%0 Journal Article %A Granick, Jennifer L. %A Reneer, Dexter V. %A Carlyon, Jason A. %A Borjesson, Dori L. %T Anaplasma phagocytophilum infects cells of the megakaryocytic lineage through sialylated ligands but fails to alter platelet production %D 2008 %J Journal of Medical Microbiology, %V 57 %N 4 %P 416-423 %@ 1473-5644 %R https://doi.org/10.1099/jmm.0.47551-0 %K sLex, sialyl Lewis x %K PLPs, platelet-like particles %K p.i., post-infection %K PSGL-1, P-selectin glycoprotein-1 %K MK, megakaryocyte %K GA, granulocytic anaplasmosis %K FBS, fetal bovine serum %I Microbiology Society, %X Anaplasma phagocytophilum is an obligate intracellular bacterial pathogen that principally inhabits neutrophils. However, infection with A. phagocytophilum results in a moderate to marked thrombocytopenia. In host neutrophils, A. phagocytophilum uses sialylated ligands, primarily P-selectin glycoprotein ligand-1 (PSGL-1), to enter its host cell. PSGL-1 is expressed on a wide array of haematopoietic cells, including megakaryocytes. In this study, it was hypothesized that (i) cells of the megakaryocytic lineage (MEG-01 cells) would be susceptible to A. phagocytophilum infection and (ii) infection may induce alterations in platelet production contributing to infection-induced thrombocytopenia. It was found that MEG-01 cells are susceptible to infection. MEG-01 cells expressing abundant sialylated ligands were the most susceptible to infection, and the absence of sialylation, or blocking of PSGL-1, limited infection susceptibility. However, infected MEG-01 cells produced proplatelets and platelet-like particles comparable to uninfected cells. These results highlight a novel target of pathogen infection and suggest that the pathogen may utilize similar strategies to gain access to megakaryocytes. Direct pathogen modification of platelet production may not play a role in infection-induced thrombocytopenia. %U https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.47551-0