Which factors influence Demodex proliferation? A retrospective pilot study highlighting a possible role of subtle immune variations and sebaceous gland status

Forton, F.; Maertelaer, Viviane De

doi:10.1111/1346-8138.15910

Cited by 20 publications

(27 citation statements)

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“…Demodex spp. are tiny mites living in the pilosebaceous follicles ( Boxberger et al, 2021 ; Forton and De Maertelaer, 2021 ). Viruses have been the less investigated elements of the skin microbiota, cutaneous β and γ human papillomaviruses are commonly found on the skin surface but are scarce contrasted to the phages of the bacterial flora inhabiting the skin ( Boxberger et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

The Human Skin Microbiome in Selected Cutaneous Diseases

Carmona-Cruz

Orozco‐Covarrubias

Sáez‐de‐Ocariz

2022

Front. Cell. Infect. Microbiol.

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The human skin harbors a wide variety of microbes that, together with their genetic information and host interactions, form the human skin microbiome. The role of the human microbiome in the development of various diseases has lately gained interest. According to several studies, changes in the cutaneous microbiota are involved in the pathophysiology of several dermatoses. A better delineation of the human microbiome and its interactions with the innate and adaptive immune systems could lead to a better understanding of these diseases, as well as the opportunity to achieve new therapeutic modalities. The present review centers on the most recent knowledge on skin microbiome and its participation in the pathogenesis of several skin disorders: atopic and seborrheic dermatitis, alopecia areata, psoriasis and acne.

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Section: Introductionmentioning

confidence: 99%

The Human Skin Microbiome in Selected Cutaneous Diseases

Carmona-Cruz

Orozco‐Covarrubias

Sáez‐de‐Ocariz

2022

Front. Cell. Infect. Microbiol.

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“…190 Corticosteroids (of which abnormal endogenous synthesis is encountered in rosacea) 140 may favour proliferation when Demodex densities (Dds) are low, via an immunosuppressive effect, and thus cause steroid-induced rosacea, 33,52,53,133,191,198,199 but could limit excessive proliferation of Demodex when Dds are high, by an atrophic action on the pilosebaceous follicles. 170,190,200 Good facial hygiene may also potentially reduce mite proliferation. 4,191,201 Genetic influences may play a role at different levels (black asterisks), including a possible specific immune defect that limits defence against the mite.…”

Section: Etr Seems To Favour Demodex Proliferationmentioning

confidence: 99%

“…This schema builds on our previously published schemas. 9,11,190 immunomodulatory and pro-angiogenic effects of VEGF may explain why Dds can be normal in as many as half of subjects with ETR. 33,138 This action of VEGF on mite proliferation may also explain why, in patients who have both conditions, PPR is more often observed after ETR than the inverse.…”

Section: Etr Seems To Favour Demodex Proliferationmentioning

confidence: 99%

“…These factors can induce flushes and ETR, may potentially aggravate/amplify the immunogenic reaction against the mite and, via VEGF production, could indirectly promote Demodex proliferation 33. Age and sex influence Demodex proliferation likely via the production of androgens and their effects on sebaceous glands, where the mites live 170,190. Immune defects (IDs) of various origins may favour Demodex proliferation: marked immunodepression (rare, for example, associated with HIV [human immunodeficiency virus] infection),107,115,122,125,126,196 and, more frequently, more subtle immunodeficiency, for example, associated with thymic stromal lymphopoietin (TSLP, increased in sebaceous gland rich areas),30 Staphylococcus epidermidis (via the action of its lipoteichoic acid)6,190,197 and, potentially, pregnancy and hypothyroidism 190.…”

mentioning

confidence: 99%

“…Good facial hygiene may also potentially reduce mite proliferation 4,191,201. Genetic influences may play a role at different levels (black asterisks), including a possible specific immune defect that limits defence against the mite 190,202. The primary factors initially favouring mite proliferation (in green) influence the initial phenotype (i.e.…”

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confidence: 99%

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Rosacea, an infectious disease: why rosacea with papulopustules should be considered a demodicosis. A narrative review

Forton¹

2022

Acad Dermatol Venereol

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Rosacea and demodicosis are common facial conditions in dermatology practice. While demodicosis is clearly the result of Demodex mite infestation, the pathogenicity of rosacea is still not sufficiently explained, so that it is defined by its symptoms, and not by its cause. It is usually considered as a disease of the immune system associated with neurogenic inflammation triggered by various factors (ultraviolet light, heat, spicy food, alcohol, stress and microorganisms). Its links with demodicosis remain controversial, although there is increasing evidence that Demodex mites may play a key role in the inflammatory process. Indeed, high Demodex densities are observed in nearly all cases of rosacea with papulopustules (PPR) and the papulopustules of rosacea can be effectively treated with topical acaricidal agents. Recent studies suggest that Demodex induces two opposite actions on host immunity: a defensive immune response aimed at eliminating the mite and an immunosuppressive action aimed at favouring its own proliferation. Moreover, the initial defensive immune response is likely diverted towards benefit for the mite, via T‐cell exhaustion induced by the immunosuppressive properties of vascular endothelial growth factor, which may also explain the favourable influence that the altered vascular background of rosacea seems to exert on Demodex proliferation. In this review, the evidence for and against a causal role of Demodex in rosacea is discussed, applying three systems traditionally used to attribute causality to a disease (modified Koch criteria, Hill criteria for causality and Rothman model). The findings suggest that PPR can reasonably be attributed to Demodex proliferation, which appears to be a necessary factor in the centre of a causal network in which multiple co‐factors interact and influence the occurrence and severity of inflammatory symptoms, from limited (pityriasis folliculorum) to more marked (PPR). PPR could, therefore, be considered as a chronic infection by Demodex mites with associated T‐cell exhaustion.

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Impact of house dust mite in vitiligo skin: environmental contribution to increased cutaneous immunity and melanocyte detachment

Bzioueche

Boniface

Drullion

et al. 2023

British Journal of Dermatology

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Background Vitiligo is an autoimmune skin disorder characterized by loss of melanocytes. Protease-mediated disruption of junctions between keratinocytes and/or keratinocyte intrinsic dysfunction may directly contribute to melanocyte loss. House dust mite (HDM), an environmental allergen with potent protease activity, contributes to respiratory and gut disease but also to atopic dermatitis and rosacea. Objective To verify if HDM can contribute to melanocyte detachment in vitiligo and if so, by which mechanism(s). Methods Using primary human keratinocytes, human skin biopsies from healthy and vitiligo patients, and 3D reconstructed human epidermis, we studied the effect of HDM on cutaneous immunity, tight and adherent junction expression and melanocyte detachment. Results HDM increased keratinocyte production of vitiligo-associated cytokines and chemokines and increased expression of TLR-4. This was associated with increased in situ MMP-9 activity, reduced cutaneous expression of adherent protein E-cadherin, increased soluble E-cadherin in culture supernatant and significantly increased number of supra-basal melanocytes in the skin. This effect was dose-dependent and driven by cysteine protease Der p1 and MMP-9. Selective MMP-9 inhibitor, Ab142180 restored E-cadherin expression and inhibited HDM-induced melanocyte detachment. Keratinocytes from vitiligo patients were more sensitive to HDM-induced changes than healthy keratinocytes. All results were confirmed in 3D model of healthy skin and in human skin biopsies. Conclusions Our results highlight that environmental mite may act as an external source of PAMPs in vitiligo and topical MMP-9 inhibitors may be useful therapeutic targets. Whether HDM contributes to onset of flares in vitiligo remains to be tested in carefully controlled trials.

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Which factors influence Demodex proliferation? A retrospective pilot study highlighting a possible role of subtle immune variations and sebaceous gland status

Abstract: The study was approved by our local institutional review board (Erasme Hospital, P 2014/117).

Cited by 20 publications

References 73 publications

The Human Skin Microbiome in Selected Cutaneous Diseases

The Human Skin Microbiome in Selected Cutaneous Diseases

Rosacea, an infectious disease: why rosacea with papulopustules should be considered a demodicosis. A narrative review

Impact of house dust mite in vitiligo skin: environmental contribution to increased cutaneous immunity and melanocyte detachment

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