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Morphine disrupts interleukin-23 (IL-23)/IL-17-mediated pulmonary mucosal host defense against Streptococcus

Jing Ma1, Jinghua Wang, Jing Wan

  • 1Division of Basic and Translational Research, Department of Surgery, University of Minnesota, MMC 195, 420 Delaware Street SE, Minneapolis, MN 55455, USA.

Infection and Immunity
|December 10, 2009
PubMed

Insights

Morphine impairs immune responses to Streptococcus pneumoniae lung infections by disrupting interleukin-23 (IL-23)/IL-17 pathways. This leads to reduced neutrophil activity and increased infection severity in drug abuse populations.

Area of Science:

  • Immunology
  • Infectious Disease
  • Pharmacology

Background:

  • Streptococcus pneumoniae causes severe infections, particularly in immunocompromised individuals, including those with drug abuse issues.
  • The mechanisms by which drug abuse compromises immune defenses against pulmonary S. pneumoniae are not fully understood.

Purpose of the Study:

  • To investigate the impact of morphine, a common opiate, on the interleukin-23 (IL-23)/IL-17 immune axis during S. pneumoniae lung infection.
  • To explore how morphine affects innate immune cell function and antimicrobial protein production in response to pneumococcal infection.

Main Methods:

  • Utilized a murine model of opiate abuse and S. pneumoniae lung infection.
  • Assessed IL-23 and IL-17 levels, neutrophil migration, bacterial clearance, and the phosphorylation of key immune signaling molecules (IRF3, ATF2, NF-kappaBp65).
  • Examined the role of T-cell receptor delta (TCRdelta) and the production of S100A8/A9 antimicrobial proteins.

Main Results:

  • Morphine treatment significantly impaired early IL-23 and IL-17 production, delaying neutrophil recruitment and reducing pneumococcal clearance.
  • Morphine inhibited MyD88-dependent IL-23 production in macrophages and dendritic cells and suppressed key signaling pathways.
  • TCRdelta-deficient mice exhibited reduced IL-17 and impaired bacterial clearance, while morphine decreased antimicrobial S100A8/A9 protein secretion.

Conclusions:

  • Morphine disrupts IL-23-producing dendritic cells/macrophages and IL-17-producing gammadelta T cells during S. pneumoniae lung infection.
  • This immune dysfunction results in diminished antimicrobial protein release, compromised neutrophil function, and exacerbated infection severity.
  • Findings highlight a critical link between opiate abuse and impaired host defense against bacterial pneumonia.

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