title: Neutrophils from pulmonary tuberculosis patients show augmented levels of chemokines MIP-1α, IL-8 and MCP-1 which further increase upon in vitro infection with mycobacterial strains.
abstract: Neutrophils being innate cells initiate the immune defence against mycobacteria by sending signals to other immune cells. Chemokines being the vital link in signaling processes, it is of interest to study their secretion by neutrophils as a response to tuberculosis infection. The levels of various chemokines (MIP-1α, MCP-1, IL-8 and IP-10) and chemokine receptors (CXCR1, CXCR2 and CCR1) in neutrophils from healthy individuals and pulmonary tuberculosis patients were studied following infection with Mycobacterium tuberculosis strains (clinical--S7 and S10 and laboratory--H37Rv). The release of MIP-1α, IL-8 and MCP-1 is found to be greatly increased in patient neutrophils. Mycobacterial strains differentially influenced neutrophils affecting the release of chemokines to different extent. H37Rv significantly increased the release of MIP-1α and IL-8 in both normals and tuberculosis patients, while S10 up regulated only the release of MIP-1α in patients. Thus, during tuberculosis, neutrophils undergo functional alteration to combat infection. While H37Rv is greatly recognized by neutrophils and triggers the release of chemokines, clinical strains by some means try to suppress immune activation of neutrophils in their favor.
authors.affiliation: Department of Immunology, National Institute for Research in Tuberculosis, Chetput, Chennai 600031, India.
authors.forename: J Nancy
authors.initials: JN
authors.lastname: Hilda
authors.affiliation: Institute for Thoracic Medicine, Chetput, Chennai 600031, India.
authors.forename: Meenakshi
authors.initials: M
authors.lastname: Narasimhan
authors.affiliation: Department of Immunology, National Institute for Research in Tuberculosis, Chetput, Chennai 600031, India. Electronic address: sulochanadas@gmail.com.
authors.forename: Sulochana D
authors.initials: SD
authors.lastname: Das
mesh_terms: D000328:Adult; D018932:Chemokine CCL2 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D054405:Chemokine CCL3 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D054884:Host-Pathogen Interactions; D006801:Humans; D016209:Interleukin-8 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D061251:Primary Cell Culture; D054389:Receptors, CCR1 / Q000235:genetics / Q000276:immunology; D023062:Receptors, Interleukin-8A / Q000235:genetics / Q000276:immunology; D023063:Receptors, Interleukin-8B / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction; D014397:Tuberculosis, Pulmonary / Q000235:genetics / Q000276:immunology* / Q000382:microbiology / Q000473:pathology
chemical_list: C111835:CCL2 protein, human; C515429:CCL3 protein, human; C515300:CCR1 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D016209:Interleukin-8; D054389:Receptors, CCR1; D023062:Receptors, Interleukin-8A; D023063:Receptors, Interleukin-8B
keywords: Chemokine; Chemokine receptor; H37Rv; Mycobacterium; Neutrophil