Review of the Innate Immune Response in Acne vulgaris: Activation of Toll-Like Receptor 2 in Acne Triggers Inflammatory Cytokine Responses

@article{Kim2005ReviewOT,
  title={Review of the Innate Immune Response in Acne vulgaris: Activation of Toll-Like Receptor 2 in Acne Triggers Inflammatory Cytokine Responses},
  author={Jenny Kim},
  journal={Dermatology},
  year={2005},
  volume={211},
  pages={193 - 198}
}
  • Jenny Kim
  • Published 1 October 2005
  • Biology, Medicine
  • Dermatology
Acne vulgaris is a common disorder that affects 40–50 million people in the USA alone. The pathogenesis of acne is multifactorial, including hormonal, microbiological and immunological mechanisms. One of the factors that contributes to the pathogenesis of acne is Propionibacterium acnes; yet, the molecular mechanism by which P. acnes induces inflammation is not known. Recent studies have demonstrated that microbial agents trigger cytokine responses via Toll-like receptors (TLRs). TLRs are… 
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Toll-like receptor 2 plays a critical role in pathogenesis of acne vulgaris
TLDR
This review focuses on the molecular structure of TLR2 as well as mechanism howTLR2 recognize P. acnes to induce inflammatory cytokines, which is related to acne vulgaris pathogenesis.
Propionibacterium acnes induces an interleukin-17 response in acne vulgaris that is regulated by vitamin A and vitamin D
TLDR
It is demonstrated that IL-17 is induced by P. acnes and expressed in acne lesions and that both vitamin A and vitamin D could be effective tools to modulate Th17-mediated diseases such as acne.
TLR2 and TLR4 Polymorphisms Are Not Associated with Acne Vulgaris
TLDR
Two mutations of the TLR2 gene as well as two polymorphisms of theTLR4 gene causing the amino acid changes Asp299Gly and Thr399Ile are investigated in 101 Caucasian subjects, 63 with acne vulgaris and 38 healthy controls.
Propionibacterium acnes and lipopolysaccharide induce the expression of antimicrobial peptides and proinflammatory cytokines/chemokines in human sebocytes.
Tumour Necrosis Factor Alpha-induced Protein 3 Negatively Regulates Cutibacterium acnes-induced Innate Immune Events in Epidermal Keratinocytes.
TLDR
The results suggest that TNFAIP3 may have a general role in fine regulation of microbiota-induced cutaneous immune homeostasis, and its role in these regulatory events is suggested.
Role of Cytokines in the Pathogenesis of Acne
TLDR
It was concluded that acne is a model of chronic immunodeficiency inflammatory dermatoses with the activation of innate immunity and the subsequent development of the adaptive T-cell immune response.
Toll‐like receptor 2 mediates inflammatory cytokine induction but not sensitization for liver injury by Propioni‐ bacterium acnes
TLDR
Results suggest that although P. acnes triggers TLR2‐mediated cell activation, TLR 2‐independent but MyD88‐dependent mechanisms mediate in vivo sensitization by P. Acnes for LPS‐induced liver injury.
The protective effects of melittin on Propionibacterium acnes-induced inflammatory responses in vitro and in vivo.
TLDR
The feasibility of applying melittin for the prevention of inflammatory skin diseases induced by P. acnes is demonstrated andMelittin treatment significantly suppressed the expression of pro-inflammatory cytokines through regulation of the NF-κB and MAPK signaling pathways.
In vitro modulation of TLR‐2, CD1d and IL‐10 by adapalene on normal human skin and acne inflammatory lesions
Abstract  The anti‐inflammatory mechanisms of adapalene, a synthetic retinoid used for the treatment of acne patients, are partially understood. They seem particularly related to the modulation of…
Establishment of an Anti-acne Vulgaris Evaluation Method Based on TLR2 and TLR4-mediated Interleukin-8 Production
TLDR
An assay that evaluates acne by determining TLR2 and 4 expression and activation and can be used for the evaluation of anti-acne treatment is presented.
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