Staphylococcus aureus and Influenza A Virus: Partners in Coinfection

Abstract

Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commensal to pathogenic organism in this setting. The ability of virus-driven danger signals to cause S. aureus to transition from commensalism to pulmonary infection was explored in a recent study by Reddinger et al. R. M. Reddinger, N. R. Luke-Marshall, A. P. Hakansson, and A. A. Campagnari, mBio 7(6):e01235-16, 2016, http://dx.doi.org/10.1128/mBio.01235-16. The authors report that physiological host changes, including febrile temperature and a combination of host stress response signals, caused S. aureus biofilms to disperse from the nasal environment and cause active pulmonary infection. This commentary discusses the new finding in light of the current understanding of the mechanisms behind staphylococcal coinfection with IAV. In addition, it considers the mechanisms behind staphylococcal dispersal in this model. Overall, the study indicates that interkingdom signaling may occur following IAV infection and this likely contributes to sensitizing the IAV-infected host to secondary staphylococcal pneumonia.

Influenza Pathogenesis: The Effect of Host Factors on Severity of Disease

“…Similarly, does an altered respiratory or gut microbiome predispose to virus infection and severe disease? For example, colonization with certain pathogenic bacteria such as Staphylococcus or Streptococcus may affect the risk of secondary bacterial infections following primary IAV disease (69).…”

<p>Functional aspects, phenotypic heterogeneity, and tissue immune response of macrophages in infectious diseases</p>

“…Furthermore, these lung lesions might be attenuated in coinfection by Staphylococcus aureus, which is normally present in the airway mucosal microbiota, because of the bacterium's ability to stimulate the expression of M2 macrophages. [292][293][294] Conversely, in the pathogenesis of coronavirus and cytomegalovirus infections, the lesions that develop are related to the induction of an inflammatory environment mediated by M2 macrophages, which indicates that viral agents can still benefit from the induction of specific tissue environments related to the Th2 response and, consequently, tissue repair and induction of tissue fibrosis. 287,[295][296][297][298][299] In mice experimentally infected with Schistosoma japonica, liver fibrosis was associated with the presence of M2 macrophages, which exhibited increased regulation of Notch1/Jagged1 signals, and the blockade of this expression reversed the M2 phenotype and, subsequently, the associated fibrosis.…”

Розвиток Імунної Відповіді При Стафілококовій Пневмонії (Частина 3)

“…Избыток продукции IFN-λ способствует пораже-нию легочной ткани при пневмонии, вызванной Staphylococcus aureus, особенно, штаммом USA300 MRSA [24]. Повышение резистентности у мутант-ных мышей Il28r -/-к Staphylococcus aureus, вероятно, обусловлено увеличением IL-22-зависимой про-дукции АМП [75]. Установлено, что у нокаутных мышей Il28r -/-заметно увеличена конститутивная экспрессия IL-22.…”