2.50
Hdl Handle:
http://hdl.handle.net/10033/621025
Title:
IL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections.
Authors:
Leech, John M; Lacey, Keenan A ( 0000-0002-9242-0170 ) ; Mulcahy, Michelle E ( 0000-0002-0138-5630 ) ; Medina, Eva; McLoughlin, Rachel M ( 0000-0003-4553-018X )
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.
Citation:
IL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections. 2017, 198 (6):2352-2365 J. Immunol.
Journal:
Journal of immunology (Baltimore, Md. : 1950)
Issue Date:
15-Mar-2017
URI:
http://hdl.handle.net/10033/621025
DOI:
10.4049/jimmunol.1601018
PubMed ID:
28167629
Type:
Article
Language:
en
ISSN:
1550-6606
Appears in Collections:
publications of the research group immunology of infection (INI)

Full metadata record

DC FieldValue Language
dc.contributor.authorLeech, John Men
dc.contributor.authorLacey, Keenan Aen
dc.contributor.authorMulcahy, Michelle Een
dc.contributor.authorMedina, Evaen
dc.contributor.authorMcLoughlin, Rachel Men
dc.date.accessioned2017-07-31T14:37:09Z-
dc.date.available2017-07-31T14:37:09Z-
dc.date.issued2017-03-15-
dc.identifier.citationIL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections. 2017, 198 (6):2352-2365 J. Immunol.en
dc.identifier.issn1550-6606-
dc.identifier.pmid28167629-
dc.identifier.doi10.4049/jimmunol.1601018-
dc.identifier.urihttp://hdl.handle.net/10033/621025-
dc.description.abstractIL-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.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleIL-10 Plays Opposing Roles during Staphylococcus aureus Systemic and Localized Infections.en
dc.typeArticleen
dc.identifier.journalJournal of immunology (Baltimore, Md. : 1950)en

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