The development of neurologic melioidosis was linked to the elicitation of Burkholderia pseudomallei-infected L-selectinCD11b BALB/c cells in our previous study. However， whether monocytic L-selectin (CD62L， encoded by the sell gene) is a key factor remains uncertain. In the present study， after establishing multi-organ foci via hematogenous routes， we demonstrated that B. pseudomallei GFP steadily persisted in blood， splenic， hepatic and bone marrow (BM) Ly6C monocytes; however， the circulating CD16/32CD45GFP brain-infiltrating leukocytes (BILs) derived from the blood Ly6C monocytes were expanded in BALB/c but not in C57BL/6 bacteremic melioidosis. Consistent with these results， 60% of BALB/c m... More
The development of neurologic melioidosis was linked to the elicitation of Burkholderia pseudomallei-infected L-selectinCD11b BALB/c cells in our previous study. However， whether monocytic L-selectin (CD62L， encoded by the sell gene) is a key factor remains uncertain. In the present study， after establishing multi-organ foci via hematogenous routes， we demonstrated that B. pseudomallei GFP steadily persisted in blood， splenic， hepatic and bone marrow (BM) Ly6C monocytes; however， the circulating CD16/32CD45GFP brain-infiltrating leukocytes (BILs) derived from the blood Ly6C monocytes were expanded in BALB/c but not in C57BL/6 bacteremic melioidosis. Consistent with these results， 60% of BALB/c mice but only 10% of C57BL/6 mice exhibited neurologic melioidosis. In a time-dependent manner， B. pseudomallei invaded C57BL/6 BM-derived phagocytes and monocytic progenitors by 2 d. The number of Ly6CCD62LGFP inflamed cells that had expanded in the BM and that were ready for emigration peaked on d 21 post-infection. Hematogenous B. pseudomallei-loaded sellLy6C monocytes exacerbated the bacterial loads and the proportion of Ly6CGFP BILs in the recipient brains compared to sell infected Ly6C cells when adoptively transferred. Moreover， a neutralizing anti-CD62L antibody significantly depleted the bacterial colonization of the brain following adoptive transfer of B. pseudomallei-loaded C57BL/6 or BALB/c Ly6C cells. Our data thus suggest that Ly6CCD62L infected monocytes served as a Trojan horse across the cerebral endothelium to induce brain infection. Therefore， CD62L should be considered as not only a temporally elicited antigen but also a disease-relevant leukocyte marker during the development of neurologic melioidosis.
