Transient and reversible reduction of stratum corneum filaggrin degradation products after allergen challenge in experimentally mite‐sensitised atopic dogs

Olivry, Thierry; Paps, Judy S.; Amalric, Nicolas

doi:10.1111/vde.13026

Cited by 5 publications

(3 citation statements)

References 32 publications

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“…It is still unknown if the demonstrated alterations of these proteins, enzymes and NMFs represent a primary defect or are secondary to an inflammatory state. A very recent study, using experimentally sensitised atopic dogs, 21 indirectly suggested that some of these alterations may be a result of cutaneous allergic inflammation rather than being a primary defect.…”

Section: Updates On Stratum Corneum Structural Proteinsmentioning

confidence: 99%

Update on the skin barrier, cutaneous microbiome and host defence peptides in canine atopic dermatitis

Santoro,

Saridomichelakis,

Eisenschenk

et al. 2023

Veterinary Dermatology

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BackgroundCanine atopic dermatitis (AD) is a complex inflammatory skin disease associated with cutaneous microbiome, immunological and skin barrier alterations. This review summarises the current evidence on skin barrier defects and on cutaneous microbiome dysfunction in canine AD.ObjectiveTo this aim, online citation databases, abstracts and proceedings from international meetings on skin barrier and cutaneous microbiome published between 2015 and 2023 were reviewed.ResultsSince the last update on the pathogenesis of canine AD, published by the International Committee on Allergic Diseases of Animals in 2015, 49 articles have been published on skin barrier function, cutaneous/aural innate immunity and the cutaneous/aural microbiome in atopic dogs. Skin barrier dysfunction and cutaneous microbial dysbiosis are essential players in the pathogenesis of canine AD. It is still unclear if such alterations are primary or secondary to cutaneous inflammation, although some evidence supports their primary involvement in the pathogenesis of canine AD.Conclusion and Clinical RelevanceAlthough many studies have been published since 2015, the understanding of the cutaneous host–microbe interaction is still unclear, as is the role that cutaneous dysbiosis plays in the development and/or worsening of canine AD. More studies are needed aiming to design new therapeutic approaches to restore the skin barrier, to increase and optimise the cutaneous natural defences, and to rebalance the cutaneous microbiome.

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Section: Updates On Stratum Corneum Structural Proteinsmentioning

confidence: 99%

Update on the skin barrier, cutaneous microbiome and host defence peptides in canine atopic dermatitis

Santoro,

Saridomichelakis,

Eisenschenk

et al. 2023

Veterinary Dermatology

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“…Skin barrier dysfunction and abnormalities in keratinocyte differentiation appear to play an important role in canine atopic dermatitis (AD) [ 1 , 2 , 3 ]. Debate exists as to whether some of these changes are primary and linked to genetic mutations [ 4 , 5 ] or whether they are mainly observed due to inflammation [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Differences in Behavior between Normal and Atopic Keratinocytes in Culture: Pilot Studies

Marsella

Ahrens

Wilkes

2022

Veterinary Sciences

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Skin barrier dysfunction is important in atopic dermatitis and can be secondary to inflammation. Observation of keratinocytes in culture may show intrinsic differences. TransEpithelial Electrical Resistance (TEER) measures epithelial permeability. We cultured normal and atopic keratinocytes and found that TEER of atopic keratinocytes was significantly lower (p < 0.0001) than that of normals. Atopic keratinocytes grew upwards, first creating isolated dome-like structures and later horizontally into a monolayer. At time of confluence (D0), atopic keratinocytes were more differentiated, with higher filaggrin gene expression than normals. No differences existed between groups for TJ proteins (claudin, occludin, and Zonula Occludens-1) on D0 and D6. On D6, claudin and occludin were higher than D0, in normal (p = 0.0296 and p = 0.0011) and atopic keratinocytes (p = 0.0348 and 0.0491). Immunofluorescent staining showed nuclear location of filaggrin on D0 and cytoplasmic on D6. ANOVA showed increased cell size from D0 to D6 in both groups (effect of time, p = 0.0076) but no differences between groups. Significant subject effect (p = 0.0022) was found, indicating that cell size was subject-dependent but not disease-dependent. No difference for continuity for TJ protein existed between groups. These observations suggest that decreased TEER in atopics is not linked to TJ differences but is possibly linked to different growth behavior.

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“…One of the main targets of the multimodal approach to CAD management is restoring epidermal barrier function and integrity [ 4 ]. Although it is still not clear whether the defective skin barrier is pre-existing or is secondary to allergic inflammation, it has been suggested that some of the skin barrier anomalies may develop secondary to the underlying skin inflammation [ 9 ]. Lipid alterations have been reported in CAD with decreased levels of free fatty acid and ceramides in the stratum corneum (SC) [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Enhanced In Vitro Expression of Filaggrin and Antimicrobial Peptides Following Application of Glycosaminoglycans and a Sphingomyelin-Rich Lipid Extract

Segarra

Naiken²,

Garnier³

et al. 2022

Veterinary Sciences

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Filaggrin is an epidermal protein involved in skin barrier formation and hydration, whose expression is altered in canine atopic dermatitis (CAD). CAD patients also present an abnormal immune response with an altered expression of antimicrobial peptides (AMPs), such as β-defensins and cathelicidins. Sphingolipids and glycosaminoglycans (GAGs) have been reported to improve the skin barrier in several animal species, including dogs. Our objective was to evaluate the in vitro effects of a sphingomyelin-rich lipid extract (LE), a hyaluronic acid-rich GAG matrix, and their combination, on the expression of filaggrin and human β-defensin 2 (hBD-2). Filaggrin expression was quantified in a reconstructed human epidermis (RHE), and hBD-2 in normal human epidermal keratinocyte (NHEK) cultures. LE and GAGs were tested at 0.02 mg/mL, with or without adding a cytokine mix. A significant increase in mean hBD-2, compared to the control (99 pg/mL) was achieved with LE (138 pg/mL) and LE+GAGs (165 pg/mL). Filaggrin increased with GAGs (202% ± 83) and LE (193% ± 44) vs. the stimulated control, but this difference was statistically significant (p < 0.05) only with LE+GAGs (210% ± 39). In conclusion, the tested GAGs and LE enhance filaggrin and AMP expression in vitro, which might benefit CAD patients if applied in vivo.

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Transient and reversible reduction of stratum corneum filaggrin degradation products after allergen challenge in experimentally mite‐sensitised atopic dogs

Cited by 5 publications

References 32 publications

Update on the skin barrier, cutaneous microbiome and host defence peptides in canine atopic dermatitis

Update on the skin barrier, cutaneous microbiome and host defence peptides in canine atopic dermatitis

Differences in Behavior between Normal and Atopic Keratinocytes in Culture: Pilot Studies

Enhanced In Vitro Expression of Filaggrin and Antimicrobial Peptides Following Application of Glycosaminoglycans and a Sphingomyelin-Rich Lipid Extract

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