RGD Reference Report - Protective immunity against recurrent Staphylococcus aureus skin infection requires antibody and interleukin-17A. - Rat Genome Database

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Protective immunity against recurrent Staphylococcus aureus skin infection requires antibody and interleukin-17A.

Authors: Montgomery, CP  Daniels, M  Zhao, F  Alegre, ML  Chong, AS  Daum, RS 
Citation: Montgomery CP, etal., Infect Immun. 2014 May;82(5):2125-34. doi: 10.1128/IAI.01491-14. Epub 2014 Mar 10.
RGD ID: 9068425
Pubmed: PMID:24614654   (View Abstract at PubMed)
PMCID: PMC3993461   (View Article at PubMed Central)
DOI: DOI:10.1128/IAI.01491-14   (Journal Full-text)

Although many microbial infections elicit an adaptive immune response that can protect against reinfection, it is generally thought that Staphylococcus aureus infections fail to generate protective immunity despite detectable T and B cell responses. No vaccine is yet proven to prevent S. aureus infections in humans, and efforts to develop one have been hampered by a lack of animal models in which protective immunity occurs. Our results describe a novel mouse model of protective immunity against recurrent infection, in which S. aureus skin and soft tissue infection (SSTI) strongly protected against secondary SSTI in BALB/c mice but much less so in C57BL/6 mice. This protection was dependent on antibody, because adoptive transfer of immune BALB/c serum or purified antibody into either BALB/c or C57BL/6 mice resulted in smaller skin lesions. We also identified an antibody-independent mechanism, because B cell-deficient mice were partially protected against secondary S. aureus SSTI and adoptive transfer of T cells from immune BALB/c mice resulted in smaller lesions upon primary infection. Furthermore, neutralization of interleukin-17A (IL-17A) abolished T cell-mediated protection in BALB/c mice, whereas neutralization of gamma interferon (IFN-gamma) enhanced protection in C57BL/6 mice. Therefore, protective immunity against recurrent S. aureus SSTI was advanced by antibody and the Th17/IL-17A pathway and prevented by the Th1/IFN-gamma pathway, suggesting that targeting both cell-mediated and humoral immunity might optimally protect against secondary S. aureus SSTI. These findings also highlight the importance of the mouse genetic background in the development of protective immunity against S. aureus SSTI.




  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
IL17AHumanStaphylococcal Skin Infections  ISOIl17a (Mus musculus) RGD 
Il17aRatStaphylococcal Skin Infections  ISOIl17a (Mus musculus) RGD 
Il17aMouseStaphylococcal Skin Infections  IMP  RGD 


Genes (Rattus norvegicus)
Il17a  (interleukin 17A)

Genes (Mus musculus)
Il17a  (interleukin 17A)

Genes (Homo sapiens)
IL17A  (interleukin 17A)