Abstract:
:Atopic dermatitis (AD) shows an increased susceptibility to Staphylococcus aureus infection partly due to decreased expression of human beta-defensin-2 (HBD-2). Interestingly, it was reported that the nasal carrier S. aureus down-regulates the expression of HBD-2 and -3, thereby the carrier strains of S. aureus retain an advantage to epithelial colonization and infection. In this study, we tried to isolate and characterize S. aureus from an AD patient, with recurrent oozing on his face. We studied the increased expression of inflammatory cytokines, such as IL-1beta, -6, -8, and TNF-alpha in S. aureus treated-HaCaT cells, which are mediated by secreting superantigens (SAgs), structural component, or both. In addition, we investigated whether the SAgs from S. aureus can down-regulate the expression of HBD-2 in HaCaT cells making favorable conditions for colonization on skin. Our data showed that the isolated S. aureus has the exotoxin gene, sea exotoxin. The SEA producing-S. aureus induced the expression of IL-1beta, -6, -8 cytokines, and TNF-alpha in HaCaT cells. The expression of HBD-2 was increased in S. aureus-treated HaCaT cells. Furthermore IL-8 was also induced by the structure component of S. aureus. Taken together, the SEA producing S. aureus induced the up-regulation of pro-inflammatory cytokines as well as HBD-2, thereby resulting in induction of the persistent eczematous skin lesions in AD. Thus, our data may give insight into understanding the pathogenesis by which S. aureus induces and aggravates eczematous skin lesions in AD.
journal_name
Int J Mol Medjournal_title
International journal of molecular medicineauthors
Cho JW,Cho SY,Lee KSdoi
10.3892/ijmm_00000135subject
Has Abstractpub_date
2009-03-01 00:00:00pages
331-5issue
3eissn
1107-3756issn
1791-244Xjournal_volume
23pub_type
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