IL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections.
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2017Access:
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Leech, J.M., Lacey, K.A., Mulcahy, M.E., Medina, E. & Mc Loughlin, R.M. IL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections., 2017, 198, 6Download Item:
Abstract:
IL-10 is a potent anti-inflammatory mediator that plays a crucial role in limiting host immunopathology during bacterial infections by controlling effector T cell activation. Staphylococcus aureus has previously been shown to manipulate the IL-10 response as a mechanism of immune evasion during chronic systemic and biofilm models of infection. In the present study, we demonstrate divergent roles for IL-10 depending on the site of infection. During acute systemic S. aureus infection, IL-10 plays an important protective role and is required to prevent bacterial dissemination and host morbidity by controlling effector T cells and the associated downstream hyperactivation of inflammatory phagocytes, which are capable of host tissue damage. CD19+CD11b+CD5+ B1a regulatory cells were shown to rapidly express IL-10 in a TLR2-dependent manner in response to S. aureus, and adoptive transfer of B1a cells was protective during acute systemic infection in IL-10–deficient hosts. In contrast, during localized s.c. infection, IL-10 production plays a detrimental role by facilitating bacterial persistence via the same mechanism of controlling proinflammatory T cell responses. Our findings demonstrate that induction of IL-10 has a major influence on disease outcome during acute S. aureus infection. Too much IL-10 at one end of the scale may suppress otherwise protective T cell responses, thus facilitating persistence of the bacteria, and at the other end, too little IL-10 may tend toward fatal host-mediated pathology through excessive activation of T cells and associated phagocyte-mediated damage.
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Science Foundation Ireland
12/IP/1532
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http://people.tcd.ie/mclougrmDescription:
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198;6;
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IL-10, T cell activation, Staphylococcus aureusDOI:
http://dx.doi: 10.4049/jimmunol.1601018Metadata
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