期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 5, 页码 3313-3318出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.5.3313
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资金
- Medical Research Council [G0400300] Funding Source: researchfish
- MRC [G0400300] Funding Source: UKRI
- Medical Research Council [G0400300] Funding Source: Medline
- Wellcome Trust [060574] Funding Source: Medline
Properdin is a positive regulator of complement activation so far known to be instrumental in the survival of infections with certain serotypes of Neisseria meningitidis. We have generated a fully backcrossed properdin-deficient mouse line by conventional gene-specific targeting. In vitro, properdin-deficient serum is impaired in alternative pathway-dependent generation of complement fragment C3b when activated by Escherichia coli DH5 alpha. Properdin-deficient mice and wild-type littermates compare in their levels of C3 and IgM. In an in vivo model of polymicrobial septic peritonitis induced by sublethal cecal ligation and puncture, properdin-deficient mice appear immunocompromised, because they are significantly impaired in their survival compared with wild-type littermates. We further show that properdin localizes to mast cells and that properdin has the ability to directly associate with E. coli DH5 alpha. We conclude that properdin plays a significant role in the outcome of polymicrobial sepsis.
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