Changes in interleukin-1 and tumor necrosis factor production by peripheral blood monocytes after specific bronchoprovocation test in occupational asthma

Am Rev Respir Dis. 1992 Aug;146(2):408-12. doi: 10.1164/ajrccm/146.2.408.

Abstract

The pathogenetic mechanisms of occupational asthma (OA) due to low-molecular-weight compounds have been poorly defined, and further studies are required to clarify the role of immunologic mechanisms in OA. Until now cellular mechanisms have been less investigated than humoral ones. We have evaluated interleukin-1 (IL-1) and tumor necrosis factor (TNF) production by peripheral blood monocytes (PBM), and peripheral T-cell subpopulations in 22 subjects with possible OA before and after specific bronchoprovocation test (SBPT). After SBPT, three subjects had an immediate reaction, seven a late reaction, and two a dual reaction. Ten subjects had no asthmatic reaction to SBPT. Spontaneous release of IL-1 from PBM did not change significantly after SBPT. TNF activity was increased 48 h after SBPT in immediate reactions and 72 h after SBPT in late-dual reactions. These results suggest that exposure to occupational agents may induce activation of PBM with increased spontaneous release of cytokines, such as TNF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / blood*
  • Asthma / diagnosis
  • Asthma / immunology
  • Bronchial Provocation Tests
  • Evaluation Studies as Topic
  • Humans
  • Hypersensitivity, Delayed / blood*
  • Hypersensitivity, Delayed / diagnosis
  • Hypersensitivity, Delayed / immunology
  • Hypersensitivity, Immediate / blood*
  • Hypersensitivity, Immediate / diagnosis
  • Hypersensitivity, Immediate / immunology
  • Interleukin-1 / metabolism*
  • Leukocyte Count
  • Methacholine Chloride
  • Middle Aged
  • Molecular Weight
  • Monocytes / metabolism*
  • Occupational Diseases / blood*
  • Occupational Diseases / diagnosis
  • Occupational Diseases / immunology
  • T-Lymphocyte Subsets
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-1
  • Tumor Necrosis Factor-alpha
  • Methacholine Chloride