Open AccessMononuclear cell response in the liver of mice infected with hepatotoxigenic Campylobacter jejuni
Author(s) -
Eisuke Kita,
Fumiko Nishikawa,
Noriaki Kamikaidou,
Adelino K. Nakano,
Noriaki Katsui,
Shuzo Kashiba
Publication year - 1992
Publication title -
journal of medical microbiology/journal of medical microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.91
H-Index - 117
eISSN - 1473-5644
pISSN - 0022-2615
DOI - 10.1099/00222615-37-5-326
Subject(s) - campylobacter jejuni , enteritis , peripheral blood mononuclear cell , microbiology and biotechnology , mononuclear cell infiltration , lesion , biology , immunology , infiltration (hvac) , pathology , medicine , in vitro , bacteria , biochemistry , genetics , physics , thermodynamics
Intragastric inoculation with hepatotoxigenic strains of Campylobacter jejuni led to the death of mice during the late phase of infection. Histological study disclosed a massive infiltration of mononuclear cells in the liver, mimicking intrahepatic hypersensitivity. Neither enterotoxigenic nor enteroinvasive Escherichia coli induced such a lesion. However, the same histopathological change was induced by injecting the hepatotoxic factor of hepatotoxigenic C. jejuni intravenously on two occasions separated by 14 days. Neither a single injection of an increased dose of the hepatotoxic factor nor two injections, the second of which was heat-inactivated, induced this change. Pre-treatment with rabbit antibody to the hepatotoxic factor inhibited the development of the hepatic lesion. These results suggest that C. jejuni-induced hepatic lesions in mice may be caused, at least in part, by the active moiety of the hepatotoxic factor. The possible mechanisms by which the toxic factor induces hepatitis as a consequence of hypersensitivity are discussed in relation to Guillain-Barré syndrome and Reiter's syndrome associated with C. jejuni enteritis.