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Related Experiment Videos

Ciprofloxacin enhances T cell function by modulating interleukin activities.

K G Stünkel1, G Hewlett, H J Zeiler

  • 1Bayer AG, Pharma Research Centre, Wuppertal, Germany.

Clinical and Experimental Immunology
|December 1, 1991
PubMed
Summary
This summary is machine-generated.

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Ciprofloxacin (CIP) enhances immune responses by boosting DNA synthesis in mouse spleen cells and human lymphocytes. It also increases Interleukin-2 (IL-2) and Interleukin-1 (IL-1) production, suggesting modulation of T cell and macrophage functions.

Area of Science:

  • Immunology
  • Pharmacology
  • Microbiology

Background:

  • Ciprofloxacin (CIP) is a quinolone antibiotic with broad-spectrum antibacterial activity.
  • The immunomodulatory effects of ciprofloxacin are not fully understood.

Purpose of the Study:

  • To investigate the effect of ciprofloxacin on immune cell DNA synthesis and cytokine production.
  • To determine if ciprofloxacin modulates T cell and/or monocyte/macrophage functions.

Main Methods:

  • Assessed DNA synthesis in mouse spleen cells and human peripheral blood lymphocytes (PBL) stimulated with mitogens or alloantigens in the presence of CIP.
  • Measured Interleukin-2 (IL-2) and Interleukin-1 (IL-1) levels in cell culture supernatants.
  • Evaluated the effect of CIP on primary antibody responses in vitro and in vivo.

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Main Results:

  • Ciprofloxacin (0.1-30 µg/ml) enhanced DNA synthesis in activated mouse spleen cells and human PBL.
  • CIP increased IL-2 production in phytohemagglutinin (PHA)-stimulated human PBL.
  • CIP augmented IL-1 release from activated mouse macrophages and human monocyte/macrophages, but not from freshly isolated monocytes or keratinocytes.
  • CIP enhanced IL-2 release from a T cell line in combination with IL-1.
  • CIP did not affect primary antibody responses in vitro or in vivo.

Conclusions:

  • Ciprofloxacin modulates the immune response by enhancing T cell function and macrophage/T cell interactions.
  • The immunomodulatory effects of CIP appear to be specific to T cell and monocyte/macrophage pathways, not affecting primary antibody production.