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Background   Staphylococcus aureus  ( S. aureus ) arthritis is one of the most detrimental joint diseases known and leads to severe joint destruction within days. We hypothesized that the provision of auxiliary immunoregulation via an expanded compartment of T regulatory cells (Tregs) could dampen detrimental aspects of the host immune response whilst preserving its protective nature. Administration of low-dose interleukin 2 (IL2) preferentially expands Tregs, and is being studied as a treatment choice in several autoimmune conditions. We aimed to evaluate the role of IL2 and Tregs in septic arthritis using a well-established mouse model of haematogenously spred  S. aureus  arthritis.    Methods  C57BL/6 or NMRI mice we intravenously (iv) injected with a defined dose of  S. aureus  LS-1 or Newman and the role of IL2 and Tregs were assessed by the following approaches: IL2 was endogenously delivered by intraperitoneal injection of a recombinant adeno-associated virus vector (rAAV) before iv  S. aureus  inoculation; Tregs were depleted before and during  S. aureus  arthritis using antiCD25 antibodies; Tregs were adoptively transferred before induction of  S. aureus  arthritis and finally, recombinant IL2 was used as a treatment starting day 3 after  S. aureus  injection .  Studied outcomes included survival, weight change, bacterial clearance, and joint damage.    Results  Expansion of Tregs induced by IL2 gene therapy prior to disease onset does not compromise host resistance to  S. aureus  infection, as the increased proportions of Tregs reduced the arthritis severity as well as the systemic inflammatory response, while simultaneously preserving the host’s ability to clear the infection.    Conclusions  Pre-treatment with IL2 gene therapy dampens detrimental immune responses but preserves appropriate host defense, which alleviates  S. aureus  septic arthritis in a mouse model.

Pre-treatment with IL2 gene therapy alleviates Staphylococcus aureus arthritis in mice