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Effect of antipyretic agents on uptake, transport, and release of antimicrobial agents by human polymorphonuclear

Gerald L Mandell1, Elizabeth J Coleman

  • 1Department of Medicine, University of Virginia Health System, Charlottesville, VA 22908, USA. gm@virginia.edu

The Journal of Infectious Diseases
|May 10, 2002
PubMed

Insights

Common fever reducers like ibuprofen and acetaminophen can reduce the effectiveness of antibiotics azithromycin and moxifloxacin by inhibiting their transport and release from immune cells (PMNL). This interaction may compromise therapy efficacy.

Area of Science:

  • Pharmacology
  • Immunology
  • Microbiology

Background:

  • Polymorphonuclear leukocytes (PMNL) are crucial for concentrating, transporting, and releasing antimicrobial agents.
  • Antipyretic agents are commonly co-administered with antimicrobials in febrile patients.
  • The potential impact of antipyretics on antimicrobial delivery by PMNL requires investigation.

Purpose of the Study:

  • To investigate the influence of ibuprofen, acetaminophen, and acetylsalicylic acid on the uptake, transport, and release of azithromycin and moxifloxacin by human PMNL.
  • To assess the clinical implications of co-administering these antipyretics with PMNL-dependent antibiotics.

Main Methods:

  • Quantification of antimicrobial uptake by human PMNL using bioassays of released agents.
  • Assessment of antimicrobial transport and release via chemotactic plates with sentinel bacteria.
  • Evaluation of antipyretic effects on PMNL chemotaxis.

Main Results:

  • Acetylsalicylic acid significantly inhibited azithromycin uptake, while other antipyretics did not.
  • Therapeutic levels of all studied antipyretics inhibited the transport and release of both azithromycin and moxifloxacin by PMNL.
  • PMNL directed and non-directed movement remained unaffected by the antipyretics.

Conclusions:

  • Co-administration of common antipyretics (ibuprofen, acetaminophen, acetylsalicylic acid) with azithromycin or moxifloxacin may compromise antimicrobial therapy efficacy.
  • The inhibition of antimicrobial transport and release by PMNL is a key mechanism for this potential compromise.
  • Clinicians should consider the interaction between antipyretics and PMNL-dependent antibiotics when managing febrile patients.

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