In Tuberculous Pleural Effusions, Activated Neutrophils Undergo Apoptosis and Acquire a Dendritic Cell–Like Phenotype
1Departamento de Inmunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, and 2División de Tisioneumonología, Hospital F. J. Muñiz, Buenos Aires, Argentina
Tuberculous pleuritis usually shows lymphocytic preponderance, but neutrophils are also present. Therefore, pleuritis is a good model for the study of neutrophil fate at sites of active Mycobacterium tuberculosis infection. We have previously demonstrated in vitro that M. tuberculosis–induced neutrophil apoptosis involves p38 mitogen protein kinase activation through Toll‐like receptor 2. Herein, we demonstrate that, in tuberculous pleuritis, neutrophil apoptosis increases together with the expression of Toll‐like receptor 2 and phosphorylated p38 (p‐p38) kinase. In addition, receptors associated with activation/apoptotis (CD11b, CD64, tumor necrosis factor receptor, and Fas ligand) are up‐regulated, together with a loss of CD16 expression. However, neutrophils express CD86, CD83, and major histocompatibility complex class II antigens, acquiring dendritic cell (DC) characteristics. Therefore, the cytokine milieu in the pleural space may influence signaling pathways on activated neutrophils, thereby inducing apoptosis and inhibiting their proinflammatory capacity, as well as allowing them acquire DC characteristics that influence the immune response.
Received 30 December 2004; accepted 12 March 2005; electronically published 28 June 2005.
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Online publication date: 1-Jan-2009.
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Online publication date: 1-Jul-2007.
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Financial support: Agencia Nacional de Promoción Científica y Tecnológica (ANPCyT, 05‐14060); Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET, PIP 0711/98).
Potential conflicts of interest: none reported.