title: Expression of chemokines and induction of rapid cell death in human blood neutrophils by Mycobacterium tuberculosis.
abstract: To elucidate the role of neutrophils in the early inflammatory response to mycobacterial infection, expression of chemokines interleukin (IL)-8 and macrophage inflammatory protein-1alpha (MIP-1alpha) was examined in human blood neutrophils in response to the lipopolysaccharide (LPS) of Escherichia coli, which induces acute inflammation, or to Mycobacterium tuberculosis or purified protein derivative (PPD), which induce chronic mycobacterial inflammation. Neutrophils stimulated with LPS, M. tuberculosis, or PPD expressed both IL-8 and MIP-1alpha. Expression of IL-8 and MIP-1alpha was lower after stimulation with M. tuberculosis or PPD than after stimulation with LPS, but the kinetics of expression did not differ significantly. In contrast, both M. tuberculosis and PPD with tumor necrosis factor-alpha induced neutrophils to undergo rapid cell death, which might remove neutrophils and activate macrophages at sites of mycobacterial inflammation. The findings suggest that neutrophils play important roles in the host defense against mycobacterial infection.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kasahara
authors.forename: I
authors.initials: I
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Ogura
authors.forename: H
authors.initials: H
authors.lastname: Takeuchi
authors.forename: K
authors.initials: K
authors.lastname: Kobayashi
authors.forename: M
authors.initials: M
authors.lastname: Adachi
mesh_terms: D017209:Apoptosis; D002470:Cell Survival; D002478:Cells, Cultured; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007124:Immunoenzyme Techniques; D007375:Interleukin-1 / Q000494:pharmacology; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000235:genetics; D008070:Lipopolysaccharides / Q000276:immunology* / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis* / Q000235:genetics; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D009504:Neutrophils / Q000166:cytology / Q000276:immunology*; D012333:RNA, Messenger; D013997:Time Factors; D014373:Tuberculin / Q000276:immunology* / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D007375:Interleukin-1; D016209:Interleukin-8; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D014373:Tuberculin; D014409:Tumor Necrosis Factor-alpha