Staphylococcal adaptation to diverse physiologic niches: an overview of transcriptomic and phenotypic changes in different biological environments

Abstract

Host niches can differ strongly regarding, for example, oxygen tension, pH or nutrient availability. Staphylococcus aureus and other staphylococci are common colonizers of human epithelia as well as important human pathogens. The phenotypes that they show in different host environments, and the corresponding bacterial transcriptomes and proteomes, are currently under intense investigation. In this review, we examine the available literature describing staphylococcal phenotypes, such as expression of virulence factors, gross morphologic characteristics and growth patterns, in various physiological environments. Going forward, these studies will help researchers and clinicians to form an enhanced and more detailed picture of the interactions existing between the host and staphylococci as some of its most frequent colonizers and invaders.

Keywords: gene expression; host–pathogen interaction; niche adaptation; staphylococci.

Figure 1.. Staphylococcus aureus in joint infections visualized by scanning electron microscopy.

(A) Biofilm isolated from a patient with orthopedic infection. (B) Rapid aggregation of S. aureus after 20 min incubation in synovial fluid.

Figure 2.. Aggregation of bacteria and formation of biofilm in response to host fibrin.

(A) Staphylococcus aureus binds to human matrix proteins present in traumatized joints (such as fibrin) using dedicated, surface-located binding proteins (ClfA, ClfB, FnbA, FnbB). (B) The low activity of Agr in fibrin-mediated aggregates causes low production of the surfactant PSMs, with the result of pronounced cell-to-cell attachment and retention of biofilm macromolecules on the cell surface. This ultimately leads to the formation of enormous, macroscopic cellular aggregates with high resistance to antibiotics.