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Calcium channel antagonist (nifedipine) attenuates Plasmodium berghei-specific T cell immune responses in Balb/C mice

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Abstract:

Moshal KS, Adhikari JS, Bist K, Nair U, Dwarakanath BS, Katyal A, Chandra R. Calcium channel antagonist (nifedipine) attenuates Plasmodium berghei-specific T cell immune responses in Balb/C mice. Apmis 2007;115:911–20.

Nifedipine and verapamil (Martin et al. Science 1987;235:899–901) are a class of calcium channel blockers involved in the reversal of chloroquine (CQ) drug resistance in CQ-sensitive Plasmodium spp. Nifedipine alters calcium-dependent functions of macrophages and neutrophils during Plasmodium berghei malaria. However, knowledge of nifedipine-induced immunomodulation of T cell functions during P. berghei malaria is still limited. We investigated the effect of nifedipine on the immune status of splenic T cells during P. berghei malaria. The intracellular calcium levels were determined in the FURA-2A/M loaded T cells by spectrofluorometry. Splenic T cell proliferation, phosphatidylserine (PS) externalization, Fas expression and Bcl2/Bax expression were determined by flow cytometry. We report a significant increase in mean percent parasitemia in nifedipine-treated and P. berghei-infected mice. Although nifedipine treatment alone did not affect the resting state free calcium levels in splenic T cells, the rise in intracellular calcium levels of T cells following P. berghei infection was significantly less in nifedipine-treated mice compared to untreated groups at various parasitemia levels. Antigen-specific splenic T cell proliferation and apoptosis was ablated in nifedipine-treated and untreated groups at various parasitemia levels. The study unequivocally reflects the suppression of P. berghei-specific T cell immune responses by nifedipine.

Keywords: T cell physiology; apoptosis; drug resistance; intracellular calcium; splenomegaly

Document Type: Research Article

DOI: https://doi.org/10.1111/j.1600-0463.2007.apm_659.x

Affiliations: 1: B. R. Ambedkar Center for Biomedical Research, University of Delhi, 2: Institute of Nuclear Medicine and Allied Sciences (INMAS), Delhi and 3: Central JALMA Institute for Leprosy, Agra, India

Publication date: 2007-08-01

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