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.

Keywords: adhesion; cell invasion; fibronectin-binding protein; non-professional phagocytic cell; staphylococci.

FIGURE 1

Staphylococcal mechanisms of adherence to and internalization into host cells. (A) Schematic diagram of structural organization of FnBP from S. aureus. Gray items (A, B1, B2, C, D1, D2, D3, D4) represent an alternative nomenclature to the fibronectin-binding repeats. (B) The Fibronectin α5β1 integrin pathway for adherence and internalization of S. aureus (FnBP A/B), S. pseudintermedius (SpsD/L) and S. epidermidis (Embp). This internalization pathway was hypothesized for S. epidermidis (Embp) but refuted. (C) Staphylococcal secondary mechanisms involved in adherence to and internalization into host cells. Bacterial adhesins presented in the figure’s panel are FnBP A/B, adhesion/autolysin family (Atl), fibrinogen binding adhesion (Fbl and ClfA), sdrD, Tet38, SraP, Eap, and GapC. The internalization pathway including Fbl, fibrinogen and host receptor was hypothesized for S. lugdunensis but refuted. Please refer to Table 1 for adhesin/Staphylococccus species concordance.