Alveolar macrophages from patients with asbestos exposure release increased levels of leukotriene B4

Journal Article · Thu Jun 01 00:00:00 EDT 1989 · Am. Rev. Respir. Dis.; (United States)

DOI:https://doi.org/10.1164/ajrccm/139.6.1494· OSTI ID:5926143

Garcia, J G; Griffith, D E; Cohen, A B; Callahan, K S

The alveolar influx and subsequent activation of inflammatory cells such as neutrophils and eosinophils are believed to be important in the pathogenesis of many interstitial lung disorders, including asbestosis. Indices of lower respiratory tract abnormalities detected by bronchoalveolar lavage (BAL) were investigated in 93 asbestos-exposed workers as well as in smoking (n = 12) and nonsmoking (n = 10) control subjects. Patients with clinical asbestosis (n = 12) exhibited increases in both BAL neutrophils and BAL eosinophils, expressed as both percentage of total cells and total numbers, when compared to asbestos-exposed workers without asbestosis (n = 81) and control subjects. Significantly greater numbers of BAL neutrophils were also found in asbestos-exposed workers without asbestosis than in either smoking or nonsmoking control subjects. These abnormalities correlated significantly with in vitro BAL alveolar macrophage production of the potent leukocyte chemotaxin, leukotriene B4 (LTB4). For example, basal, unstimulated LTB4 production was 3.1 +/- 0.8 ng/10(6) alveolar macrophages for patients with asbestosis, 1.05 +/- 0.2 ng/10(6) cells in asbestos workers without asbestosis, 0.9 +/- 0.2 ng/10(6) cells in control nonsmokers, and 0.2 +/- 0.05 ng/10(6) cells in control smokers. Stimulated LTB4 release from BAL alveolar macrophages (A23187 or arachidonate) was even more pronounced in asbestos workers with or without asbestosis, suggesting an in vivo priming effect on alveolar macrophage synthesis of LTB4. Cell-free BAL supernatants from asbestos-exposed patients with or without asbestosis also contained significantly greater amounts of LTB4 than did those from control subjects, indicating enhanced in vivo production of this inflammatory mediator.

• Research Organization: Indiana Univ. School of Medicine, Indianapolis (USA)
• OSTI ID: 5926143
• Journal Information: Am. Rev. Respir. Dis.; (United States), Vol. 139:6
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ASBESTOS
TOXICITY
PROSTAGLANDINS
BIOSYNTHESIS
RESPIRATORY SYSTEM DISEASES
PATHOGENESIS
LAVAGE
MACROPHAGES
NEUTROPHILS
OCCUPATIONAL EXPOSURE
PATIENTS
PERSONNEL
TOBACCO SMOKES
AEROSOLS
ANIMAL CELLS
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BODY FLUIDS
COLLOIDS
CONNECTIVE TISSUE CELLS
DISEASES
DISPERSIONS
LEUKOCYTES
MATERIALS
PHAGOCYTES
RESIDUES
SMOKES
SOLS
SOMATIC CELLS
SYNTHESIS
560300* - Chemicals Metabolism & Toxicology