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Cutaneous Immune Defenses Against Staphylococcus aureus Infections.

Choi JH, Seo HS, Lim SY, Park K - J Lifestyle Med (2014)

Bottom Line: Staphylococcus aureus (S. aureus) is a virulent bacterium that abundantly colonizes inflammatory skin diseases.In this review, we summarize not only the pathogenesis and key elements of S. aureus skin infections, but also the cutaneous immune system against its infections and colonization.The information obtained from this area may provide the groundwork for further immunomodulatory therapies or vaccination strategies to prevent S. aureus infections.

View Article: PubMed Central - PubMed

Affiliation: Research Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup, Korea;

ABSTRACT
Staphylococcus aureus (S. aureus) is a virulent bacterium that abundantly colonizes inflammatory skin diseases. Since S. aureus infections occur in an impaired skin barrier, it is important to understand the protective mechanism through cutaneous immune responses against S. aureus infections and the interaction with Staphylococcal virulence factors. In this review, we summarize not only the pathogenesis and key elements of S. aureus skin infections, but also the cutaneous immune system against its infections and colonization. The information obtained from this area may provide the groundwork for further immunomodulatory therapies or vaccination strategies to prevent S. aureus infections.

No MeSH data available.


Related in: MedlinePlus

The mechanism of Staphylococcal skin infection and cutaneous immune defense.
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f2-jlm-04-39: The mechanism of Staphylococcal skin infection and cutaneous immune defense.

Mentions: Of these AMPs, CAMP is the first AMP found in the skin. The Vitamin D3-mediated Vitamin D Receptor (VDR) activation is the primary transcriptional regulatory mechanism of CAMP generation in the skin [44,45]. Alternatively, we recently demonstrated that subtoxic external stresses such as UVB irradiation that induce endoplasmic reticulum (ER) stress and increase cellular ceramide production in parallel with stimulated metabolic conversion of sphingosine to sphingosine-1-phosphate (S1P) lead to enhanced CAMP production via an NF-κB activation, independent of the VDR pathway [46,47]. Although a detailed mechanism of how the ER stress-mediated increase in S1P activates NF-B still remains unresolved, our recent studies further demonstrated that CAMP generation likely occurs by an S1P receptor independent mechanism (Fig. 2). CAMP has potent, broad-spectrum antimicrobial activities against virulent S. aureus. It is generally accepted that CAMP disrupts the integrity of the cell membrane of S. aureus, which accounts for their ability to kill invaded S. aureus [40,48]. In addition to antimicrobial activity, CAMP is known to have other functions, e.g., cytokine production, cellular differentiation, and adaptive immunity [49]. Interestingly, CAMP expression is highly increased in skin wounds, and decreased after wound closure, suggesting an important role of CAMP in wound healing [50].


Cutaneous Immune Defenses Against Staphylococcus aureus Infections.

Choi JH, Seo HS, Lim SY, Park K - J Lifestyle Med (2014)

The mechanism of Staphylococcal skin infection and cutaneous immune defense.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4390763&req=5

f2-jlm-04-39: The mechanism of Staphylococcal skin infection and cutaneous immune defense.
Mentions: Of these AMPs, CAMP is the first AMP found in the skin. The Vitamin D3-mediated Vitamin D Receptor (VDR) activation is the primary transcriptional regulatory mechanism of CAMP generation in the skin [44,45]. Alternatively, we recently demonstrated that subtoxic external stresses such as UVB irradiation that induce endoplasmic reticulum (ER) stress and increase cellular ceramide production in parallel with stimulated metabolic conversion of sphingosine to sphingosine-1-phosphate (S1P) lead to enhanced CAMP production via an NF-κB activation, independent of the VDR pathway [46,47]. Although a detailed mechanism of how the ER stress-mediated increase in S1P activates NF-B still remains unresolved, our recent studies further demonstrated that CAMP generation likely occurs by an S1P receptor independent mechanism (Fig. 2). CAMP has potent, broad-spectrum antimicrobial activities against virulent S. aureus. It is generally accepted that CAMP disrupts the integrity of the cell membrane of S. aureus, which accounts for their ability to kill invaded S. aureus [40,48]. In addition to antimicrobial activity, CAMP is known to have other functions, e.g., cytokine production, cellular differentiation, and adaptive immunity [49]. Interestingly, CAMP expression is highly increased in skin wounds, and decreased after wound closure, suggesting an important role of CAMP in wound healing [50].

Bottom Line: Staphylococcus aureus (S. aureus) is a virulent bacterium that abundantly colonizes inflammatory skin diseases.In this review, we summarize not only the pathogenesis and key elements of S. aureus skin infections, but also the cutaneous immune system against its infections and colonization.The information obtained from this area may provide the groundwork for further immunomodulatory therapies or vaccination strategies to prevent S. aureus infections.

View Article: PubMed Central - PubMed

Affiliation: Research Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup, Korea;

ABSTRACT
Staphylococcus aureus (S. aureus) is a virulent bacterium that abundantly colonizes inflammatory skin diseases. Since S. aureus infections occur in an impaired skin barrier, it is important to understand the protective mechanism through cutaneous immune responses against S. aureus infections and the interaction with Staphylococcal virulence factors. In this review, we summarize not only the pathogenesis and key elements of S. aureus skin infections, but also the cutaneous immune system against its infections and colonization. The information obtained from this area may provide the groundwork for further immunomodulatory therapies or vaccination strategies to prevent S. aureus infections.

No MeSH data available.


Related in: MedlinePlus