TITLE

Panton-Valentine Leukocidin Facilitates the Escape of Staphylococcus aureus From Human Keratinocyte Endosomes and Induces Apoptosis

AUTHOR(S)
Chi, Chia-Yu; Lin, Chia-Chun; Liao, I-Chuang; Yao, Yi-Chuan; Shen, Fan-Ching; Liu, Ching-Chuan; Lin, Chiou-Feng
PUB. DATE
January 2014
SOURCE
Journal of Infectious Diseases;Jan2014, Vol. 209 Issue 2, p224
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Skin and soft-tissue infections (SSTIs) caused by community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) have emerged as major health problems throughout the world. Most SSTI CA-MRSA strains produce Panton-Valentine leukocidin (PVL), but its contribution to CA-MRSA pathogenesis is poorly defined. Here, we used an endemic PVL-positive SSTI-causing CA-MRSA strain from Taiwan, together with an isogenic PVL-knockout mutant (Δpvl) and complemented PVL-positive derivative, to evaluate the role of PVL in the pathogenesis of CA-MRSA in the RHEK-1 human keratinocyte cell line and a rabbit skin infection model. We found that both PVL-positive CA-MRSA and isogenic Δpvl strains attached and were engulfed into endosomes of RHEK-1 cells within 1 hour following infection. However, by 2 hours after infection PVL-positive CA-MRSA more effectively disrupted endosomes, escaped into the cytoplasm, and replicated intracellularly. By 6 hours after infection, the PVL-positive strain caused significantly more caspase-dependent keratinocyte apoptosis than the isogenic Δpvl mutant. In the rabbit infection model, 1 week following infection the wild-type strain produced significantly more widespread lesions and cell apoptosis than the isogenic Δpvl mutant. These findings indicate that PVL is an important virulence factor that enables CA-MRSA to produce necrotizing skin infections by allowing the bacteria to escape from endosomes, replicate intracellularly, and induce apoptosis.
ACCESSION #
93399108

 

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