Staphylococcal Adhesion and Host Cell Invasion: Fibronectin-Binding and Other Mechanisms

Abstract

Opportunistic bacteria from the genus Staphylococcus can cause life-threatening infections such as pneumonia, endocarditis, bone and joint infections, and sepsis. This pathogenicity is closely related to their capacity to bind directly to the extracellular matrix or to host cells. Adhesion is indeed the first step in the formation of biofilm or the invasion of host cells, which protect the bacteria from the host immune system and facilitate chronic infection. Adhesion relies on the expression of a repertoire of surface proteins called adhesins, notably microbial surface components recognizing adhesive matrix molecules. In this short review, we discuss the main pathway (FnBP-Fn-α5β1 integrin), as well as alternatives, through which Staphylococcus aureus adheres to and then invades non-professional phagocytic cells. We then examine the corresponding mechanisms for coagulase negative staphylococci. There is currently a little understanding of the molecular mechanisms that lead to internalization. Filling this gap in the literature would therefore be an important step toward limiting the duration of staphylococci infections in clinical practice.

Folliculitis decalvans is characterized by a persistent, abnormal subepidermal microbiota

“…This step may be preceded or accompanied by the colonization of the non‐lesional skin of the scalp by opportunistic bacteria. The greater prevalence of S aureus rather than that of other potentially pathogenic bacteria can be attributed to its greater colonizing abilities . Antibiotic therapy may be effective in reducing the bacterial load below the threshold that triggers innate immune system and its inflammatory response, but fails to restore a normal composition due to the persistence of an unbalanced follicular microbiota (ie follicular dysbiosis).…”

A new host cell internalisation pathway for SadA‐expressing staphylococci triggered by excreted neurochemicals

“…One protein is the major autolysin, Atl and AtlE from S. aureus and Staphylococcus epidermidis, respectively, that interacts with the heat shock cognate protein Hsc70 as a host cell receptor to trigger internalisation (Hirschhausen et al, 2010). Some other staphylococcal surface proteins involved in internalisation were reviewed recently (Josse, Laurent, & Diot, 2017). Another class of proteins involved in internalisation comprises the lipoproteins (Lpls) encoded in an S. aureus pathogenicity island, νSaα (Nguyen et al, 2015).…”

CD8α− conventional dendritic cells control Vβ T‐cell immunity in response to Staphylococcus aureus infection in mice

“…Therefore, the receptors in the DCs may contribute to the recognition and phagocytosis of the S. aureus . The other receptors such as CD36, integrin β v and TNF‐ α receptor 1 also contribute to the recognition of S. aureus . We plan to examine whether the human BDCA1 + mDCs and mouse CD8 α − cDCs express these receptors and contribute to immune activation against S. aureus in our future research.…”