Cholera Caused by Vibrio cholerae O1 Induces T-Cell Responses in the Circulation

Author:

Bhuiyan Taufiqur Rahman12,Lundin Samuel B.2,Khan Ashraful Islam1,Lundgren Anna2,Harris Jason B.3,Calderwood Stephen B.3,Qadri Firdausi1

Affiliation:

1. International Centre for Diarrhoeal Disease Research, Bangladesh, G.P.O. Box 128, Dhaka 1000, Bangladesh

2. Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, 405 30 Gothenburg, Sweden

3. Division of Infectious Diseases, Massachusetts General Hospital, Gray-Jackson 504, 55 Fruit Street, Boston, Massachusetts 02114

Abstract

ABSTRACT Considerable effort is being made to understand the acute and memory antibody responses in natural cholera infection, while rather less is known about the roles of cellular immune responses involving T and B lymphocytes. We studied responses in adult patients hospitalized with cholera caused by Vibrio cholerae O1. Peripheral blood mononuclear cells from patients ( n = 15) were analyzed by flow cytometry after stimulation with V. cholerae O1 membrane protein (MP) or toxin-coregulated pilus antigen (TcpA). The gamma interferon (IFN-γ) and interleukin-13 (IL-13) responses in stimulated-lymphocyte supernatants were studied. The responses were compared with those of healthy controls ( n = 10). Patients responded with increased frequencies of gut-homing CD4 + T cells (CD4 + β7 + ), gut-homing CD8 + T cells (CD8 + β7 + ), and gut-homing B cells (CD19 + β7 + ) at the early and/or late convalescent stages compared to the acute stage. After stimulation with MP or TcpA, proliferation of CD4 + and CD8 + T cells was increased at the acute stage and/or early convalescent stage compared to healthy controls. Increased IL-13 and IFN-γ responses were observed after antigenic stimulation at the acute and convalescent stages compared to healthy controls. Thus, increases in the levels of gut-homing T and B cells, as well as involvement of CD8 and CD4 Th1-mediated (IFN-γ) and CD4 Th2-mediated (IL-13) cytokine responses, take place in acute dehydrating disease caused by V. cholerae O1. Further studies are needed to determine if such responses are also stimulated after immunization with oral cholera vaccines and if these responses play a role in protection following exposure to cholera.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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