title: Enhanced interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha production by LPS stimulated human monocytes isolated from HIV+ patients.
abstract: Periodontal disease and tooth loss is a common finding among advanced HIV+ patients. In addition to local oral lipopolysaccharide (LPS) stimulation, systemic up-regulation of monocyte pro-inflammatory cytokine secretion may also be involved in the pathogenesis of HIV disease. A study was undertaken to investigate IL-1beta, IL-6 and TNF-alpha production by resting and LPS stimulated monocytes isolated from HIV+ patients and also to investigate the relationship of the patient's HIV viral load status to the cytokine production. Whole blood samples in EDTA were collected from 39 HIV-1 infected patients and 20 age and sex matched uninfected controls. Plasma was separated by centrifugation. Viral load was determined using a quantitative RT-PCR. Monocytes were isolated by Ficoll-hypaque gradient separation followed by overnight plastic adherence. Cultured monocytes (1x10(6)/ml) were stimulated with LPS (1 microg/ml) of either P. gingivalis or F. nucleatum for 2, 8, 24 and 48 h and supernatant fluids were collected. IL-1beta, IL-6, and TNF-alpha levels in supernatant fluids were estimated by ELISA. Increased overall production of IL-1beta, IL-6 and TNF-alpha by LPS stimulated monocytes isolated from HIV-1 infected patients was observed when compared to HIV-1 uninfected controls. LPS stimulated monocytes from HIV-1 infected patients with high viral load (HVL) produced significant (p<0.05) elevations in these pro-inflammatory cytokines when compared to HIV-1 uninfected controls. Both LPS of P. gingivalis and F. nucleatum produced a comparable cytokine production by monocytes after 8 h of stimulation. These data suggest that enhanced IL-1beta, IL-6 and TNF-alpha is produced by monocytes/macrophages isolated from HVL HIV+ patients and may be involved in the overall pathogenesis of HIV-1 infection.
authors.affiliation: Department of Oral Medicine, Dental School University of Maryland, Baltimore 21201, USA.
authors.forename: A A
authors.initials: AA
authors.lastname: Baqui
authors.forename: M A
authors.initials: MA
authors.lastname: Jabra-Rizk
authors.forename: J I
authors.initials: JI
authors.lastname: Kelley
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.forename: W A
authors.initials: WA
authors.lastname: Falkler
authors.forename: T F
authors.initials: TF
authors.lastname: Meiller
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005260:Female; D016967:Fusobacterium nucleatum / Q000276:immunology; D015658:HIV Infections / Q000276:immunology*; D015497:HIV-1; D006801:Humans; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D007375:Interleukin-1 / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000096:biosynthesis*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000276:immunology*; D016966:Porphyromonas gingivalis / Q000276:immunology; D012367:RNA, Viral / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D014766:Viremia / Q000276:immunology
chemical_list: D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D012367:RNA, Viral; D014409:Tumor Necrosis Factor-alpha