RGD Reference Report - Epicutaneous exposure to staphylococcal superantigen enterotoxin B enhances allergic lung inflammation via an IL-17A dependent mechanism. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Epicutaneous exposure to staphylococcal superantigen enterotoxin B enhances allergic lung inflammation via an IL-17A dependent mechanism.

Authors: Yu, J  Oh, MH  Park, JU  Myers, AC  Dong, C  Zhu, Z  Zheng, T 
Citation: Yu J, etal., PLoS One. 2012;7(7):e39032. doi: 10.1371/journal.pone.0039032. Epub 2012 Jul 27.
RGD ID: 9068417
Pubmed: PMID:22848348   (View Abstract at PubMed)
PMCID: PMC3407176   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0039032   (Journal Full-text)

Atopic dermatitis (AD) is the initial step of the atopic march: the progression from AD to allergic rhinitis and asthma. There is a close association between skin barrier abnormalities and the development of AD and the atopic march. One of cardinal features of AD is that the lesional skin of the majority of AD patients is chronically colonized with Staphylococcus aureus with half isolates producing superantigen enterotoxin B (SEB). Although diverse roles of SEB in the pathogenesis and severity of AD have been recognized, whether SEB contributes to the dermal inflammation that drives lung inflammation and airway hyperresponsiveness (AHR) has not been examined. Here we show a novel role of S. aureus superantigen SEB in augmenting allergen ovalbumin (Ova) induced atopic march through an IL-17A dependent mechanism. When mice epicutaneously (EC) sensitized with allergen Ova, addition of topical SEB led to not only augmented systemic Th2 responses but also a markedly exaggerated systemic Th17/IL-17 immune environment. The ability of SEB in enhancing Th17/IL-17 was mediated through stimulating lymphocytes in spleen and draining lymph nodes to promote IL-6 production. Epicutaneous sensitization of mice with a combination of Ova and SEB significantly enhanced Ova-induced AHR and granulocytic lung inflammation than Ova allergen alone. When IL-17A was deleted genetically, the effects of SEB on augmenting lung inflammation and AHR were markedly diminished. These findings suggest that chronic heavy colonization of enterotoxin producing S. aureus in the skin of patients with atopic dermatitis may have an important role in the development of atopic march via an IL-17A dependent mechanism.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
atopic dermatitis  ISOIl17a (Mus musculus)9068417; 9068417protein:increased expression:epidermis (mouse)RGD 
atopic dermatitis  IEP 9068417protein:increased expression:epidermis (mouse)RGD 
pneumonia  ISOIl17a (Mus musculus)9068417; 9068417 RGD 
pneumonia  IMP 9068417 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il17a  (interleukin 17A)

Genes (Mus musculus)
Il17a  (interleukin 17A)

Genes (Homo sapiens)
IL17A  (interleukin 17A)


Additional Information