title: Impaired cytokine production by neutrophils isolated from patients with AIDS.
abstract: OBJECTIVE
  To determine the ability of neutrophils isolated from HIV-seropositive patients to produce proinflammatory cytokines.
  
  
  METHODS
  The in vitro responsiveness of polymorphonuclear neutrophils (PMN) and peripheral blood mononuclear cells (PBMC) to lipopolysaccharide (LPS), used in the presence or absence of interferon (IFN)gamma, was determined in 47 HIV-positive patients with advanced stages of virus infection.
  
  
  METHODS
  Cytokines in cell-free supernatants were measured by enzyme-linked immunosorbent assay or radioimmunoassay.
  
  
  RESULTS
  Cell-free supernatants from PMN isolated from the peripheral blood of HIV-positive patients and stimulated with LPS contained increased amounts of tumour necrosis factor (TNF)-alpha and interleukin (IL)-8 with respect to supernatants obtained from PMN of normal donors. In contrast, release of IL-1beta and IL-1ra (IL-1 receptor antagonist) in response to LPS, or LPS plus IFNgamma, was found to be lower in PMN from HIV-positive patients than in PMN from controls, but was significant only in the case of IL-1ra. Furthermore, the release of IL-12 induced by LPS or LPS plus IFNgamma did not significantly differ between PMN from HIV-positive patients and healthy donors. Concerning PBMC, the production of TNF-alpha and IL-12 in response to LPS, or LPS plus IFNgamma, was found to be significantly higher in cells isolated from HIV-positive patients, whereas the release of IL-1beta was significantly lower. In the case of IL-8, no statistically significant difference was found between PBMC isolated from HIV-positive patients and healthy donors.
  
  
  CONCLUSIONS
  Collectively, the data suggest that in HIV-positive patients with advanced stages of disease, the ability of PMN to produce specific cytokines in response to LPS is significantly altered. Alterations in this ability might contribute to the evolution of HIV disease.
authors.affiliation: Department of General Pathology, University of Verona, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Gasperini
authors.forename: R
authors.initials: R
authors.lastname: Zambello
authors.forename: C
authors.initials: C
authors.lastname: Agostini
authors.forename: L
authors.initials: L
authors.lastname: Trentin
authors.forename: C
authors.initials: C
authors.lastname: Tassinari
authors.forename: P
authors.initials: P
authors.lastname: Cadrobbi
authors.forename: G
authors.initials: G
authors.lastname: Semenzato
authors.forename: M A
authors.initials: MA
authors.lastname: Cassatella
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D054407:Chemokine CCL4; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D005260:Female; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D053590:Interleukin 1 Receptor Antagonist Protein; D007378:Interleukins / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000096:biosynthesis; D008297:Male; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology*; D011863:Radioimmunoassay; D012795:Sialoglycoproteins / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D054407:Chemokine CCL4; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007378:Interleukins; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma