Abstract：
:The immune responses of males and females to bacterial infections display differences. The mechanisms that underlie this sexual dimorphism are multifactorial. Lipopolysaccharide (LPS) contributes to the pathogenesis of endotoxaemia. We have previously demonstrated that the plasma protein beta-2 glycoprotein-1 (β2GPI) reduces LPS-induced inflammation in male mice. In the present study using a more robust infection model of septicaemia the role of β2GPI is examined in both male and female wild type (WT) and β2GPI deficient (β2GPI-/-) mice challenged with Escherichia coli (E. coli) intravenously. β2GPI deficiency led to an increase of E. coli colony forming units (CFU) in the circulation of both male and female mice. In male β2GPI-/- mice this was associated with a worse clinical severity score. This difference was not observed between female β2GPI-/- and female WT mice. Male WT mice had decreased levels of total and increased levels of free thiol β2GPI following administration of LPS or E. coli. This pattern of sexual dimorphic response was also observed in our cohort of humans with sepsis. These findings support a role for β2GPI in modulating the sex-specific susceptibility to gram-negative septicaemia.
journal_name
Sci Repjournal_title
Scientific reportsauthors
El-Assaad F,Qi M,Gordon AK,Qi J,Dong S,Passam F,Weaver JC,Giannakopoulos B,Krilis SAdoi
10.1038/s41598-017-07945-8subject
Has Abstractpub_date
2017-08-15 00:00:00pages
8201issue
1issn
2045-2322pii
10.1038/s41598-017-07945-8journal_volume
7pub_type
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