Moumita Ghosh1, Koushik Roy, Syamal Roy. 1. Department of Infectious Diseases and Immunology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Abstract
OBJECTIVES: The commonly used antileishmanial drugs are sodium antimony gluconate (SAG), amphotericin B, miltefosine and paromomycin. There are a number of reports that antileishmanial drugs show immunomodulatory properties. Here, we attempt to understand how the innate arm of the immune system is modulated in response to these antileishmanial drugs. METHODS: BALB/c peritoneal macrophages were treated with miltefosine, SAG, amphotericin B or paromomycin. The membrane fluidity of macrophages following drug treatment was studied in terms of fluorescence anisotropy. The T cell-stimulating ability, production of cytokines and nitrogen and oxygen metabolite production in drug-treated macrophages were also studied. The study was also carried out using peritoneal macrophages from drug-treated BALB/c mice. RESULTS: The antileishmanial drugs altered macrophage membrane fluidity, except amphotericin B. The drug-treated macrophages showed enhanced T cell-stimulating ability and generation of reactive oxygen species, nitrite, interleukin-12 and tumour necrosis factor-α. CONCLUSIONS: Antileishmanial drugs can stimulate the innate arm of the immune system, which may have a significant bearing on the cellular arm of the immune system.
OBJECTIVES: The commonly used antileishmanial drugs are sodium antimony gluconate (SAG), amphotericin B, miltefosine and paromomycin. There are a number of reports that antileishmanial drugs show immunomodulatory properties. Here, we attempt to understand how the innate arm of the immune system is modulated in response to these antileishmanial drugs. METHODS: BALB/c peritoneal macrophages were treated with miltefosine, SAG, amphotericin B or paromomycin. The membrane fluidity of macrophages following drug treatment was studied in terms of fluorescence anisotropy. The T cell-stimulating ability, production of cytokines and nitrogen and oxygen metabolite production in drug-treated macrophages were also studied. The study was also carried out using peritoneal macrophages from drug-treated BALB/c mice. RESULTS: The antileishmanial drugs altered macrophage membrane fluidity, except amphotericin B. The drug-treated macrophages showed enhanced T cell-stimulating ability and generation of reactive oxygen species, nitrite, interleukin-12 and tumour necrosis factor-α. CONCLUSIONS: Antileishmanial drugs can stimulate the innate arm of the immune system, which may have a significant bearing on the cellular arm of the immune system.
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