toll-like receptor 2 or the complement system, which stimulates the release of cytokines that lead to the activation of adhesion molecules. The aim of this study was to investigate the involvement of immune pathways and of the intercellular and vascular cell adhesion molecules (intercellular adhesion molecule and vascular cell adhesion molecule, respectively) in the lungs of patients with pulmonary involvement of leptospirosis. We studied the lungs of 18 patients who died of leptospirosis and compared them with 2 groups of controls: normal and noninfectious hemorrhagic lungs. Using immunohistochemistry and image analysis, we quantified the expression of the C3a anaphylatoxin receptor, intercellular adhesion molecule, vascular cell adhesion molecule, and Toll-like receptor 2 in small pulmonary vessels and in the alveolar septa. There was an increased expression of intercellular adhesion molecule (P <.03) and C3a anaphylatoxin receptor (P <.008) in alveolar septa in the leptospirosis group compared with the normal and hemorrhagic controls. In the vessels of the leptospirosis group, there was an increased expression of intercellular adhesion molecule (P=.004), vascular cell adhesion molecule (P=.030), and Toll-like receptor 2 (P=.042) compared with the normal group. Vascular cell adhesion molecule expression in vessels was higher in the leptospirosis group compared with the hemorrhagic group (P=.015). Our results indicate that immune receptors and adhesion molecules participate in the phenomena leading to pulmonary hemorrhage in leptospirosis. (C) 2012 Elsevier Inc. All rights reserved.

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)

Identificador

HUMAN PATHOLOGY, PHILADELPHIA, v. 43, n. 10, supl. 1, Part 1, pp. 1601-1610, OCT, 2012

0046-8177

http://www.producao.usp.br/handle/BDPI/33470

10.1016/j.humpath.2011.11.017

http://dx.doi.org/10.1016/j.humpath.2011.11.017

Idioma(s)

eng

Publicador

W B SAUNDERS CO-ELSEVIER INC

PHILADELPHIA

Relação

HUMAN PATHOLOGY

Direitos

closedAccess

Copyright W B SAUNDERS CO-ELSEVIER INC

Palavras-Chave #ADHESION MOLECULES #AUTOPSY #INNATE IMMUNITY #LEPTOSPIROSIS #LUNG HEMORRHAGE #OUTER-MEMBRANE PROTEINS #CELL-ADHESION #HEMORRHAGE #MECHANISM #IMMUNOGLOBULIN #INTERROGANS #COMPLEMENT #DEPOSITION #INFECTION #PATHOLOGY #PATHOLOGY
Tipo

article

original article

publishedVersion