Abstract
Staphylococcus aureus is a prominent etiological agent of suppurative abscesses. In principle, abscess formation and purulent exudate are classical physiological features of healing and tissue repair. However, S. aureus deploys two coagulases that can usurp this classical host response and form distinct abscess lesions. Here, we establish that during coinfection with coagulase producers and non-producers, coagulases are shared public goods that contribute to staphylococcal persistence, abscess formation, and disease progression. Coagulase-negative mutants that do not produce the public goods themselves are able to exploit those cooperatively secreted by producers and thereby thrive during coinfection at the expense of others. This study shows the importance of social interactions among pathogens concerning clinical outcomes.
Highlights
Staphylococcus aureus engages a large set of its adhesin/invasins, pore-forming toxins, superantigens, and immune evasion factors upon entering tissues or the bloodstream via trauma, surgical wounds, or medical devices[1,2]
Using an in vitro infection model and ex vivo human blood, we recently showed that S. aureus coagulases, staphylocoagulase (Coa) and von Willebrand factor binding protein, act as “public goods” during bloodstream-related infection[4]
We dissect the relative contribution of coagulases from a microbial interactions perspective—whether or not they can function as public goods in mixed S. aureus communities of coagulase-positive and -negative isogenic strains during systemic spread and abscess formation
Summary
P values calculated using general linear hypotheses test with manual contrast). b Number of mice that had abscesses on either one or both of their kidneys; images are of kidneys representing the pathology observed within each cohort. c Splenomegaly plotted as the weight of each spleen (adjusted P values calculated using general linear hypotheses test with manual contrast). d Plot showing Pearson correlation between splenomegaly and pyelonephritis. Mice that were monoinfected with LAC had a higher bacterial load in their kidneys and spleen compared with those monoinfected with Δcoa or ΔcoaΔvwbp (P < 0.001) (Fig. 1e, f), indicating that cheats were impaired in their ability to persist and replicate in host tissue owing to the absence of coagulases. There was a slight decrease in the LAC bacterial load in the kidneys and spleen during coinfection compared to monoinfection These data indicate that the cooperative secretion of coagulases can enhance staphylococcal fitness in host tissues. LAC and ΔcoaΔvwbp had abscess lesions in their kidneys (×2 obj.) (Fig. 2) These demarcated hypercellular regions had a central nidus of staphylococci (×100 obj.) enclosed within an amorphous pseudocapsule (×20 and ×40 obj.) and were circumscribed by zones of apparently dead immune cells. When coinfected together with producers, cheats become shielded (Fig. 2) and are able to persist within the necropurulent foci
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