Anaplasma phagocytophilum infects cells of the megakaryocytic lineage through sialylated ligands but fails to alter platelet production.
Anaplasma phagocytophilum infects cells of the megakaryocytic lineage through sialylated ligands but fails to alter platelet production.
复制标题
嗜吞噬细胞无形体通过唾液酸化配体感染巨核细胞谱系的细胞，但不能改变血小板的产生。
DOI：
10.1099/jmm.0.47551-0
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发表时间：
2008
影响因子：
3
通讯作者：
Borjesson,DoriL
中科院分区：
文献类型：
--
作者：
Granick,JenniferL;Reneer,DexterV;Carlyon,JasonA;Borjesson,DoriL
Anaplasma phagocytophilumis an obligate intracellular bacterial pathogen that principally inhabits neutrophils. However, infection withA. phagocytophilumresults in a moderate to marked thrombocytopenia. In host neutrophils,A. phagocytophilumuses 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 toA. phagocytophiluminfection 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.
