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In vitro studies have shown that many microbial pathogens can adhere to cell surface heparan sulfate proteoglycans (HSPGs) to promote cell infection; whether such HSPG-pathogen interactions occur in vivo, however, remains to be clearly established. In this Paper of the Week, Atsuko Hayashida and colleagues examined whether the major HSPG syndecan-1 plays any role in Staphylococcus aureus corneal infection in mice. They found that syndecan-1 knock-out mice (Sdc1−/−) displayed significant resistance to S. aureus corneal infection compared to wild type mice. However, subsequent studies showed that syndecan-1 did not bind to S. aureus, nor was it required for bacterial colonization of cultured corneal cells, suggesting that this proteoglycan does not mediate S. aureus attachment in vivo. Rather, Hayashida and colleagues found that shed syndecan-1 mediated bacterial infectivity, as topical administration of purified syndecan-1 ectodomains or heparan sulfate (HS) significantly increased bacterial burden in corneal tissues. The shed syndecan-1 particles could inhibit the activity of surrounding neutrophils, preventing these immune cells from destroying the invading S. aureus. This study reveals a previously unknown infection tactic whereby a pathogen can exploit the capacity of syndecan-1 ectodomains to inhibit neutrophil-mediated killing to promote its pathogenesis, a finding that may point to new therapeutic strategies.
Anti-syndecan-1-immunostained eye sections of wild type mice before and after S. aureus infection show a dramatic decrease in syndecan-1 expression in the corneal epithelium, suggestive of increased syndecan-1 shedding.
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