In vitro ethanol suppresses alveolar macrophage TNF-alpha during simian immunodeficiency virus infection.

Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

In vitro ethanol suppresses alveolar macrophage TNF-alpha during simian immunodeficiency virus infection.

Am J Respir Crit Care Med. 2000 Jan;161(1):135-40. Unique Identifier : AIDSLINE MED/20087336
Stoltz DA; Nelson S; Kolls JK; Zhang P; Bohm RP Jr; Murphey-Corb M; Bagby GJ; Department of Medicine, Section of Pulmonary/Critical Care,; Alcohol Research Center, New Orleans, Louisiana, USA.

Abstract: Pulmonary infections are a significant cause of morbidity and mortality in patients with alcohol abuse and human immunodeficiency virus (HIV) infection, two immunocompromising conditions that frequently coexist. This study examined the separate and combined effects of in vivo lentiviral infection and in vitro alcohol exposure on alveolar macrophage (AM) production of tumor necrosis factor- alpha (TNF-alpha), a proinflammatory cytokine that is critical to normal pulmonary host defense. AMs, recovered by bronchoalveolar lavage (BAL) from uninfected and simian immunodeficiency virus (SIV)-infected rhesus macaques, at the asymptomatic and terminal stages of infection, were cultured in ethanol 2 h prior to stimulation with lipopolysaccharide (LPS). Median TNF-alpha concentrations were measured 15 h later. Spontaneous TNF-alpha production was similar in all groups examined. LPS increased TNF-alpha protein production similarly in SIV(-) (2, 381 +/- 359 pg/ml) and SIV(+) animals at the terminal stage of infection (2,019 +/- 507 pg/ml). In contrast, cells from SIV(+) asymptomatic animals had a depressed response (763 +/- 304 pg/ml). Ethanol (100 mM) suppressed the LPS-induced AM TNF-alpha response by approximately 50% in both SIV(-) and (+) animals. Ethanol-induced suppression of the TNF-alpha response occurred at a post-transcriptional level. These data suggest that ethanol-induced suppression of the pulmonary TNF-alpha response may further increase the susceptibility to and severity of secondary infectious complications in HIV-infected hosts.

Keywords: JOURNAL ARTICLE Animal Antibodies, Viral/ANALYSIS Biological Markers Bronchoalveolar Lavage Fluid/CHEMISTRY/CYTOLOGY Cells, Cultured Comparative Study CD4-CD8 Ratio DNA Primers/CHEMISTRY Ethanol/*PHARMACOLOGY Female Macaca mulatta Macrophages, Alveolar/DRUG EFFECTS/*METABOLISM Male Polymerase Chain Reaction RNA, Messenger/ANALYSIS Simian Acquired Immunodeficiency Syndrome/IMMUNOLOGY/*METABOLISM/ PATHOLOGY Support, U.S. Gov't, P.H.S. *SIV/IMMUNOLOGY Tumor Necrosis Factor/*ANTAGONISTS & INHIB/BIOSYNTHESIS/GENETICS
000530
A0052199

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