Activation of peripheral blood neutrophils from patients with active advanced tuberculosis

Activation of peripheral blood neutrophils (PMN) was investigated in order to determine whether they might contribute to the inflammatory process during active advanced tuberculosis. Receptors for the Fc portion of IgG (FcγR) (FcγRI, FcγRII, and FcγRIIIB), CD66 (degranulation marker), and receptors...

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Detalles Bibliográficos
Autores: de la Barrera, Silvia Susana, Sasiain, María del Carmen, Alemán, Mercedes, Beigier Bompadre, Macarena, Borghetti, Claudio, Abbate, Pablo Eduardo, Isturiz, Martín Amadeo
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2001
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/54743
Acceso en línea:http://hdl.handle.net/11336/54743
Access Level:acceso abierto
Palabra clave:Neutrophils
Tuberculosis
https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
Descripción
Sumario:Activation of peripheral blood neutrophils (PMN) was investigated in order to determine whether they might contribute to the inflammatory process during active advanced tuberculosis. Receptors for the Fc portion of IgG (FcγR) (FcγRI, FcγRII, and FcγRIIIB), CD66 (degranulation marker), and receptors for tumor necrosis factor-α (TNF-R55 and TNF-R75) were analyzed on PMN obtained from normal controls and tuberculosis patients (TB-PMN). Functional parameters such as cytotoxicity, superoxide anion generation triggered by N-formyl-methionyl-leucyl-phenyl-alanine (FMLP), and TNF-α and IL-1β production were evaluated. A high expression of TNF-R55, CD66, and FcγRIIIB and the appearance of FcγRI were detected in TB-PMN. In addition, cytotoxicity, superoxide anion release, and TNF-α and IL-1β production were enhanced in TB-PMN. Thus, in tuberculosis, the activation of PMN outside the focus of infection strongly suggests the possibility of a systemic inflammation that could modulate the inflammatory response.