期刊论文详细信息
Journal of Leukocyte Biology
Nitric oxide-dependent killing of Cryptococcus neoformans by B-1-derived mononuclear phagocyte
Eliver Eid Bou Ghosn1  Sandro Rogerio Almeida1  Montchilo Russo2 
[1] Departamento de Analises Clinicas e Toxicologicas, Faculdade de Ciências Farmacêuticas, Departamento de Analises Clinicas e Toxicologicas, Faculdade de Ciências Farmacêuticas, Departamento de Analises Clinicas e Toxicologicas, Faculdade de Ciências Farmacêuticas,;#Departamento de Imunologia, Universidade de São Paulo, Brazil #Departamento de Imunologia, Universidade de São Paulo, Brazil #Departamento de Imunologia, Universidade de São Paulo, Brazil
关键词: inflammation;    fungus;    lymphocyte;   
DOI  :  10.1189/jlb.1005603
学科分类:生理学
来源: Federation of American Societies for Experimental Biology
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【 摘 要 】

The role of B lymphocytes in protecting the host against pulmonary Cryptococcus neoformans infection is until now, uncertain. A recent study using B lymphocyte-deficient mice suggests that B lymphocytes play a protective role in cryptococcal infection. It has been well established that at least three B cell subsets, B-1a, B-1b, and B-2, are present in the mouse periphery. B-1 cells constitute a minor fraction of the B cell population in the spleen and are not detected in lymph nodes of mice. We demonstrated that B-1 cells migrate to a nonspecific, inflammatory focus and differentiate into macrophage-like cells. However, the role these cells might play on the kinetics and evolution of the inflammatory response and on fungal infection has not yet been established. Based on these data, we decided to investigate the interaction of B-1-derived mononuclear phagocytes (BDMP) with C. neoformans to elucidate the possible influence of this cell in the progression of the disease. In this study, we demonstrated that the BDMP cell internalized C. neoformans and that this process was mediated by complement receptor 3. Thus, our results showed that the BDMP cell was more fungicidal than a macrophage and up-regulated major histocompatibility complex type II and the CD86 costimulatory molecule with the production of proinflammatory cytokines. The phagocytosis of C. neoformans results in the nitric oxide (NO)-mediated death of the fungus, as demonstrated by experiments using NO synthase 2 knockout and aminoguanidine-treated, wild-type mice.

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