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

被引:12
|
作者
Vuckovic, D
Abram, M
Bubonja, M
Wraber, B
Doric, M
机构
[1] Univ Rijeka, Fac Med, Dept Microbiol, HR-51000 Rijeka, Croatia
[2] Univ Ljubljana, Fac Med, Inst Microbiol & Immunol, Ljubljana 1000, Slovenia
关键词
Campylobacter jejuni; mice; depletion; T cells;
D O I
10.1016/j.micpath.2005.10.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Campylobocter 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 carnpylobacteriosis will be the subject of our further research.
引用
收藏
页码:35 / 39
页数:5
相关论文
共 50 条
  • [1] A comparison of the behavior of C57BL/6 and C57BL/10 mice
    Deacon, R. M. J.
    Thomas, C. L.
    Rawlins, J. N. P.
    Morley, B. J.
    BEHAVIOURAL BRAIN RESEARCH, 2007, 179 (02) : 239 - 247
  • [2] DETERMINATION OF THE HISTOCOMPATIBILITY LOCUS INVOLVED IN THE RESISTANCE OF MICE STRAINS C57BL/10-X, C57BL/6-X, AND C57BL/6KS TO C57BL TUMORS
    SNELL, GD
    BORGES, PRF
    JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1953, 14 (03) : 481 - 484
  • [3] Genetic analysis of resistance to infections in mice: A/J meets C57BL/6J
    Marquis, J. -F
    Gros, P.
    IMMUNOLOGY, PHENOTYPE FIRST: HOW MUTATIONS HAVE ESTABLISHED NEW PRINCIPLES AND PATHWAYS IN IMMUNOLOGY, 2008, 321 : 27 - 57
  • [4] C57BL/6 and congenic interleukin-10-deficient mice can serve as models of Campylobacter jejuni colonization and enteritis
    Mansfield, L. S.
    Bell, J. A.
    Wilson, D. L.
    Murphy, A. J.
    Elsheikha, H. M.
    Rathinam, V. A. K.
    Fierro, B. R.
    Linz, J. E.
    Young, V. B.
    INFECTION AND IMMUNITY, 2007, 75 (03) : 1099 - 1115
  • [5] Differences in resistance of C57BL/6 and C57BL/10 mice to infection by Mycobacterium avium are independent of gamma interferon
    Appelberg, R
    Leal, IS
    Pais, TF
    Pedrosa, J
    Flórido, M
    INFECTION AND IMMUNITY, 2000, 68 (01) : 19 - 23
  • [6] Responses to ethanol in C57BL/6 versus C57BL/6 x 129 hybrid mice
    Lim, Jana P.
    Zou, Mimi E.
    Janak, Patricia H.
    Messing, Robert O.
    BRAIN AND BEHAVIOR, 2012, 2 (01): : 22 - 31
  • [7] Resistance to Development of Collagen-Induced Arthritis in C57BL/6 Mice Is Due to a Defect in Secondary, but Not in Primary, Immune Response
    Meng Pan
    Insoo Kang
    Joe Craft
    Zhinan Yin
    Journal of Clinical Immunology, 2004, 24 : 481 - 491
  • [8] Resistance to development of collagen-induced arthritis in C57BL/6 mice is due to a defect in secondary, but not in primary, immune response
    Pan, M
    Kang, I
    Craft, J
    Yin, ZN
    JOURNAL OF CLINICAL IMMUNOLOGY, 2004, 24 (05) : 481 - 491
  • [9] HAEMOGLOBINS OF FOETAL C57BL/6 MICE
    BARROWMAN, J
    CRAIG, M
    NATURE, 1961, 190 (477) : 819 - &
  • [10] METABOLISM OF GLUCOSE BY C57BL/6 MICE
    ADAMS, JT
    KITOS, PA
    WEIR, JA
    AMERICAN JOURNAL OF PHYSIOLOGY, 1967, 213 (01): : 231 - &