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Crosstalk between CD93, C1q and GIPC in the Regulation of Pneumococcal Meningitis Inflammation.

OBJECTIVE
Pneumococcal meningitis is a common and serious infectious disease that threatens human health worldwide. Recent studies have shown that various regulatory proteins of the immune system may be potential targets for adjuvant therapy. The aim of this study was to investigate CD93 expression and potential signaling pathways in rat models of pneumococcal meningitis.


METHODS
The levels of sCD93 (soluble CD93), IL-6 (Interleukin-6) and TNF-α (tumor necrosis factor-α) in cerebrospinal fluid were assessed by ELISA, and the levels of iNOS (inducible nitric oxide synthase), CD93, complement C1q, and GIPC (C-terminal of the regulator of G protein signaling-G alpha interacting protein) in the brain tissue were evaluated by Western Blotting. The interaction between CD93 and complement C1q was investigated by co-immunoprecipitation, and the interaction between CD93 and GIPC was detected by immunofluorescence colocalization.


RESULTS
Our results showed a significant increase in the levels of IL-6, TNF-α, sCD93, CD93, complement C1q, GIPC, and iNOS in the Streptococcus pneumoniae infection group. CD93 interacted with complement C1q, and CD93 and GIPC colocalized on the cell membrane of the cerebral cortex.


CONCLUSIONS
This study suggests that CD93 may be a new inflammatory factor in pneumococcal meningitis. C1q and GIPC may mediate downstream signaling pathways of CD93 in pneumococcal meningitis.