Atopic Skin Research Articles

Risk of skin atrophy induced by short-term topical corticosteroid use in atopic dermatitis lesional skin: A systematic review

Risk of skin atrophy induced by short-term topical corticosteroid use in atopic dermatitis lesional skin: A systematic review

A CCR4 antagonist attenuates atopic dermatitis-like skin inflammation by inhibiting the recruitment and expansion of Th2 cells and Th17 cells.

CCR4 is a major trafficking receptor for T-helper (Th) 2 cells and Th17 cells and is considered as a potential therapeutic target for atopic dermatitis (AD). The CCR4 ligands CCL17 and CCL22 have been reported to be upregulated in the skin lesions of AD patients. Of note, thymic stromal lymphopoietin (TSLP), a master regulator of the Th2 immune response, promotes the expression of CCL17 and CCL22 in AD skin lesions. Here, we investigated the role of CCR4 in an AD mouse model induced by MC903, a TSLP inducer. Topical application of MC903 to ear skin increased the expression of not only TSLP but also CCL17, CCL22, the Th2 cytokine IL-4, and the Th17 cytokine IL-17A. Consistently, MC903 induced AD-like skin lesions as shown by increased epidermal thickness; increased infiltration of eosinophils, mast cells, type 2 innate lymphoid cells, Th2 cells, and Th17 cells; and elevated serum levels of total IgE. We also found increased expansion of Th2 cells and Th17 cells in the regional lymph nodes (LNs) of AD mice. Compound 22, a CCR4 inhibitor, ameliorated AD-like skin lesions with reduction of Th2 cells and Th17 cells in the skin lesions and regional LNs. We further confirmed that compound 22 diminished the expansion of Th2 cells and Th17 cells in the coculture of CD11c+ dendritic cells (DCs) and CD4+ T cells derived from the regional LNs of AD mice. Collectively, CCR4 antagonists may exhibit anti-allergic effects by inhibiting both the recruitment and expansion of Th2 cells and Th17 cells in AD.

Foxp3 and Bcl6 deficiency synergistically induces spontaneous development of atopic dermatitis-like skin disease.

Atopic dermatitis (AD) is a common chronic skin disease caused by immune dysfunction, specifically the hyperactivation of Th2 immunity. AD is a complex disease with multiple factors contributing to its development; however, the interaction between these factors is not fully understood. In this study, we demonstrated that the conditional deletion of both the forkhead box p3 (Foxp3) and B-cell lymphoma 6 (Bcl6) genes induced the spontaneous development of AD-like skin inflammation with hyperactivation of type 2 immunity, skin barrier dysfunction, and pruritus, which were not induced by the single deletion of each gene. Furthermore, the development of AD-like skin inflammation was largely dependent on IL-4/13 signaling but not on immunoglobulin E (IgE). Interestingly, we found that the loss of Bcl6 alone increased the expression of thymic stromal lymphopoietin (TSLP) and interleukin (IL)-33 in the skin, suggesting that Bcl6 controls Th2 responses by suppressing TSLP and IL-33 expression in epithelial cells. Our results suggest that Foxp3 and Bcl6 cooperatively suppress the pathogenesis of AD. Furthermore, these results revealed an unexpected role of Bcl6 in suppressing Th2 responses in the skin.

Analysis of the Effective Components of Cocos nucifera L. Oil on Atopic Dermatitis Skin Disease and Staphylococcus Aureus Bacteria

The major objective of the research was to investigate the in vitro antibacterial susceptibility to particular fatty acids contained in coconut oil on a collection of clinical isolates. especially, the chronic skin condition Atopic dermatitis (Atopic eczema). caused by gram-positive bacteria (Staphylococcus aureus). Clinical isolates were collected from Shar Hospitals, and the organisms went through a typical biochemical examination evolution. While coconut oil was obtained using the centrifuge method to extract coconut oil (CE VCO). The sensitivity evaluation was conducted using the disc diffusion method. Lastly, used a measuring tool to estimate the inhibitory zones' diameter. In another hand, after analysis of the oil by GC-MASS, Coconut oil contained numerous chemical components and the highest amount was Oleic acid 54.62%, while the smallest amount was N-Hexadecanoic acid, N-Hexadecanoic acid, (Myristic acid), % 3.34. Sequentially, Heneicosane, 9-Octadecenoic acid (Z)- % 13.78, with 9,12-Octadecadienoic acid 11.23%, and Nonadecane and his isomers 5.77% percent. Coconut oil doesn't show any sensitivity and a high potential for antibacterial activity due to the high contents of medium and long-chain saturated and unsaturated fatty acids so This study recommends further studies should be done on the oil and its derivative both in vitro and in vivo for showing its mechanisms of actions.

The Quality of Life of Allergic Cats, Treated with Allergen-Specific Immunotherapy – A Retrospective Study

Abstract Feline atopic skin syndrome (FASS) describes allergic skin diseases in cats associated with sensitivity to environmental allergens. Allergen-specific immunotherapy (ASIT) aims to reduce or eliminate symptoms associated with subsequent exposure to the causative allergen. The primary outcome of this study was to determine if the quality of life (QoL) of cats and owners improved as a result of ASIT. The secondary outcome was to determine whether the QoL improved in cats treated with ASIT compared with cats treated symptomatically. Eight cats were included in the ASIT group (AG) and 6 cats in the control group (CG). Validated quality of life questionnaires were retrospectively completed by cat owners for the period before and after treatment. The QoL of cats improved significantly with ASIT. Cats were significantly less lazy, nervous, aggressive, restrained, preened less while sleeping and hid less, were less disturbed by consultations, were more playful and interactive with their environment, and had better appetites than before treatment. Owners felt significantly less physically exhausted and less emotionally distressed compared to before ASIT treatment and their expenses were significantly lower. On the contrary various symptomatic treatments did not significantly improve the quality of life of the cats or their owners in any of the terms. No serious side effects were observed with ASIT. The quality of life of animals suffering from chronic diseases is important as it determines the decisions of owners and veterinarians on the modalities of lifelong treatment. Validated questionnaires are still rarely used in veterinary practice and research.

A systematic review of allergen immunotherapy, a successful therapy for canine atopic dermatitis and feline atopic skin syndrome.

Canine atopic dermatitis and feline atopic skin syndrome are common presentations in small animal practice. Numerous drugs are used for symptomatic therapy. The only definitive treatment based on the cause of the disease is allergen immunotherapy. Classical allergen immunotherapy (AIT) consists of subcutaneous injections of an extract containing offending allergens, with increasing doses and allergen concentrations at short intervals during the induction phase of several weeks to months followed by a maintenance phase, where a fixed dose is typically given at longer intervals. Dose and interval are tailored to the individual patient. Newer types of AIT include rush immunotherapy, where the induction phase is abbreviated, intralymphatic immunotherapy, and oromucosal or sublingual immunotherapy. AIT aims at inducing a regulatory T-cell response and subsequently downregulating the exaggerated immune response to offending allergens leading to clinical signs. This article reviews the published knowledge about allergen immunotherapy in dogs and cats for small animal practitioners.

ВЛАГОЧУВСТВИТЕЛЬНЫЕ IN SITU СИСТЕМЫ В КОМПЛЕКСНОЙ ТЕРАПИИ АТОПИЧЕСКОГО ДЕРМАТИТА

Self-emulsifying drug delivery systems (SEDDS) are modern forms for drug agent delivery with improved biopharmaceutical characteristics. By their formation mechanism they belong to the group of in situ systems - forms formed at the application site, under the influence of specific physiological or pathological factors. Dermatological SEDDS for external use that form an emulsion at the absorption site upon contact with water are characterized by a number of advantages, both in terms of use and technology. Moisture-sensitive SEDDS are compositions of oil, surfactant, emollients and co-surfactants. Emulsification occurs with minimal mechanical action, and the emulsion formed provides effective transdermal absorption of the active ingredients, soothing, moisturizing, and protective effects on the skin. All these advantages can be effectively applied in local symptomatic treatment of atopic dermatitis. Topical SEDDS are currently known to be developed for the treatment of melanoma, viral and fungal diseases, protection against ultraviolet radiation. Atopic dermatitis (AD) is a chronic dermatological disease accompanied by itching, burning, dry and flaky skin, reduced protective function of the epidermis, susceptibility to fungal and bacterial infections. Using alkaline skin care products for patients with AD negatively affects the pH of the skin and affects it accordingly. In addition, the using of soaps causes thinning of the skin in both normal and atopic skin, which can aggravate the course of the disease. Therefore, the use of moisture-activated SEDDS in the complex external treatment of AD is reasonable both as agents for daily skin care, maintenance of its basic functions, and as drugs for transdermal delivery of active ingredients.

Staphylococcus epidermidis isolates from atopic or healthy skin have opposite effect on skin cells: potential implication of the AHR pathway modulation.

Staphylococcus epidermidis is a commensal bacterium ubiquitously present on human skin. This species is considered as a key member of the healthy skin microbiota, involved in the defense against pathogens, modulating the immune system, and involved in wound repair. Simultaneously, S. epidermidis is the second cause of nosocomial infections and an overgrowth of S. epidermidis has been described in skin disorders such as atopic dermatitis. Diverse isolates of S. epidermidis co-exist on the skin. Elucidating the genetic and phenotypic specificities of these species in skin health and disease is key to better understand their role in various skin conditions. Additionally, the exact mechanisms by which commensals interact with host cells is partially understood. We hypothesized that S. epidermidis isolates identified from different skin origins could play distinct roles on skin differentiation and that these effects could be mediated by the aryl hydrocarbon receptor (AhR) pathway. For this purpose, a library of 12 strains originated from healthy skin (non-hyperseborrheic (NH) and hyperseborrheic (H) skin types) and disease skin (atopic (AD) skin type) was characterized at the genomic and phenotypic levels. Here we showed that strains from atopic lesional skin alter the epidermis structure of a 3D reconstructed skin model whereas strains from NH healthy skin do not. All strains from NH healthy skin induced AhR/OVOL1 path and produced high quantities of indole metabolites in co-culture with NHEK; especially indole-3-aldehyde (IAld) and indole-3-lactic acid (ILA); while AD strains did not induce AhR/OVOL1 path but its inhibitor STAT6 and produced the lowest levels of indoles as compared to the other strains. As a consequence, strains from AD skin altered the differentiation markers FLG and DSG1. The results presented here, on a library of 12 strains, showed that S. epidermidis originated from NH healthy skin and atopic skin have opposite effects on the epidermal cohesion and structure and that these differences could be linked to their capacity to produce metabolites, which in turn could activate AHR pathway. Our results on a specific library of strains provide new insights into how S. epidermidis may interact with the skin to promote health or disease.

The Diagnostic Value of Delayed-Type Reactions to Perennial Aeroallergens for Atopic Disease.

Background: Delayed-type reactions to aeroallergens have been observed, however, their clinical significance continues to be debated. Objective: We assessed the prevalence and significance of delayed-type reactions to aeroallergens in atopic patients. Methods: Retrospective study including 266 patients with history or evidence of atopic disease (atopic dermatitis [AD], allergic rhinitis, and/or allergic asthma) and tested via either the intradermal skin test (IDT) or atopy patch test for common aeroallergens, specifically house dust mites (Dermatophagoides farinae, Dermatophagoides pteronyssinus) and perennial molds (Aspergillus fumigatus, Penicillium notatum). All patients were tested via IDT with both immediate (15 minute) and delayed (2 and 4 days) readings. Delayed reading was considered positive if the IDT injection site demonstrated at least 5 mm induration 48 hours after inoculation. Results: In total, 195 (73.3%) patients demonstrated an immediate-type reaction, whereas 118 (44.4%) had a delayed-type reaction. In total, 75 (28.2%) patients experienced both immediate- and delayed-type reactions, 43 (16.2%) reacted delayed-type only, and 85.3% of delayed-type reactions to individual aeroallergens were associated with eczematous lesions predominantly in air-exposed areas. Conclusion: Delayed-type reactions to aeroallergens are prevalent and clinically significant as a component of extrinsic AD and atopic diseases. The data support delayed reading of the IDT to guide diagnosis and management in these patients.

Loss of microRNA-29 in B cells leads to atopic skin phenotype in mice

Abstract Developing B cells are highly dependent on microRNA (miRNA) regulation. We have previously demonstrated the miR-29 family of miRNAs contributes to the regulation of B cell survival through fine-tuning of PTEN expression, a negative regulator of B cell receptor (BCR) signaling. When the miR-29 alleles are selectively deleted in B cells, this leads to reduced survival which can be rescued by ablating one copy of Ptento restore normal BCR signaling. We observed that mice with B cells lacking miR-29 also develop an inflammatory skin phenotype associated with lesions, leukocyte infiltration into the skin, and persistent pruritis. Nearly 50% of miR-29-deficient animals die within 6 months of birth, and ablation of Ptento restore BCR signaling did not improve the survival rate. This suggests that additional targets of miR-29 in B lymphocytes are involved in promoting this inflammatory skin condition. Epidermal thickening, granulocyte plasma cell infiltration in the skin, and high serum IgE titers suggest that miR-29 may contribute to the regulation of IgE-driven immune responses and that in the absence of this miRNA family, animals develop atopic dermatitis. Our bioinformatic analysis revealed that miR29 is predicted to regulate the expression of the Il4Ratranscript, and in vitrodifferentiation assays revealed that miR-29-deficient B cells have a higher propensity for IgE class switch recombination in response to IL-4 and/or IL-13 stimulation compared to wild-type control B cells. We conclude that miR-29 is critical in the regulation of both Ptenand Il4raexpression in mature B cells thereby influencing the survival and function of peripheral B lymphocytes, which can have profound repercussions for the development of autoimmune disease. The Bernard Levine Fellowship

956 Epidermal keratinocyte-specific STAT3 deficiency aggravated atopic dermatitis-like skin inflammation in mice through TSLP upregulation

956 Epidermal keratinocyte-specific STAT3 deficiency aggravated atopic dermatitis-like skin inflammation in mice through TSLP upregulation

414 Identification of metagenes for prediction of therapeutic efficacy and disease monitoring by decomposing atopic dermatitis skin mRNA-seq data

414 Identification of metagenes for prediction of therapeutic efficacy and disease monitoring by decomposing atopic dermatitis skin mRNA-seq data

Development and validation of the atopic dermatitis and infant skincare knowledge, attitude, and practice (ADISKAP 1.0) scale.

Preserving skin health is crucial for atopic dermatitis control as well as for the thriving of children. However, a well-developed and validated tool that measures the knowledge, attitude, and practice of skin care is lacking. To develop and validate the atopic dermatitis and infant skincare knowledge, attitude, and practice (ADISKAP 1.0) scale that measures parental health literacy on atopic dermatitis and skin care. We conducted a review of the literature, a focus group (two dermatologists and 12 parents), and a panel discussion in order to generate the ADISKAP prototype. Two samples of parents with knowingly superior (dermatologists, n = 59) and inferior (general population, n = 395) knowledge traits participated in the validation of ADISKAP. Cronbach's alpha was reported as a measure of internal consistency, and the intraclass correlation coefficient (ICC) was calculated to assess the test-retest validity. The known-groups technique was used to evaluate construct validity. The ADISKAP scale contained 17 items after content and face validity validation. After removing items that displayed poor test-retest reliability (n = 4) and construct validity (n = 3), 12 items were retained in the ADISKAP 1.0. ADISKAP 1.0 is a reliable and valid tool for assessing parental knowledge, attitude, and practice on infantile atopic dermatitis and skin care.

Influence of the cream with filaggrin activity modulator for dry and sensitive skin in children with mild to moderate severity atopic dermatitis on objective indicators of skin barrier function and disease severity indices

BACKGROUND: Atopic dermatitis is a chronic, relapsing and severely itchy dermatitis that usually occurs in childhood and has a characteristic age-related distribution. Atopic dermatitis is relatively frequent, affecting 1020% of children in developed countries. Atopic dermatitis in children associated with poor school performance, low self-esteem and family problems. Recent studies show importance in atopic dermatitis pathogenesis of protein filaggrin and modulation of its activity may be a promising direction in the pathogenic therapy of atopic dermatitis.
 AIM: to study the effect of a cream for dry, sensitive and atopic skin with a modulator of filaggrin activity on the course of mild and moderate atopic dermatitis.
 MATERIAL AND METHODS: An open, prospective, multicentre, non-comparative, single-group clinical trial was organized to test the effectiveness of a cream with a filaggrin activity modulator. The study was on outpatients in the participated centers and included 5 visits with a screening visit 1, and 5th visit ― therapy completion. Cream was used for 12 weeks. In total, the study involved 60 children aged 3 to 18 years with diagnoses of atopic dermatitis of mild and moderate severity. The severity of atopic dermatitis was measured with the SCORAD, EASI, IGA scales, also measured was skin pH and transepidermal water loss (TEWL), as well as the severity of xerosis according to visual analogue scale.
 RESULTS: The severity of atopic dermatitis in children whose therapy regimens included Admera cream decreased by 19.6 points according to the SCORAD index, including in children who did not receive mometasone furoate in the therapy schemes, the SCORAD index decreased statistically significantly compared to the baseline data (p 0.001). The overall decline in the EASI index ― by 3.0 points, the IGA global assessment index ― by 2.0 points, the severity of xerosis decreased by 3 points (in all cases, p 0.001). Transepidermal water loss decreased (by 4.5 g/m2 per hour, p 0.001); Skin pH did not change (difference 0.02, p=0.34). The smell was rated as "excellent" by 86.7% (95% CI 75.494.1), the consistency ― by 83.3% (95% CI 71.591.7) of the respondents, and overall satisfaction was noted by ― 88.3% (95% CI 77.495.2) of the respondents.
 CONCLUSION: Сream for dry and sensitive skin with a modulator of filaggrin activity during the study showed good efficacy and tolerability and can be used in atopic dermatitis treatment regimens as a basic care product, both during exacerbation and remission.

Cytokine transcriptome profiling in acute experimental canine atopic dermatitis skin lesions after IL-31 inhibition with lokivetmab.

The caninised monoclonal antibody lokivetmab (LKV), directed at interleukin (IL)-31, is very effective at controlling pruritus in most dogs with atopic dermatitis (AD). However, evidence exists that IL-31 is not required for the induction of acute allergic skin inflammation, which might explain why this treatment is less efficacious in some dogs with AD. To compare the comprehensive transcriptome analysis of house dust mite (HDM)-sensitised dogs with and without treatment with LKV to attest our hypothesis that LKV does not majorly affect acute cytokine/chemokine production. Six HDM-sensitised atopic Maltese-beagle dogs. In this cross-over study, the cytokine profiling of acute AD skin lesions was compared by RNA sequencing (RNA-Seq), with or without LKV-induced inhibition of IL-31. Skin biopsies were obtained from each dog at 0, 6, 12, 24, 48, and 96 h after epicutaneous HDM allergen provocation. Macroscopic and microscopic skin lesion scores were not significantly different between the LKV- and nontreatment groups at any time points. Likewise, the results of RNA-Seq analysis revealed no significant difference in the messenger (m)RNA expression of the major cytokines between these two groups. In LKV-treated dogs, IL6, IL9, IL13, IL33, CCL17, and CCL22 were significantly upregulated compared to their baseline expression levels, suggesting that these cytokines are unaffected by IL-31 inhibition. IL-31 inhibition is insufficient to prevent the expression of other proinflammatory mediators in acute AD and these could be considered as other potential therapeutic targets.

Feline Atopic Skin Syndrome: an Introduction to Recently Proposed Terminology and How to Work Up the Case

Atopic disease remains as an enigmatic hypersensitivity disorder in feline patients. Studies of cutaneous atopic syndrome in cats have reported several reaction patterns in cats, presenting as a diagnostic challenge, and a recent literature review has proposed a new set of terminologies for such diagnoses. This paper aims to report a case workup of feline atopic skin syndrome in a patient presented with severe pruritus and reaction patterns of self-inducd alopecia and facial excoriation. Feline food allergy and flea allergic dermatitis were ruled out by a 6-week elimination diet and use of fluralaner respectively. Clinical symptoms were successfully managed with the use of oral glucocorticoid (GC) and systemic and topical antimicrobial, the use of all of which for 8 weeks was deemed successful based on the degree of clinical relief provided. It is concluded that feline atopic skin syndrome is a clinical diagnosis and pharmacological interventions, including drugs to treat skin inflammation and secondary infection, are warranted.

Altered expression of S100 fused-type proteins in an atopic dermatitis skin model.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder with elevated interleukin (IL)-4 and IL-13 signatures and extensive barrier dysfunction, which is correlated with the downregulation of filaggrin (FLG). FLG is a member of the S100 fused-type protein family and this family also includes cornulin (CRNN), filaggrin-2 (FLG2), hornerin (HRNR) repetin (RPTN), trichohyalin (TCHH) and trichohyalin-like 1 (TCHHL1). The present study aimed to examine the effects of IL-4 and IL-13 and the downregulation of FLG on the expression of S100 fused-type proteins using a three-dimensional (3D) AD skin model by immunohistochemical study and quantitative polymerase chain reaction. In the 3D AD skin model, which was generated by a stimulation of recombinant IL-4 and IL-13, the expression of FLG, FLG2, HRNR and TCHH was decreased, while that of RPTN was increased in comparison to the 3D control skin. In the FLG knockdown (KD) 3D skin model, which was generated using FLG siRNA, the expression of HRNR was increased. The expression of the other proteins did not differ to a statistically significant extent. The expression of fused-S100 type protein family members may differ in AD skin. This suggests that these proteins play different roles in the pathogenesis of AD.

Regnase-1 plays an essential role in maintaining skin immune homeostasis via regulation of chemokine expression

Regnase-1 is an endoribonuclease that regulates the stability of target genes. Here, we investigated whether Regnase-1 plays a regulatory role in the pathophysiology of atopic dermatitis, a chronic inflammatory skin disease. Regnase-1 levels were decreased in skin and serum of atopic dermatitis patients and mice. Regnase-1+/- mice exhibited more severe atopic dermatitis symptoms than wild-type mice in a house dust mite allergen-induced atopic dermatitis model. Regnase-1 deficiency led to the global changes in gene expression related with innate immune and inflammatory responses, in particular chemokines. The skin Regnase-1 level had an inverse relationship with chemokine expression when we analyzed samples of atopic dermatitis patients and Regnase-1-deficient mice, suggesting that potentiated chemokine production contributes to the augmented inflammation at lesion sites. Subcutaneous administration of recombinant Regnase-1 to mice significantly ameliorated atopic dermatitis-like skin inflammation with reduced chemokine production in a house dust mite-induced atopic dermatitis NC/Nga mouse model. These results indicate that Regnase-1 plays an essential role in maintaining skin immune homeostasis as a regulator of chemokine expression. Modulating Regnase-1 activity may be an efficient therapeutic strategy for treating chronic inflammatory diseases, including atopic dermatitis.

The epidemiology of antimicrobial resistance and transmission of cutaneous bacterial pathogens in domestic animals.

As the primary agents of skin and soft tissue infections in animals, Staphylococcus spp and Pseudomonas aeruginosa are among the most formidable bacterial pathogens encountered by veterinarians. Staphylococci are commensal inhabitants of the surfaces of healthy skin and mucous membranes, which may gain access to deeper cutaneous tissues by circumventing the stratum corneum's barrier function. Compromised barrier function occurs in highly prevalent conditions such as atopic dermatitis, endocrinopathies, and skin trauma. P aeruginosa is an environmental saprophyte that constitutively expresses virulence and antimicrobial resistance genes that promote its success as an animal pathogen. For both organisms, infections of the urinary tract, respiratory tract, joints, central nervous system, and body cavities may occur through ascension along epithelial tracts, penetrating injuries, or hematogenous spread. When treating infections caused by these pathogens, veterinarians now face greater therapeutic challenges and more guarded outcomes for our animal patients because of high rates of predisposing factors for infection and the broad dissemination of antimicrobial resistance genes within these bacterial species. This review considers the history of the rise and expansion of multidrug resistance in staphylococci and P aeruginosa and the current state of knowledge regarding the epidemiologic factors that underly the dissemination of these pathogens across companion animal populations. Given the potential for cross-species and zoonotic transmission of pathogenic strains of these bacteria, and the clear role played by environmental reservoirs and fomites, a one-health perspective is emphasized.

Food allergy in dogs and cats; current perspectives on aetiology, diagnosis, and management.

Food allergy is a recognized clinical entity in dogs and cats and is an important differential to consider in the workup of a pruritic animal. Food can be a trigger factor for canine atopic dermatitis, and food allergy may coexist with feline atopic skin syndrome. Other clinical signs such as urticaria, recurrent pyoderma, and dorsolumbar pruritus can be seen in dogs, and urticaria, conjunctivitis, and respiratory signs can be seen in cats. In both species, gastrointestinal signs may be present. The pathogenesis in dogs and cats is complex and incompletely understood, which limits the development of reliable diagnostic laboratory tests. The diagnosis currently relies on an appropriately performed diet trial with subsequent provocation. This paper briefly reviews food allergies in people and explores our current knowledge of the disorder in dogs and cats.