Open AccessMitogenic Component in Polar Lipid-Enriched Anaplasma phagocytophilum Membranes
Author(s) -
Kwang Shik Choi,
J. Stephen Dumler
Publication year - 2007
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00204-07
Subject(s) - anaplasma phagocytophilum , biology , splenocyte , innate immune system , anaplasma , immune system , microbiology and biotechnology , immunology , virology , antibody , tick , borrelia burgdorferi
Human granulocytic anaplasmosis is an emerging tick-borne disease caused byAnaplasma phagocytophilum. A. phagocytophilum cells activate Toll-like receptor 2 signaling and possess mitogenic activity, andA. phagocytophilum infection in vivo activates NKT cells unrelated to major surface protein 2 (Msp2) hypervariable region expression. Thus, we hypothesized that lipoprotein or glycolipid components ofA. phagocytophilum membranes could be important triggers of the innate immune response and immunopathology.A. phagocytophilum membranes depleted of Msp2 and protein antigens enhanced the proliferation of naïve mouse splenocytes beyond that of untreated membranes. Protein-depleted and polar lipid-enriched membranes from low-passageA. phagocytophilum cultures enhanced naïve splenocyte lymphoproliferation to a much greater degree than did these fractions from high-passage cultures of bacterial membranes (1.8- to 3.7-fold for protein-depleted fractions and 4.8- to ≥17.7-fold for polar lipid-enriched fractions). These results support the hypothesis that components that are enriched among polar lipids in theA. phagocytophilum membrane stimulate innate immune cell proliferation, possibly activating NKT cells that link innate and adaptive immunity, and immunopathology.