The aim of this study is to quantify D. folliculorum colonisation in rosacea subtypes and age-matched controls and to determine the relationship between D. folliculorum load, rosacea subtype and skin innate immune system activation markers. We set up a multicentre, cross-sectional, prospective study in which 98 adults were included: 50 with facial rosacea, including 18 with erythematotelangiectatic rosacea (ETR), and 32 with papulopustular rosacea (PPR) and 48 age- and sex-matched healthy volunteers. Non-invasive facial samples were taken to quantify D. folliculorum infestation by quantitative PCR and evaluate inflammatory and immune markers. Analysis of the skin samples show that D. folliculorum was detected more frequently in rosacea patients than age-matched controls (96% vs 74%, P < 0.01). D. folliculorum density was 5.7 times higher in rosacea patients than in healthy volunteers. Skin sample analysis showed a higher expression of genes encoding pro-inflammatory cytokines (Il-8, Il-1b, TNF-a) and inflammasome-related genes (NALP-3 and CASP-1) in rosacea, especially PPR. Overexpression of LL-37 and VEGF, as well as CD45RO, MPO and CD163, was observed, indicating broad immune system activation in patients with rosacea. In conclusion, D. folliculorum density is highly increased in patients with rosacea, irrespective of rosacea subtype. There appears to be an inverse relationship between D. folliculorum density and inflammation markers in the skin of rosacea patients, with clear differences between rosacea subtypes.
Sciences (grant no. UL1TR000039), and Arkansas Biosciences Institute (to R.C.K.). S.S.A has salary support from CEGIR (U54 AI117804) which is part of the Rare Diseases Clinical Research Network (RDCRN), an initiative of the Office of Rare Diseases Research (ORDR), NCATS, and is funded through collaboration between NIAID, NIDDK, and NCATS, funded by AI114585 (to T.A.D.). Disclosure of potential conflict of interest: E. Tkachenko owns stock in MuWells Inc (supplier of elastic cell substrates
Background: Tissue-resident memory T (Trm) cells are detrimental in patients with numerous chronic inflammatory diseases, including allergic contact dermatitis (ACD).Objectives: We sought to analyze the contribution of Trm cells to the chronicity and severity of ACD and to define the local parameters regulating their development and functions. Methods: We used an experimental model of ACD (ie, contact hypersensitivity to 2,4-dinitrofluorobenzene) that is mediated by CD8 1 T cells. Results: Our data show that early effector T cells accumulated in the skin during the acute contact hypersensitivity reaction and gave rise to epidermal CD8 1 Trm cells expressing a specific set of inhibitory checkpoint receptors (ICRs), such as programmed cell death protein 1 (PD-1) and T cell immunoglobulin and mucin domain 3 (TIM-3). Those Trm cells remained in the epidermis for several weeks and mediated the eczema exacerbations, which developed on allergen re-exposure without the contribution of circulating specific T cells. Furthermore, allergen-induced Trm cell reactivation was constrained because treatment with ICR antagonists dramatically enhanced the magnitude and severity of eczema exacerbations. Finally, we show that the persistence of the
Interactions between the immune system and skin bacteria are of major importance in the pathophysiology of atopic dermatitis (AD), yet our understanding of them is limited. From a cohort of very young AD children (1 to 3 years old), sensitized to Dermatophagoides pteronyssinus allergens (Der p), we conducted culturomic analysis of skin microbiota, cutaneous transcript profiling and quantification of anti-Der p CD4+ T cells. This showed that the presence of S. aureus in inflamed skin of AD patients was associated with a high IgE response, increased expression of inflammatory and Th2/Th22 transcripts and the prevalence of a peripheral Th2 anti-Der p response. Monocyte-derived dendritic cells (moDC) exposed to the S. aureus and S. epidermidis secretomes were found to release pro-inflammatory IFN-γ and anti-inflammatory IL-10, respectively. Allogeneic moDC exposed to the S. aureus secretome also induced the proliferation of CD4+ T cells and this effect was counteracted by concurrent exposure to the S. epidermidis secretome. In addition, whereas the S. epidermidis secretome promoted the activity of regulatory T cells (Treg) in suppressing the proliferation of conventional CD4+ T cells, the Treg lost this ability in the presence of the S. aureus secretome. We therefore conclude that S. aureus may cause and promote inflammation in the skin of AD children through concomitant Th2 activation and the silencing of resident Treg cells. Commensals such as S. epidermidis may counteract these effects by inducing the release of IL-10 by skin dendritic cells.
The report describes a method for the assay of five enzymatic activities involved in establishing the stratum corneum permeability barrier: β-glucocerebrosidase, acid phosphatase, phospholipase A2 (PLA2) and two serine proteases: chymotrypsin and its activator in the stratum corneum, trypsin. The specific activities of these different enzymes have been determined along with their pH profiles and sensivities to specific inhibitors. It can be noted that only two presented a pH optimum similar to the pH of the stratum corneum. This could suggest that their activities are regulated by local variations in pH. The method was applied to a pathological situation, that of a non-eczematous dry atopic dermatitis. Atopic skin had significantly reduced trypsin activity, increased acid phosphatase and no change in the activities of three other studied enzymes. Understanding these activities can provide a tool for the characterization of skin pathologies and for the development of a certain number of applications in cosmetology and therapeutics.
Background/ObjectivesThe use of emollients is widely recommended for the management of atopic dermatitis (AD), especially between flares. An imbalance of skin microflora is suspected of playing a key role in exacerbations of AD. Our aim was to evaluate the effect of a new emollient balm on clinical parameters (SCORing Atopic Dermatitis [SCORAD], xerosis, pruritus), skin barrier function (transepidermal water loss and loricrin, filaggrin, corneodesmosin, and involucrin expression], skin microflora biodiversity, and Staphylococcus aureus and Staphylococcus epidermidis balance in children with mild AD.MethodsFifty‐four children (1–4 yrs old) were enrolled in this randomized, controlled study. Subjects applied a hygiene product and the emollient balm (emollient group, n = 28) or the hygiene product only (control group, n = 26) twice a day for 28 days.ResultsWe found improvement in favor of the emollient group in SCORAD (p < 0.001), pruritus (p = 0.06), and xerosis (p = 0.06) after 28 days of application. Moreover, transepidermal water loss decreased in the emollient group by 34% (p = 0.06) and involucrin expression by 37% (p = 0.001) at day 28 from baseline in association with improvement in barrier function, whereas other barrier‐specific proteins did not vary. S. aureus increased significantly in the control group only (6.5 times, p = 0.01), whereas S. epidermidis remained stable in both groups. The Shannon index (H′ = 2.3) did not vary with treatment in either group.ConclusionTwice‐daily application of a new emollient balm in children with mild AD protected the skin from S. aureus proliferation and preserved microflora biodiversity.
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