Backgrounds: As an infectious agent, B. pseudomallei is capable of persisting in CD11b phagocytes and escapes from innate immunity during subacute or chronic melioidosis. We hypothesized that those infected cells were used as a vehicle that facilitate the bacterial invading to CNS (central nerve system).

Materials and Methods: The BALB/c and C57BL/6 respectively as subacute and chronic infectious models were used to evaluate the murine melioidosis with CNS syndromes via an intravenous injection of B. pseudomallei GFP or through an adoptively transferred by CD11b cells harboring B. pseudomallei GFP. Observation on occurrence of CNS melioidosis was performed by histological examination, cytokine analysis and bacterial loads in brain.

Results: We found that, during an initial 14 d-infection, by injecting B. pseudomallei GFP, the sL-selectin, sP-selectin, sICAM-1, MCP-1 and IFN-gamma were increased in blood and CSF specimens for the mice with melioidosis. After a 14 d-infection, the CD11b⁺CD45⁺ subpopulation of brain infiltrating leukocytes (BILs) were significantly increased. Approximately 6.5% of BILs were harbored with B. pseudomallei GFP. After adoptive transfer of infected CD11b cells that collected from C57BL/6 WT (wild-type) with melioidosis, the bacterial colonization in the brain and neutrophil infiltration in meninges were obviously occurred while they did not occur in recipients after adoptively transferred if the donor cells were isolated from C57BL sel^-/- (selectin knock-out mice).

Conclusions/Significance: We suggest that B. pseudomallei-infected CD11b⁺CD62L⁺ cells play an important role in inducing melioidosis with meningitis that could be due to the migration of infected leukocyte involving in a selectin-dependent manner.