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Prostaglandin E2 in tick saliva regulates host cell migration and cytokine profile
Author(s) -
Poole Nina M,
Mamidanna Gayatri,
Smith Richard A,
Coons Lewis,
Cole Judith
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb436
Subject(s) - saliva , fibroblast , lipopolysaccharide , prostaglandin e2 , tumor necrosis factor alpha , macrophage , cytokine , immune system , prostaglandin , biology , immunology , chemistry , medicine , endocrinology , cell culture , biochemistry , in vitro , genetics
Ticks are obligate ectoparasites that suppress the host's responses by secreting immunomodulatory and anti‐inflammatory molecules in their saliva. Previously, we have shown that tick salivary constituents from Dermacentor variabilis have distinctive effects on macrophage and fibroblast migration. Since tick saliva contains a high concentration of prostaglandin E 2 (PGE 2 ), we examined the effects of tick saliva on IC‐21 macrophage and NIH3T3‐L1 fibroblast migration in the absence and presence of a PGE 2 antagonist. Assessment of macrophage and fibroblast migration showed the saliva‐induced changes in migration are reversed by the receptor antagonist AH 6809. Tick saliva induces macrophages to secrete copious amounts of PGE 2 , and conditioned medium from these cells caused a PGE 2 antagonist‐sensitive inhibition on fibroblast migration. Using a cytokine antibody array, we showed tick saliva decreases the secretion of the pro‐inflammatory cytokines r egulated a nd n ormal T cell e xpressed and s ecreted (RANTES/CCL5), tumor necrosis factor‐alpha (TNF‐α), and s oluble TNF R eceptor I (sTNFRI), through a PGE 2 ‐dependent mechanism mediated by cyclic adenosine monophosphate (cAMP). Saliva also had similar effects on lipopolysaccharide (LPS) stimulated macrophages. Our data indicate ticks use PGE 2 to regulate the acitivities of macrophages and fibroblast, cells important in the wound healing response.