Host resistance to primary and secondary Campylobacter jejuni infections in C57Bl/6 mice

• Published in: Microbial pathogenesis 2006, Vol.40 (1), p.35-39
• Main Authors: Vučković, Darinka, Abram, Maja, Bubonja, Marina, Wraber, Branka, Dorić, Miljenko
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Bacterial - biosynthesis; Antibodies, Bacterial - blood; Campylobacter Infections - immunology; Campylobacter jejuni; Campylobacter jejuni - growth & development; Campylobacter jejuni - immunology; CD4-Positive T-Lymphocytes - physiology; CD8-Positive T-Lymphocytes - physiology; Depletion; Female; Humans; Immunologic Memory; Liver - immunology; Liver - microbiology; Liver - pathology; Male; Mice; Mice, Inbred C57BL; Recurrence; Spleen - immunology; Spleen - microbiology; T cells
• ISSN: 0882-4010; 1096-1208
• DOI: 10.1016/j.micpath.2005.10.004

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.