Impairment of neutrophil migration to remote inflammatory site during lung histoplasmosis

• Autor(a) principal: Medeiros, Alexandra Ivo de [UNESP]
• Data de Publicação: 2015
• Outros Autores: Secatto, Adriana, Belanger, Caroline, Sorgi, Carlos Artério, Borgeat, Pierre, Marleau, Sylvie, Faccioli, Lucia Helena
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://www.hindawi.com/journals/bmri/2015/409309/; http://hdl.handle.net/11449/129366

Histoplasma capsulatum (Hc) induces a pulmonary disease in which leukotrienes promote activation and recruitment of effectors cells. It is also well-recognized that leukotriene B 4 (LTB 4) and platelet-activating factor (PAF) induce leukocyte recruitment to inflammatory sites. We investigated the impact of pulmonary Hc infection on PMN migration to a remote inflammatory site. Our results show that pulmonary Hc infection impairs LTB4- or PAF-stimulated PMN recruitment to air pouch. Yet, remote inflammation did not modify PMN numbers in the bronchoalveolar lavage fluid (BALF) of Hc-infected mice. Interestingly, the concomitant administration of PAF and LTB 4 receptor antagonists inhibited PMN recruitment to both BALF and the remote site, demonstrating cooperation between both mediators. Along that line, our results show that PAF-elicited PMN chemotaxis was abrogated in 5-lipoxygenase-deficient animals. These results suggest caution in the indiscriminate use of anti-inflammatory drugs during infectious diseases.