Group A Streptococcus translocates across an epithelial barrier via degradation of intercellular junctions

Sumitomo, Tomoko

doi:10.1016/j.job.2015.03.002

Cited by 2 publications

(1 citation statement)

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“…It is likely that intraepidermal invasion of S. pyogenes through sites of abrasions, minor trauma, or insect bites is required for development of superficial skin infection (Stevens and Bryant, 2016 ). We recently reported that S. pyogenes possesses several strategies for TJ and AJ destabilization allowing for bacterial penetration via a paracellular route, raising the possibility that disruption of the keratinocyte barrier by colonized S. pyogenes leads to pyoderma development (Sumitomo et al, 2011 , 2013 , 2016 ; Sumitomo, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Streptococcal Cysteine Protease-Mediated Cleavage of Desmogleins Is Involved in the Pathogenesis of Cutaneous Infection

Sumitomo

Mori

Nakamura

et al. 2018

Front. Cell. Infect. Microbiol.

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Streptococcus pyogenes is responsible for a wide variety of cutaneous infections ranging from superficial impetigo to fulminant invasive necrotizing fasciitis. Dysfunction of desmosomes is associated with the pathogenesis of cutaneous diseases. We identified streptococcal pyrogenic exotoxin B (SpeB) as a proteolytic factor that cleaves the extracellular domains of desmoglein 1 and 3. In an epicutaneous infection model, lesional skin infected with an speB deletion mutant were significantly smaller as compared to those caused by the wild-type strain. Furthermore, immunohistological analysis indicated cleavage of desmogleins that developed around the invasion site of the wild-type strain. In contrast, the speB mutant was preferentially found on the epidermis surface layer. Taken together, our findings provide evidence that SpeB-mediated degradation of desmosomes has a pathogenic role in development of S. pyogenes cutaneous infection.

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