Abstract
Staphylococcus aureus (S. aureus) infections are a major healthcare challenge and new treatment alternatives are needed. S. aureus septic arthritis, a debilitating joint disease, causes permanent joint dysfunction in almost 50% of the patients. S. aureus bacteremia is associated with higher mortalities than bacteremia caused by most other microbes and can develop to severe sepsis and death. The key to new therapies is understanding the interplay between bacterial virulence factors and host immune response, which decides the disease outcome. S. aureus produces numerous virulence factors that facilitate bacterial dissemination, invasion into joint cavity, and cause septic arthritis. Monocytes, activated by several components of S. aureus such as lipoproteins, are responsible for bone destructions. In S. aureus sepsis, cytokine storm induced by S. aureus components leads to the hyperinflammatory status, DIC, multiple organ failure, and later death. The immune suppressive therapies at the very early time point might be protective. However, the timing of treatment is crucial, as late treatment may aggravate the immune paralysis and lead to uncontrolled infection and death.
Highlights
We demonstrated that the virulence associated with PGN O-acetyltransferase A (OatA), in both systemic and local S. aureus-induced septic arthritis model, led to milder progression of the disease in mice infected with a ∆oatA
VWbp but not Coa expressed by S. aureus facilitates the initiation of septic arthritis and such an effect might be mediated through its interaction with a host factor, strongly suggesting bacterial adherence to blood vessels is more important than fibrin clotting function of coagulases in induction of septic arthritis [38]
Innate immunity including neutrophils and complement system plays a protective role in the development of septic arthritis
Summary
S. aureus expresses a capsular polysaccharide (CP) that functions as a virulent factor, enabling the bacteria to evade phagocytosis [4]. S. aureus SA113 ∆lgt mutant strain that lacks Lpp maturation, induced more knee swelling compared to its parental strain This coincided with increased IL-6 expression and higher bacterial burden in the local knee [14]. In a hematogenous septic arthritis model, increased bacterial persistence was observed in both C57BL/6 wild-type and TLR2 deficient murine kidneys when inoculated intravenously with the S. aureus Newman parental strain compared to its ∆lgt mutant strain [26]. This is in agreement with earlier reports showing that different organs, including the kidneys, exhibited higher bacterial loads when infected with SA113 parental strain in comparison to the ∆lgt mutant strain, independent of TLR2 and MyD88 signaling [27].
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