Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Panteleyev, Andrey A.; Bickers, David R.

doi:10.1111/j.1600-0625.2006.00476.x

Cited by 130 publications

(128 citation statements)

References 253 publications

(353 reference statements)

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“…Clinically, marked volume reduction or absence of SGs was observed in patients with dioxininduced chloracne; the latter been the marker of dioxin intoxication in humans [139]. Similar changes in SGs were also found in patients with hidradenitis suppurativa/acne inversa, in whom cigarette smoking is a high risk factor [140].…”

Section: Sebaceous Glands and Skin Skin Detoxificationsupporting

confidence: 50%

Beyond acne: Current aspects of sebaceous gland biology and function

Zouboulis¹,

Picardo

Qiang

et al. 2016

Rev Endocr Metab Disord

115

112

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The sebaceous gland is mostly found in association with a hair follicle. Its traditional function is the holocrine production of sebum, a complex mixture of lipids, cell debris, and other rather poorly characterized substances. Due to the gland central role in acne pathogenesis, early research had focused on its lipogenic activity. Less-studied aspects of the sebaceous gland, such as stem cell biology, the regulation of cellular differentiation by transcription factors, the significance of specific lipid fractions, the endocrine and specially the neuroendocrine role of the sebaceous gland, and its contribution to the innate immunity, the detoxification of the skin and skin aging have recently attracted the attention of researchers from different disciplines. Here, we summarize recent, multidisciplinary progress in sebaceous gland research and discuss how sebaceous gland research may stimulate the development of novel therapeutic strategies targeting specific molecular pathways of the pathogenesis of skin diseases.

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Section: Sebaceous Glands and Skin Skin Detoxificationsupporting

confidence: 50%

Beyond acne: Current aspects of sebaceous gland biology and function

Zouboulis¹,

Picardo

Qiang

et al. 2016

Rev Endocr Metab Disord

115

112

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“…This chronic condition is characterized by metaplasia and hyperkeratinization of the ducts of the sebaceous gland, resulting in comedone formation, along with hyperproliferation and differentiation of the interfollicular squamous epithelium (5). As for other endpoints of dioxin toxicity, the mechanism of chloracne is not known.…”

Section: Egf Receptor Signaling Blocks Aryl Hydrocarbon Receptor-medimentioning

confidence: 99%

“…As for other endpoints of dioxin toxicity, the mechanism of chloracne is not known. Also, the severity and persistence of chloracne does not correlate with the half-life or concentration of the chloracnegen, indicating that additional factors likely modulate individual susceptibility (5).…”

Section: Egf Receptor Signaling Blocks Aryl Hydrocarbon Receptor-medimentioning

confidence: 99%

EGF receptor signaling blocks aryl hydrocarbon receptor-mediated transcription and cell differentiation in human epidermal keratinocytes

Sutter

Yin

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Fig. 4. Opposing effects of TCDD and EGF on differentiation of NHEKs. (A)NHEKs were grown to confluence, and basal medium, or medium with ␣-naphthoflavone (NF, 1 M) was added 24 h before treatment. CEs were isolated after treatment with either 0.1% DMSO or TCDD (10 nM) for 5 days. (B) NHEKs were grown to confluence, and basal medium with or without EGF (10 ng/mL) was added 24 h before treatment. CEs were isolated after treatment with either 0.1% DMSO or TCDD (10 nM) for 5 days. (C) NHEKs were grown to confluence, and basal medium, or medium with EGF (10 ng/mL), was added 24 h before treatment. CEs were isolated after treatment with either 0.1% DMSO or TCDD (10 nM) in the presence or absence of PD153035 (300 nM) for 5 days. (A-C) The values for CEs are a mean of triplicate samples Ϯ SD. (D-G) NHEKs were grown to a cell density of either 50% or 100% confluence before basal medium, or medium with EGF (10 ng/mL), was added for 24 h before treatment. Total mRNA was isolated after treatment with either control vehicle (0.1% DMSO) or TCDD (10 nM) for 24 h. Real-time PCR was used to determine the relative expression of each indicated gene (y axis). Levels of mRNA [mean (n ϭ 3) Ϯ SD] are expressed in units relative to the minimum, given a value of 1. (A-G) The a indicates that the value from treatment with TCDD is significantly different from the DMSO control; the b indicates that the value from cotreatment with TCDD and NF is significantly different from TCDD alone; the c indicates that the value from cotreatment with TCDD and EGF is significantly different from with TCDD alone; the d indicates that the value from treatment with TCDD, EGF, and PD153035 is significantly different from treatment with TCDD and EGF; and the e indicates that treatment with EGF is significantly different from DMSO control treatment. For each of these comparisons, P Յ 0.01 by Student's t test. Comparisons made in D-G are within the group grown to a cell density of 100% confluence.

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“…22 Earlier views ever thought that SGs are replaced by keratinized epithelial cells because SGs undergo squamous metaplasia and keratinization in patients with chloracne. 23 Recently Panteleyev and Bickers 22 produced a hypothesis to explain the pathogenesis of chloracne based on epidermal stem cell theory that chloracnegeninduced transformation of the pilosebaceous unit is driven by activation and accelerated exit of cells from the stem cell compartment coupled with a shift from a pilosebaceous differentiation pattern to an epidermal one.…”

Section: Pathogenesis Of Chloracnementioning

confidence: 99%

Environmental pollution and acne-chloracne

Qiang

Zouboulis

Xia

2009

Dermato-Endocrinology

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Environmental pollutants can result in a variant of acne called 'chloracne'. Chloracne is caused by systemic exposure to certain halogenated aromatic hydrocarbons 'chloracnegens', and is considered to be one of the most sensitive indicators of systemic poisoning by these compounds. Dioxin is the most potent environmental chloracnegen. Most cases of chloracne have resulted from occupational and non-occupational exposures, non-occupational chloracne mainly resulted from contaminated industrial wastes and contaminated food products. Non-inflammatory comedones and straw-colored cysts are the primary clinical manifestation of chloracne. Increasing of cysts in number is a signal of aggravation of chloracne. Generalized lesions can appear on the face, neck, trunk, exterimities, genitalia, axillary and other areas. Course of chloracne is chronic. Severity of chloracne is related to dosage of exposed chloracnegens, chloracnegenic potency and individual susceptibility. Histopathology of chloracne is characterized mainly by hyperplasia of epidermal cell, while follicular and sebaceous gland are taken placed by keratinized epidermal cell. The pathogenesis of chloracne maybe related to the imbalance of epidermal stem cell. Chloracne appears to be resistant to all tested forms of treatment. The only way to control chloracne is to prevent exposure to chloracnegens.

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Dioxin‐induced chloracne – reconstructing the cellular and molecular mechanisms of a classic environmental disease

Cited by 130 publications

References 253 publications

Beyond acne: Current aspects of sebaceous gland biology and function

Beyond acne: Current aspects of sebaceous gland biology and function

EGF receptor signaling blocks aryl hydrocarbon receptor-mediated transcription and cell differentiation in human epidermal keratinocytes

Environmental pollution and acne-chloracne

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