| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 100 === Background
Streptococcus pneumoniae is a leading cause of pneumonia, otitis media, bacteremia, and one of the most severe complications of invasive pneumococcal disease is pneumococcal hemolytic uremic syndrome (pHUS). Neuraminidases, NanA, NanB, and NanC of S. pneumoniae cleaves the linkage between termanal sialic acid residues and glycoconjugates on host cells, thus exposing Thomsen-Friedenreich antigen (T-antigen). T-antigen exposure on red blood cells (RBC) and kidney glomeruli lead to pHUS which is associated with haemolytic anaemia, thrombocytopenia and acute renal failure. The role of NanA in bacterial colonization and exposing T-antigen has been reported, but little is known for NanB and NanC.
Methods
A549 cell line were used in adherence assay. BALB/c mice were used in the murine infection model. The mice were injected intravenously through the tail vein with S. pneumoniae 6B (wild type), and isogenic nanB and nanC mutants. The bloods were collected by retro-orbital puncture, and subjected to bacterial culture and T-antigen detection by flow cytometer.
Results
Animal studies showed that nanB and nanC mutants were cleared more quickly than wild-type S. pneumoniae from blood. nanB and nanC mutants exposed less T-antigen on RBC by flow cytometry. Immunofluorescence data showed that wild-type S. pneumoniae significantly exposed T-antigen in kidney, but not nanB and nanC mutants.
Conclusion
We found that NanC promoted S. pneumoniae bloodstream infection, and was also involved in T-antigen exposure on RBC and glomeruli in mice.
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