Heat‐killed <i>Propionibacterium acnes</i> is capable of inducing inflammatory responses in skin

Lyte, Peter; Sur, Runa; Nigam, Anu; Southall, Michael D.

doi:10.1111/j.1600-0625.2009.00891.x

Cited by 38 publications

(27 citation statements)

References 34 publications

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“…A large, randomized controlled trial comparing five antimicrobial regimens noted that clinical efficacy of oral antibiotics was less in those with resistant strains, suggesting that antibiotics may work through a direct antimicrobial as well as anti‐inflammatory effect. This is a concept that the majority of experimental studies have supported, although not all 152–155 . Similar bacterial resistance has been seen in other studies as well, 156,157 and in vitro experiments have shown that resistance may be due to the formation of biofilms 158 .…”

Section: Infectionsupporting

confidence: 66%

Epidemiology of acne vulgaris

Bhate¹,

Williams²

2013

British Journal of Dermatology

685

517

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SummaryDespite acne being an almost universal condition in younger people, relatively little is known about its epidemiology. We sought to review what is known about the distribution and causes of acne by conducting a systematic review of relevant epidemiological studies. We searched Medline and Embase to the end of November 2011. The role of Propionibacterium acnes in pathogenesis is unclear: antibiotics have a direct antimicrobial as well as an anti-inflammatory effect. Moderate-to-severe acne affects around 20% of young people and severity correlates with pubertal maturity. Acne may be presenting at a younger age because of earlier puberty. It is unclear if ethnicity is truly associated with acne. Black individuals are more prone to postinflammatory hyperpigmentation and specific subtypes such as 'pomade acne'. Acne persists into the 20s and 30s in around 64% and 43% of individuals, respectively. The heritability of acne is almost 80% in first-degree relatives. Acne occurs earlier and is more severe in those with a positive family history. Suicidal ideation is more common in those with severe compared with mild acne. In the U.S.A., the cost of acne is over 3 billion dollars per year in terms of treatment and loss of productivity. A systematic review in 2005 found no clear evidence of dietary components increasing acne risk. One small randomized controlled trial showed that low glycaemic index (GI) diets can lower acne severity. A possible association between dairy food intake and acne requires closer scrutiny. Natural sunlight or poor hygiene are not associated. The association between smoking and acne is probably due to confounding. Validated core outcomes in future studies will help in combining future evidence.The clinical and histological features of acne, a chronic inflammatory disease of the pilosebaceous unit, are well described. Scarring is often present following inflammation 3 as illustrated in Figure 1. The pathophysiological events occurring in acne are also relatively well studied. Lesions start when keratinocytes lining the hair follicle desquamate creating a microcomedone. At puberty increased sebum production creates an environment that can sustain the colonization of Propionibacterium acnes. As P. acnes proliferates, inflammatory and chemotactic mediators are produced, which in turn drive inflammatory processes. 4Despite advances in understanding the pathophysiology of acne, much less appears to have been written about its epidemiology, which is strange considering that acne is almost universal in teenage years. Epidemiology not only describes the burden of disease in terms of incidence, prevalence and variations according to age, sex, social class, ethnic group and geography, but also has the potential to identify specific risk factors for disease occurrence or progression, which may be amenable to manipulation. Discovery of risk factors or factors that exacerbate existing disease could lead to appropriate primary or secondary preventative measures and treatments, which in turn could lead t...

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Section: Infectionsupporting

confidence: 66%

Epidemiology of acne vulgaris

Bhate¹,

Williams²

2013

British Journal of Dermatology

685

517

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“…The pathogenetic role of IL-8 has been postulated, at least in part, in neutrophil-related skin diseases such as psoriasis [49,50], palmoplantar pustulosis [50] and acne [48,51,52]. Propionibacterium acnes is feasible for inducing IL-8 production in various cell types including NHEKs [52,53].…”

Section: [ ( ) T D $ F I G ]mentioning

confidence: 99%

An environmental contaminant, benzo(a)pyrene, induces oxidative stress-mediated interleukin-8 production in human keratinocytes via the aryl hydrocarbon receptor signaling pathway

Tsuji

Takahara

Uchi

et al. 2011

Journal of Dermatological Science

138

160

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“…Throughout the activation of TLRs, PARs and antimicrobial peptides, P. acnes upregulates the secretion of different proinflammatory cytokines (IL‐1α, IL‐1β, IL‐6, IL‐8, IL‐12, TNF‐α or granulocyte macrophage colony stimulating factor) by human keratinocytes, sebocytes or macrophages and strongly activates the inflammasome of human peripheral neutrophils …”

Section: P Acnes and Inflammationmentioning

confidence: 99%

Propionibacterium acnes: an update on its role in the pathogenesis of acne

Beylot¹,

Auffret²,

Poli³

et al. 2013

Acad Dermatol Venereol

221

159

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In recent years, significant progress has been made in the understanding of the pathophysiological mechanisms of acne and the role of Propionibacterium acnes. With this review, the authors aim to provide an update on the current understanding of the role of P. acnes in the development of acne lesions and analysing the potential implications for future treatments. A total of 188 articles published between January 1980 and March 2013 were searched using key words such as acne, P. acnes, microbiology, Corynebacterium acnes, acne vulgaris, pathogenesis, antibiotic, vaccination and a combination of those key words. From those articles, 77 were analysed in depth. Recent data confirm that P. acnes has a strong proinflammatory activity and targets molecules involved in the innate cutaneous immunity, keratinocytes and sebaceous glands of the pilosebaceous follicle and leads to the development of comedones. Furthermore, the profile of its different strains may differ between healthy subjects and acne patients. The better understanding of the role of P. acnes may allow for new perspectives in the treatment of acne. Novel therapies should target molecules implicated in the activation of innate immunity, including toll-like receptors, protease-activated receptors and topical antimicrobial peptides; the latter may be an alternative to topical antibiotics and thus a solution for limiting bacterial resistance induced by topical macrolides. Vaccines may also be promising. However, the most appropriate candidate remains to be selected.

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Heat‐killed Propionibacterium acnes is capable of inducing inflammatory responses in skin

Cited by 38 publications

References 34 publications

Epidemiology of acne vulgaris

Epidemiology of acne vulgaris

An environmental contaminant, benzo(a)pyrene, induces oxidative stress-mediated interleukin-8 production in human keratinocytes via the aryl hydrocarbon receptor signaling pathway

Propionibacterium acnes: an update on its role in the pathogenesis of acne

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