Effect of corticosteroid treatment on interleukin-1 and tumour necrosis factor secretion by monocytes from subjects with asthma

Clin Exp Allergy. 1992 Mar;22(3):365-70. doi: 10.1111/j.1365-2222.1992.tb03097.x.

Abstract

Peripheral blood monocytes (PBM) may be activated in asthmatic patients, a condition usually reverted by corticosteroid (CS) treatment. In the present research we have evaluated the spontaneous or lipopolysaccharide (LPS)-induced production of interleukin 1 (IL-1) and tumour necrosis factor (TNF) by PBM obtained from 14 asthmatic subjects during an asthmatic attack and after 1 week of CS treatment. The control group included 20 healthy volunteers. PBM obtained during severe asthma showed a pattern of IL-1 and TNF secretion similar to that of normal subjects. After CS treatment, IL-1 levels did not change significantly in comparison to baseline values, while LPS-induced TNF production was apparently related to the degree of airway obstruction after CS treatment. In fact, TNF production by PBM from CS-responsive subjects was significantly decreased in comparison to the levels determined before CS treatment, while PBM from CS-resistant subjects produced the same cytokine levels regardless of CS treatment. The present study suggests that the determination of LPS-induced TNF secretion by PBM could be used to confirm the effectiveness of CS treatment in asthma.

MeSH terms

  • Adrenal Cortex Hormones / therapeutic use*
  • Adult
  • Asthma / blood*
  • Asthma / drug therapy
  • Cells, Cultured
  • Forced Expiratory Volume / drug effects
  • Humans
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / metabolism*
  • Lipopolysaccharides
  • Middle Aged
  • Monocytes / cytology
  • Monocytes / drug effects*
  • Monocytes / metabolism
  • Prednisone / therapeutic use
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / drug effects
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Adrenal Cortex Hormones
  • Interleukin-1
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Prednisone