Nasal commensal Staphylococcus epidermidis counteracts influenza virus

Abstract

Several microbes, including Staphylococcus epidermidis (S. epidermidis), a Gram-positive bacterium, live inside the human nasal cavity as commensals. The role of these nasal commensals in host innate immunity is largely unknown, although bacterial interference in the nasal microbiome may promote ecological competition between commensal bacteria and pathogenic species. We demonstrate here that S. epidermidis culture supernatants significantly suppressed the infectivity of various influenza viruses. Using high-performance liquid chromatography together with mass spectrometry, we identified a giant extracellular matrix-binding protein (Embp) as the major component involved in the anti-influenza effect of S. epidermidis. This anti-influenza activity was abrogated when Embp was mutated, confirming that Embp is essential for S. epidermidis activity against viral infection. We also showed that both S. epidermidis bacterial particles and Embp can directly bind to influenza virus. Furthermore, the injection of a recombinant Embp fragment containing a fibronectin-binding domain into embryonated eggs increased the survival rate of virus-infected chicken embryos. For an in vivo challenge study, prior Embp intranasal inoculation in chickens suppressed the viral titres and induced the expression of antiviral cytokines in the nasal tissues. These results suggest that S. epidermidis in the nasal cavity may serve as a defence mechanism against influenza virus infection.

Manipulating the microbiome: evolution of a strategy to prevent S. aureus disease in children

“…For decades, researchers have been investigating the role that these commensal bacterial species play on a human host’s susceptibility to S. aureus colonization and disease. As a result, bacterial interference emerged as a strategy to use commensal bacterial species to eliminate or prevent the colonization of an anatomic niche by a pathogenic species 16 .…”

“…As the nasal microbiome develops, commensal species may play a direct role in host protection by eliminating or excluding pathogens from their niche 16 . Children whose microbiota contains commensals Corynebacterium or Dolosigranulum , for example, are less likely to harbor potential pathogens of genera Streptococcus , Staphylococcus , and Moraxella 44 .…”

“…Children whose microbiota contains commensals Corynebacterium or Dolosigranulum , for example, are less likely to harbor potential pathogens of genera Streptococcus , Staphylococcus , and Moraxella 44 . Although the specific mechanisms by which commensals exclude other organisms from the nasal cavity remain unclear, studies conducted on the immature nasal microbiota suggest that early acquisition of certain commensal species may impart long-term resistance to colonization by pathogens in newborns 16 , 51 .…”

Pattern recognition receptor immunomodulation of innate immunity as a strategy to limit the impact of influenza virus

“…Colonization and/or infection with specific bacteria can limit IAV infection directly via the production of microbial products. For example, a giant extracellular matrix-binding protein produced by Staphylococcus epidermis was shown to bind and block infectivity of IAV, both in vitro and in vivo [32]. In addition, stimulation of innate immunity via a crude mixture of bacterial products containing bacterial lysates and/or bacterial toxins has been investigated as an immunomodulation strategy to limit influenza virus growth, disease, and mortality.…”

Mechanisms of benzydamine action against local inflammatory process

“…Аналогичные защитные свойства демонстрирует и S. epidermidis в нормальных концентрациях, в которых он не проявляет вирулентные свойства, а, наоборот, препятствует формированию биопленок со стороны более опасного S. aureus. К тому же он подавляет активность вируса гриппа А. Таким образом, нарушение баланса нормальных микробных ассоциаций может негативно влиять на местный иммунный статус пациента, осложняя течение инфекционного процесса[3,4]. Topicality of the influence of some active substances at the stage of acute infectious inflammation…”