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Janus kinase (JAK) pathways have emerged as targets of treatment, yet localization and expression of JAK1 and JAK3 in canine atopic skin have not been studied. This study aimed to compare the localization and expression of JAK1 and JAK3 in the skin of atopic dogs before and after allergen exposure. Skin biopsies taken from atopic beagles sensitized to house dust mites (HDM) before (D0) and after four weeks (D28) of allergen exposure were stained. Staining was subjectively scored by examiners unaware of the source of the slides. Image J was used for the semiquantitative assessment of staining intensity. JAK1 and JAK3 staining was epidermal and dermal. JAK1 staining was cytoplasmic, primarily found in basal keratinocytes and dermal cells, while JAK 3 was nuclear (all epidermal levels and on dermal inflammatory cells). Epidermal thickness was significantly higher on D28 than on D0 (p < 0.0001). For JAK1, epidermal staining divided by epithelial thickness was significantly lower on D28 (p = 0.0002) compared to D0. For JAK3 staining, intensity in the dermis was significantly higher on D28 (p = 0.0405) compared to D0. We conclude that decreased expression of JAK1 in the epidermis and increased expression of JAK3 in the dermis of atopic dogs occur after allergen exposure.

Previous studies documented antibiotic resistance in horses but did not focus on skin specifically. We investigated antibiotic resistance and correlations between resistance patterns in skin infections. Records from 2009 to 2019 were searched for Staphylococcal infection and susceptibility results. Seventy-seven cases were included. Organisms identified were S. aureus (48/77), S. pseudintermedius (7/77), non-hemolytic Staphylococcus (8/77), beta-hemolytic Staphylococcus (6/77), and other species (8/77). Samples included pyoderma (36/77), wounds (10/77), abscesses (15/77), incision sites (5/77), nose (8/77), and foot (3/77). A trend analysis using non-parametric Spearman’s test showed significant upward trend of resistance (p < 0.05) for 3/15 antibiotics (ampicillin, cefazolin, penicillin). Susceptibility was significantly different by Staphylococcal species for 8/15 antibiotics. Gentamicin showed significant susceptibility differences based on source (all abscesses were susceptible to gentamicin). Steel-Dwass test showed statistically significant (p = 0.003) difference between incision sites and abscesses. A non-parametric Kendall’s T-test found significantly negative correlation between cefazolin and amikacin sensitivity (p = 0.0108) and multiple positive correlations of resistance (p < 0.05). This study confirms increasing resistance in dermatologic samples. It is unlikely that the sample source affects resistance, but Staphylococcus species may affect it. Study limitations include lack of information about previous antibiotic use and small sample size.

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.

Canine progenitor epidermal keratinocytes (CPEK) are used as canine keratinocyte cell line. Their suitability for skin barrier studies is unknown. Measurement of transepithelial electric resistance (TEER) evaluates epithelial permeability. We compared TEER and tight junction (TJ) expression in CPEKs and normal keratinocytes (NK) harvested from biopsies of normal dogs. CPEKs and NK were grown until confluence (D0) and for 13 additional days. Slides were fixed on D0 and stained with ZO-1 and claudin-1 antibodies. Five images/antibody were taken, randomized and evaluated blindly by three investigators for intensity, staining location, granularity, and continuousness. Cell size and variability were evaluated. TEER increased overtime to 2000 Ohms/cm in NK, while remained around 100–150 Ohms/cm in CPEK. ANOVA showed significant effect of time (p < 0.0001), group (p < 0.0001) and group x time interaction (p < 0.0001) for TEER. Size of CPEKs was significantly (p < 0.0001) smaller and less variable (p = 0.0078) than NK. Intensity of claudin-1 staining was greater in CPEKs (p < 0.0001) while granularity was less in CPEKs (p = 0.0012). For ZO-1, cytoplasmic staining was greater in CPEK (p < 0.0001) while membrane continuousness of staining was greater in NK (p = 0.0002). We conclude that CPEKs grown in monolayer are not representative of NK for permeability studies.

Canine atopic dermatitis (CAD) is chronic and frequently complicated by Staphylococcal infections. Understanding the role of allergen dose, frequency and duration of exposure in triggering infections requires a model. Most models elicit acute inflammation and do not mimic real-life disease. Here we describe the effects of allergen exposures on development of infections in a model of chronic CAD. Diagnosis of pyoderma was based on clinical signs and consistent cytology. Study 1 evaluated the role of duration of exposure keeping the daily dose constant (25 mg/day). The one-week protocol involved three exposures, 3 days in a row. The one-month protocol involved twice-weekly challenges for 4 weeks. The three-month protocol involved twice-weekly challenges for 12 weeks. Study 2 evaluated different daily doses while keeping constant the total weekly dose (25 mg) and duration (3 weeks). Low-dose used 5 mg/day for 5 days, each week. High-dose used 12.5 mg/day twice-weekly. In Study 1, the longer the exposure, the more dogs developed pyoderma (6/9 in the three-month study, 2/9 in the one-month and 0 in the one-week). In Study 2, low-dose daily exposure caused more infections (5/8) than high-dose infrequent exposure (0/8). It is concluded that low-grade, daily exposure for a long time is most relevant for development of staphylococcal infections.

Atopic dermatitis is a clinical syndrome that affects both people and animals. Dogs closely mimic the complexity of the human skin disease, and much progress has been made in recent years in terms of our understanding of the role of skin impairment and the identification of new treatments. Cats and horses also develop atopic syndromes which include both cutaneous and respiratory signs, yet studies in these species are lagging. It is now recognized that atopic dermatitis is not a single disease but a multifaceted clinical syndrome with different pathways in various subgroups of patients. Appreciating this complexity is clinically relevant as we develop more targeted treatments which may work well in some patients but not in others. Different phenotypes of atopic dermatitis have been described in dogs, and it is possible that phenotypes related to breed and age may exist in other animals similar to how they are described in people. The awareness of different mechanisms of disease leads to the desire to correlate different phenotypes with specific biomarkers and responses to treatment. In this review, the current understanding and updated information on atopic syndrome in animals are described, highlighting opportunities for further studies in the future.

Allergic diseases have great impact on the quality of life of both people and domestic animals. They are increasing in prevalence in both animals and humans, possibly due to the changed lifestyle conditions and the decreased exposure to beneficial microorganisms. Dogs, in particular, suffer from environmental skin allergies and develop a clinical presentation which is very similar to the one of children with eczema. Thus, dogs are a very useful species to improve our understanding on the mechanisms involved in people’s allergies and a natural model to study eczema. Animal models are frequently used to elucidate mechanisms of disease and to control for confounding factors which are present in studies with patients with spontaneously occurring disease and to test new therapies that can be beneficial in both species. It has been found that drugs useful in one species can also have benefits in other species highlighting the importance of a comprehensive understanding of diseases across species and the value of comparative studies. The purpose of the current article is to review allergic diseases across species and to focus on how these diseases compare to the counterpart in people.

Atopic Dermatitis (AD) is a prevalent disease that affects both humans and animals. Dogs share similar environments with the owners and spontaneously develop a disease that is clinically and immunologically identical to AD in humans. In past decades AD has become more and more common in both dogs and humans, possibly due to the increased exposure to indoor allergens and decreased exposure to parasites and beneficial bacteria. The allergic component plays an important role in both species. Allergen specific immunotherapy (ASIT) has been used with great success in veterinary medicine for decades for the treatment of AD and traditionally has been accomplished with subcutaneous injections. In human medicine, ASIT has been traditionally used for respiratory manifestations of atopic disease and only recently considered for the therapy of AD. Interestingly, dogs primarily express cutaneous manifestations of atopic disease and only rarely progress from cutaneous into respiratory disease, a process referred in human medicine as “atopic march”. Recently, sublingual immunotherapy has been replacing subcutaneous immunotherapy both in human and veterinary medicine due to its ease and safety, leading to increased compliance. The purpose of this mini review is to focus on the use of sublingual immunotherapy for AD highlighting similarities and differences between humans and dogs.

Atopic dermatitis is an extremely common, pruritic, and frustrating disease to treat in both people and animals. Atopic dermatitis is multifactorial and results from complex interactions between genetic and environmental factors. Much progress has been done in recent years in terms of understanding the complex pathogenesis of this clinical syndrome and the identification of new treatments. As we learn more about it, we appreciate the striking similarities that exist in the clinical manifestations of this disease across species. Both in animals and people, atopic disease is becoming increasingly common and important similarities exist in terms of immunologic aberrations and the propensity for allergic sensitization. The purpose of this review is to highlight the most recent views on atopic dermatitis in both domestic species and in people emphasizing the similarities and the differences. A comparative approach can be beneficial in understanding the natural course of this disease and the variable response to existing therapies.

Canine atopic dermatitis (CAD) is chronic and frequently complicated by Staphylococcal infections. Understanding the role of allergen dose, frequency and duration of exposure in triggering infections requires a model. Most models elicit acute inflammation and do not mimic real-life disease. Here we describe the effects of allergen exposures on development of infections in a model of chronic CAD. Diagnosis of pyoderma was based on clinical signs and consistent cytology. Study 1 evaluated the role of duration of exposure keeping the daily dose constant (25 mg/day). The one-week protocol involved three exposures, 3 days in a row. The one-month protocol involved twice-weekly challenges for 4 weeks. The three-month protocol involved twice-weekly challenges for 12 weeks. Study 2 evaluated different daily doses while keeping constant the total weekly dose (25 mg) and duration (3 weeks). Low-dose used 5 mg/day for 5 days, each week. High-dose used 12.5 mg/day twice-weekly. In Study 1, the longer the exposure, the more dogs developed pyoderma (6/9 in the three-month study, 2/9 in the one-month and 0 in the one-week). In Study 2, low-dose daily exposure caused more infections (5/8) than high-dose infrequent exposure (0/8). It is concluded that low-grade, daily exposure for a long time is most relevant for development of staphylococcal infections. [ABSTRACT FROM AUTHOR]