Host resistance to primary and secondary Campylobacter jejuni infections in C57Bl/6 mice |
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| Authors: | Vucković Darinka Abram Maja Bubonja Marina Wraber Branka Dorić Miljenko |
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| Affiliation: | 1. Department of Biology, Tekirdag Namik Kemal University, Tekirdag, Turkey;2. Department of Parasitology, Faculty of Veterinary, Ataturk University, Erzurum, Turkey;3. Zonguldak Bulent Ecevit University, Caycuma Vocational High School, Zonguldak, Turkey;4. Galveston National Laboratory, Department of Microbiology & Immunology, Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, TX, United States of America;5. Department of Parasitology, Faculty of Veterinary, Kafkas University, Kars, Turkey;1. UCLA Mattel Children''s Hospital, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA;2. Department of Pediatrics, Harbor-University of California, Los Angeles, Torrance, CA;1. Institute of Physiology 1/Neurophysiology, Jena University Hospital, Friedrich Schiller University of Jena, Teichgraben 8, 07743 Jena, Germany;2. Laboratory of Experimental Rheumatology and Neuroendocrine-Immunology, Division of Rheumatology, Department of Internal Medicine I,University Hospital Regensburg, 93042 Regensburg, Germany |
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| Abstract: | Campylobacter jejuni has been known as a main causative agent of human enterocolitis for more than 30 years. This has prompted the research on defence mechanisms of the host involved. Although the humoral immune response to C. jejuni has been addressed in many studies, relatively little is known about the role of T lymphocytes in campylobacteriosis. The current study was based on in vivo T-cell subsets depletion to evaluate the role of CD4+ and CD8+ T lymphocytes in disseminated C. jejuni infection in C57BL/6 mice. Depletion of either CD8+ or CD4+ cells did not change the overall infection kinetics of primary campylobacteriosis. To assess the role of T cells in acquired immunity that develops during primary infection in C57BL/6 mice, in vivo depletions were performed during reinfection. Depletion of CD4+ cells did not have any effect on secondary infection kinetics, whereas depletion of CD8+ cells resulted in secondary liver infection that failed to resolve during the observed period. This study showed that both CD8+ and CD4+ T cells contribute to protection of C57BL/6 mice against C. jejuni. However, the predominant role resides in the CD8+ cell subpopulation. The exact mechanisms by which CD8+ cells operate during the course of campylobacteriosis will be the subject of our further research. |
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