Premium
Listeria monocytogenes virulence proteins induce surface expression of Fas ligand on T lymphocytes
Author(s) -
Zenewicz Lauren A.,
Skinner Jason A.,
Goldfine Howard,
Shen Hao
Publication year - 2004
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2003.03931.x
Subject(s) - listeriolysin o , fas ligand , listeria monocytogenes , biology , virulence , downregulation and upregulation , listeria infection , microbiology and biotechnology , immune system , listeria , apoptosis , immunology , gene , programmed cell death , biochemistry , bacteria , genetics
Summary Virulence factors secreted by Listeria monocytogenes are known to interfere with host cellular signalling pathways. We investigated whether L. monocytogenes modulates T‐cell receptor signalling by examining surface expression of proteins known to be upregulated on activated T cells. In vitro culture of murine splenocytes with L. monocytogenes resulted in a specific and dose‐dependent upregulation of Fas ligand (FasL). Induction of FasL expression was also observed for pathogenic Listeria ivanovii but not for non‐pathogenic Listeria innocua , indicating involvement of Listeria virulence protein(s). Examination of L. monocytogenes strains deficient in different virulence genes demonstrated that FasL upregulation was dependent on the expression of two secreted proteins: listeriolysin O (LLO) and phosphatidylcholine‐preferring phospholipase C (PC‐PLC). Treatment of cells with purified proteins demonstrated that LLO was sufficient for inducing FasL, while PC‐PLC synergized with LLO for the induction of FasL expression. FasL‐expressing cells induced by L. monocytogenes were capable of killing Fas‐expressing target cells. Furthermore, L. monocytogenes infection results in upregulation of FasL on T cells in mice. These results describe a novel function for LLO and PC‐PLC and suggest that L. monocytogenes may use these virulence factors to modulate the host immune response.