Activation of peripheral blood neutrophils from patients with active advanced tuberculosis

Copyright 2001 Academic Press.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 100(2001), 1 vom: 10. Juli, Seite 87-95
1. Verfasser: Alemán, M (VerfasserIn)
Weitere Verfasser: Beigier-Bompadre, M, Borghetti, C, de la Barrera, S, Abbate, E, Isturiz, M, Sasiain, M C
Format: Aufsatz
Sprache:English
Veröffentlicht: 2001
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Antigen-Antibody Complex Antigens, CD Antigens, Differentiation CD66 antigens Cell Adhesion Molecules Immunoglobulin G Interleukin-1 Receptors, IgG mehr... Receptors, Tumor Necrosis Factor Receptors, Tumor Necrosis Factor, Type I Tumor Necrosis Factor-alpha Superoxides 11062-77-4 N-Formylmethionine Leucyl-Phenylalanine 59880-97-6
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100 1 |a Alemán, M  |e verfasserin  |4 aut 
245 1 0 |a Activation of peripheral blood neutrophils from patients with active advanced tuberculosis 
264 1 |c 2001 
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500 |a Date Revised 30.11.2018 
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500 |a Citation Status MEDLINE 
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520 |a 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 (FcgammaR) (FcgammaRI, FcgammaRII, and FcgammaRIIIB), CD66 (degranulation marker), and receptors for tumor necrosis factor-alpha (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-alpha and IL-1beta production were evaluated. A high expression of TNF-R55, CD66, and FcgammaRIIIB and the appearance of FcgammaRI were detected in TB-PMN. In addition, cytotoxicity, superoxide anion release, and TNF-alpha and IL-1beta 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 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Antigen-Antibody Complex  |2 NLM 
650 7 |a Antigens, CD  |2 NLM 
650 7 |a Antigens, Differentiation  |2 NLM 
650 7 |a CD66 antigens  |2 NLM 
650 7 |a Cell Adhesion Molecules  |2 NLM 
650 7 |a Immunoglobulin G  |2 NLM 
650 7 |a Interleukin-1  |2 NLM 
650 7 |a Receptors, IgG  |2 NLM 
650 7 |a Receptors, Tumor Necrosis Factor  |2 NLM 
650 7 |a Receptors, Tumor Necrosis Factor, Type I  |2 NLM 
650 7 |a Tumor Necrosis Factor-alpha  |2 NLM 
650 7 |a Superoxides  |2 NLM 
650 7 |a 11062-77-4  |2 NLM 
650 7 |a N-Formylmethionine Leucyl-Phenylalanine  |2 NLM 
650 7 |a 59880-97-6  |2 NLM 
700 1 |a Beigier-Bompadre, M  |e verfasserin  |4 aut 
700 1 |a Borghetti, C  |e verfasserin  |4 aut 
700 1 |a de la Barrera, S  |e verfasserin  |4 aut 
700 1 |a Abbate, E  |e verfasserin  |4 aut 
700 1 |a Isturiz, M  |e verfasserin  |4 aut 
700 1 |a Sasiain, M C  |e verfasserin  |4 aut 
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