Bacterial ribosomal immunostimulants prime alveolar macrophages in vivo to produce interleukin 1 in vitro

Chest. 1991 Sep;100(3):644-8. doi: 10.1378/chest.100.3.644.

Abstract

Alveolar macrophages (AMs) may play a key role in human respiratory immune defenses, partially by synthesizing and releasing interleukin 1 (IL = 1). D53 (Ribomunyl), a composite bacterial ribosomal immunostimulant, has been recognized as an efficient prevention of respiratory tract infections. In vitro, D53 enhances the IL-1 production by mouse spleen adherent cells. A thymocyte proliferative response assay was used to evaluate the in vitro IL-1 production by AMs in healthy subjects who received D53 immunostimulant. Twelve nonsmoking healthy subjects took part in a prospective double-blind placebo control study. On day 1, a first bronchoalveolar lavage (BAL) was performed to assess IL-1 production by unstimulated and lipopolysaccharide (LPS) stimulated AM. Then, subjects were randomized to receive D53 (n = 6) or its placebo (n = 6) by both oral and subcutaneous injection routes from day 1 to day 15. On day 15, a second BAL was done and AM IL-1 production was again tested. IL-1 production on day 15 did not significantly differ from day 1 in both D53-treated and placebo groups either when AMs were unstimulated or were stimulated with concentrations of LPS resulting in maximal IL-1 production. However, in the D53-treated group, but not in the placebo group, IL-1 production induced by low LPS concentration (5 mg/L) was significantly higher (mean +/- SEM: 1,238 +/- 287 U/10(6) AM) on day 15 in comparison with day 1 (577 +/- 113 U/10(6) AM; p less than 0.05, Wilcoxon W test) and in comparison with the control group (day 15 IL-1 production induced by 5 mg/L LPS, 758 +/- 175 U/10(6) AM; p less than 0.05, Mann-Whitney U test). Moreover, in the D53-treated group, the optimal LPS concentration (ie, LPS concentration that induced maximal IL-1 production) was significantly lower on day 15 (mean +/- SD: 11 +/- 7 mg/L) than on day 1 (16 +/- 7 mg/L; p less than 0.05 Wilcoxon W test). We conclude that D53 immunostimulant in vivo primes AM to produce IL-1 following low LPS concentration stimulation. This may partially explain the protective effect of D53 immunostimulant against respiratory tract infection.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial

MeSH terms

  • Adjuvants, Immunologic / administration & dosage
  • Adjuvants, Immunologic / pharmacology
  • Administration, Oral
  • Adult
  • Animals
  • Antigens, Bacterial / administration & dosage
  • Antigens, Bacterial / pharmacology*
  • Biological Assay
  • Bronchoalveolar Lavage Fluid / cytology
  • Dose-Response Relationship, Drug
  • Dose-Response Relationship, Immunologic
  • Double-Blind Method
  • Escherichia coli
  • Female
  • Humans
  • Injections, Subcutaneous
  • Interleukin-1 / biosynthesis*
  • Lipopolysaccharides / pharmacology
  • Lymphocyte Activation
  • Macrophages / immunology*
  • Male
  • Mice
  • Mice, Inbred C3H
  • Prospective Studies
  • Pulmonary Alveoli / cytology*
  • Pulmonary Alveoli / immunology
  • Random Allocation

Substances

  • Adjuvants, Immunologic
  • Antigens, Bacterial
  • Interleukin-1
  • Lipopolysaccharides
  • Ribomunyl