Inhibition of keratinocyte migration by lipopolysaccharide

Loryman, Chris; Mansbridge, Jonathan

doi:10.1111/j.1524-475x.2007.00290.x

Cited by 46 publications

(31 citation statements)

References 41 publications

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“…TLR2, TLR4, TLR6, and TLR13 are highly expressed and enriched as a significant group in skin wounds, but not in tongue wounds. In a recent study, migration of human epidermal keratinocytes, in in vitro scratch wounds, was inhibited by LPS and the inhibition could be blocked partially by anti-TLR4 (75%) and anti-TLR2 (40%) [26]. The emerging roles of TLRs in wound healing has received little experimental attention to date except in chemical or thermal-induced burn injuries [27-31].…”

Section: Discussionmentioning

confidence: 99%

Positional differences in the wound transcriptome of skin and oral mucosa

Chen¹,

Arbieva

Guo³

et al. 2010

BMC Genomics

168

195

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BackgroundWhen compared to skin, oral mucosal wounds heal rapidly and with reduced scar formation. Recent studies suggest that intrinsic differences in inflammation, growth factor production, levels of stem cells, and cellular proliferation capacity may underlie the exceptional healing that occurs in oral mucosa. The current study was designed to compare the transcriptomes of oral mucosal and skin wounds in order to identify critical differences in the healing response at these two sites using an unbiased approach.ResultsUsing microarray analysis, we explored the differences in gene expression in skin and oral mucosal wound healing in a murine model of paired equivalent sized wounds. Samples were examined from days 0 to 10 and spanned all stages of the wound healing process. Using unwounded matched tissue as a control, filtering identified 1,479 probe sets in skin wounds yet only 502 probe sets in mucosal wounds that were significantly differentially expressed over time. Clusters of genes that showed similar patterns of expression were also identified in each wound type. Analysis of functionally related gene expression demonstrated dramatically different reactions to injury between skin and mucosal wounds. To explore whether site-specific differences might be derived from intrinsic differences in cellular responses at each site, we compared the response of isolated epithelial cells from skin and oral mucosa to a defined in vitro stimulus. When cytokine levels were measured, epithelial cells from skin produced significantly higher amounts of proinflammatory cytokines than cells from oral mucosa.ConclusionsThe results provide the first detailed molecular profile of the site-specific differences in the genetic response to injury in mucosa and skin, and suggest the divergent reactions to injury may derive from intrinsic differences in the cellular responses at each site.

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Section: Discussionmentioning

confidence: 99%

Positional differences in the wound transcriptome of skin and oral mucosa

Chen¹,

Arbieva

Guo³

et al. 2010

BMC Genomics

168

195

View full text Add to dashboard Cite

show abstract

“…Recently, several relationships between host defense and microorganisms have been reported (23–25). Niebuhr et al (23) discussed the need for local inflammation to accelerate chronic wound‐healing, but no conclusion could be drawn from this study.…”

Section: Discussionmentioning

confidence: 99%

Biofilm formation on rat skin wounds by Pseudomonas aeruginosa carrying the green fluorescent protein gene

Emi

Toriyabe

Zhang

et al. 2010

Experimental Dermatology

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Most chronic wounds are covered by biofilms. However, questions remain about whether biofilms are a causative factor in delayed wound healing and whether the biofilm state contributes to this pathology. The purpose of this study was to develop an experimental model for convenient observation of biofilm formation on skin wounds. Full-thickness wounds were created on the backs of SD rats. Suspensions of Pseudomonas aeruginosa carrying the gene encoding green fluorescent protein were then applied to the wounds. The wounds were harvested at 8 h, and at 1, 3 and 7 days postwounding for histological and immunohistochemical examinations. Fluorescence microscopy confirmed the presence of a biofilm as early as 8 h. Comparing with non-infected wounds, epithelialization was not delayed. In conclusion, wound healing of rat acute wounds was unaffected by biofilm formation.

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“…7 A potent PAMP, lipopolysaccharide, inhibited keratinocyte migration in a dose-dependent manner and this inhibition was relieved using neutralizing antibodies to TLR4 and TLR2. 8 Recently, TLR4 was reported to be present in keratinocytes at the wound edges and epithelialization was significantly delayed in TLR4-deficient mice. 9 Moreover, increased TLR2 expression has been shown to contribute to prolonged inflammation and delayed wound healing in the experimental diabetic wounds.…”

Section: Innate Immunitymentioning

confidence: 99%