Response of corneal epithelial cells to<i>Staphylococcus aureus</i>

Heimer, Susan R.; Yamada, Ai; Russell, Hugh; Gilmore, Michael S.

doi:10.4161/viru.1.4.11466

Cited by 23 publications

(27 citation statements)

References 74 publications

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“…95 94 lends further support to this theory: a large increase in the dendritic cell chemokine CCL20 was identified when human corneal epithelial cells were stimulated with both toxigenic and non-toxigenic strains of S. aureus, which appeared to be independent of TLR2 stimulation. Bacterial lipoproteins have also been shown to activate alternative pathways to MyD88, including p38 and ERK but also JNK.…”

Section: Pattern Recognition Mechanisms Activated By Microbial Pathogmentioning

confidence: 60%

“…39,41 a crucial bactericidal agent. Interestingly, work by Heimer et al 94 suggests that on infection of human corneal epithelial cells in vitro the principal difference between toxigenic and non-toxigenic strains of S. aureus appears to be an increased activation of stress response molecules such as heat shock proteins on exposure to a toxigenic strain of S. aureus.…”

Section: Pattern Recognition Mechanisms Activated By Microbial Pathogmentioning

confidence: 99%

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Pattern recognition receptors in microbial keratitis

Taube

Cendra

Elsahn

et al. 2015

Eye

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Section: Pattern Recognition Mechanisms Activated By Microbial Pathogmentioning

confidence: 60%

Section: Pattern Recognition Mechanisms Activated By Microbial Pathogmentioning

confidence: 99%

Pattern recognition receptors in microbial keratitis

Taube

Cendra

Elsahn

et al. 2015

Eye

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“…Exposure of keratinocytes to staphylococcal alpha-toxin resulted in the doubling of the S+G2/M phase [20]. Transcriptome analyses of the human corneal epithelial cells exposed to S. aureus and S. aureus -infected bovine mammary tissue revealed an alteration in the expression profiles of genes that affect the cell cycle progression [21], [22]. To our knowledge, the implications of S. aureus in the alteration of the eukaryotic cell cycle and the biological significance of such an alteration has never been investigated.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus-Induced G2/M Phase Transition Delay in Host Epithelial Cells Increases Bacterial Infective Efficiency

et al. 2013

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Staphylococcus aureus is a highly versatile, opportunistic pathogen and the etiological agent of a wide range of infections in humans and warm-blooded animals. The epithelial surface is its principal site of colonization and infection. In this work, we investigated the cytopathic effect of S. aureus strains from human and animal origins and their ability to affect the host cell cycle in human HeLa and bovine MAC-T epithelial cell lines. S. aureus invasion slowed down cell proliferation and induced a cytopathic effect, resulting in the enlargement of host cells. A dramatic decrease in the number of mitotic cells was observed in the infected cultures. Flow cytometry analysis revealed an S. aureus-induced delay in the G2/M phase transition in synchronous HeLa cells. This delay required the presence of live S. aureus since the addition of the heat-killed bacteria did not alter the cell cycle. The results of Western blot experiments showed that the G2/M transition delay was associated with the accumulation of inactive cyclin-dependent kinase Cdk1, a key inducer of mitosis entry, and with the accumulation of unphosphorylated histone H3, which was correlated with a reduction of the mitotic cell number. Analysis of S. aureus proliferation in asynchronous, G1- and G2-phase-enriched HeLa cells showed that the G2 phase was preferential for bacterial infective efficiency, suggesting that the G2 phase delay may be used by S. aureus for propagation within the host. Taken together, our results divulge the potential of S. aureus in the subversion of key cellular processes such as cell cycle progression, and shed light on the biological significance of S. aureus-induced host cell cycle alteration.

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“…Both of these genes are likely to be induced by oxidative damage. CDKN1A encodes p21Cip1/Waf1, a potent CDKN, previously reported in corneal epithelial cells with infection23 and in the limbal stem cell of the cornea 24. CDKN1A expression is controlled by the damage-inducible transcription factor p53; recent work has shown that in UV-irradiated corneal epithelial cells, levels of p53 protein are increased, though in contrast with the damage response in most other tissues p53 gene transcription is not affected 25.…”

Section: Discussionmentioning

confidence: 96%