IgA and canine atopic dermatitis

13 November 2025

Francesca Soutter was awarded funding for a BSAVA PetSavers master’s degree by research in 2023 for a project exploring whether IgA deficiency is a feature of canine atopic dermatitis in small and medium sized dogs.

Student Abigail Robins describes her findings.

Background

Canine atopic dermatitis (CAD) is a common condition encountered on a daily basis in most companion animal veterinary practices. Dogs typically present with aural, facial, axillae and pedal pruritus with evidence of skin inflammation, which can include otitis. The disease is more common in certain breeds including Golden and Labrador retrievers, German Shepherd dogs (GSDs), Boxers, and West Highland White Terriers (Jaeger et al., 2010). It is also common in breeds that have become increasingly popular in recent years such as French Bulldogs, and in ‘designer crossbreeds’ such as Cockapoos and Cavapoos. Clinical signs typically appear between 4 months and 3 years of age, although the age of onset can vary between breeds (Favrot et al., 2010; Wilhem, Kovalik and Favrot, 2011).

CAD is a genetically predisposed condition with a complex aetiopathogenesis (Figure 1). It involves poor skin barrier function, altered skin inflammation, allergies (in most but not all dogs) to environmental, food and/or Malassezia allergens, and dysbiosis of the skin microbiome (Marsella, 2021; Meury et al., 2011). However, the causes and disease phenotype differ among breeds and between individuals, which is in part due to the varied and largely undefined genotype that varies between breeds and gene pools (Nuttall, 2013). Polymorphisms in numerous genes, mostly associated with immune regulation and skin barrier function, have previously been associated with CAD (Tengvall et al., 2013; Wood et al., 2009; Agler et al., 2019), while skin barrier dysfunction and microbial colonisation may contribute to the onset of disease and worsening of clinical signs (Marsella, 2021). A compromised skin barrier facilitates the penetration of allergens, irritants, and microbes that stimulate immune cells and inflammation. A T helper 2 (Th2)-type immune response is often involved in the initiation of disease with the release of pro-inflammatory cytokines that promote inflammation of the skin through thymic stromal lymphopoietin and innate lymphoid cells (Früh et al., 2020; Olivry et al., 2016). An itching sensation is caused by pruritogens (particularly IL-31) binding to receptors on sensory nerve endings, which send signals through the dorsal root ganglion to the spinal cord up the spinothalamic tract then into the brain (Wheeler et al., 2019; Olivry et al., 2016). The Janus kinase-signal transducer and activator of transcription (JAK-STAT) signalling pathway also mediates cellular responses in inflammation and itch (Blubaugh et al., 2024; He et al., 2024). The disrupted skin barrier and immune dysregulation foster a dysbiotic skin microbiome, with overgrowth of organisms like Staphylococcus and Malassezia spp., which further exacerbate inflammation (Pierezan et al., 2016).

What is IgA and why might it play a role in CAD?

Immunoglobulin A (IgA) is the dominant class of antibody found at mucosal surfaces such as the gastrointestinal and upper and lower respiratory and urogenital tracts (Corthésy, 2013). It plays an important role in mucosal immunity, interacting with local microbiota and epithelial and immune cells. IgA is involved in mucosal tolerance and inflammation by mediating local cytokine production through antibody receptors (Scheurer et al., 2023). In health, this balance enables the immune system to tolerate commensal microorganisms and foreign but harmless antigens such as food whilst excluding harmful pathogens (Conrey et al., 2023).

Selective IgA deficiency (IgAD) is common in humans and has been associated with atopic diseases such as eczema and asthma, although the underlying molecular mechanisms are poorly defined. Other immunoglobulins, such as IgG, are likely to compensate for a lack of IgA but it is hypothesised that interactions with commensal and pathogenic organisms are likely to be altered (Conrey et al., 2023). Previous studies have demonstrated an association between IgAD and CAD in German Shepherd dogs but this has not been examined in other breeds (Olsson et al., 2014). We therefore focused on assessing this in popular CAD-predisposed breeds and crossbreeds by measuring salivary and faecal IgA in CAD cases and breed-matched controls.

Methods

We collected faecal and saliva samples from healthy dogs and dogs with CAD through the first opinion and dermatology referral service at the R(D)SVS Hospital for Small Animals (HfSA) at the University of Edinburgh. CAD was diagnosed on the basis of a history of chronic pruritus with an inflammatory dermatitis including otitis and fulfilling at least five of Favrot’s criteria (Favrot et al., 2010). Dogs who responded completely to an elimination diet or to ectoparasite treatment were excluded. Dogs also had to be free from the effects of immunosuppressive therapy at the time of sampling, and dogs under the age of 6 months were also excluded. The control population consisted of breed-matched dogs ³4 years of age with no history of skin disease and who had not received antimicrobial or immunosuppressive medication at the time of sampling. Selecting dogs over 4 years of age precluded age-matched controls but was done to avoid inadvertently including younger dogs who could go on to develop CAD.

Enzyme-linked immunosorbent assay (ELISA) testing was performed to quantify secretory IgA concentrations in canine faeces and saliva. Faecal supernatant and saliva samples of atopic and control dogs were tested after being diluted (1:10,000) using a commercially available IgA dog ELISA kit (Abcam, Cambridge, UK) according to the manufacturer’s instructions.

Results

Key findings

• The study population consisted of 32 atopic and 35 control dogs from 20 breeds each (10 small/medium sized breeds and 10 large sized breeds). The most common atopic breeds were French bulldogs (n=4) and Labrador retrievers (n=4).
• Saliva and faecal samples were obtained from 24 atopic and 25 control dogs, saliva alone from three atopic and five control dogs, and faeces alone from five atopic and five control dogs.
• The faecal IgA concentration was significantly lower in atopic dogs where it ranged from 0.05 to 5.28 g/L (median 0.98 g/L, 95% confidence interval [CI]: 0.498–1.462) than in controls where it ranged from 0.014 to 10.27 g/L (median 1.78 g/L, 95% CI: 0.764–2.796) (p = 0.03).
• There was no significant difference in mean ranked salivary IgA between atopic dogs and controls (p = 0.23).
• Faecal and salivary IgA concentrations were not associated with age. However, it was not possible to evaluate an association with breed as only small numbers of each dog breed were included.
• Faecal and salivary IgA concentrations were highly variable in atopic dogs and were not correlated (i.e. dogs with low faecal IgA did not always have low salivary IgA).

Discussion

Faecal IgA concentration was associated with CAD in this study, with a significantly lower mean ranked faecal IgA seen in atopic than in healthy dogs. Previous studies focusing on large breed dogs found that low serum IgA was associated with CAD in GSDs (Olsson et al., 2014). In contrast we found this association in a more heterogenous group of breeds; we did not test serum IgA as none of the dogs in the study had a clinical need for blood sampling. Future work should examine whether this association is observed in larger cohorts and with longitudinal sampling of affected individuals.

Human studies have found that high levels of faecal and serum IgA are protective against IgE-mediated allergic diseases (Kukkonen et al., 2010). However, this protective effect might only be observed in very early infancy before allergen sensitisation (Seppo, Jackson and Järvinen, 2023). Therefore, studying faecal IgA in puppies from high-risk breeds could increase our understanding of its role in the development of gut tolerance versus immune dysregulation. Gut dysbiosis in atopic diseases may go beyond food allergy and be important in the development of systemic tolerance. With an abundance of genomic tools now available, further exploration of cross-talk between host IgA and the gut microbiome in dogs is required.

Funding acknowledgments and the research experience

Completing my Master of Science by Research degree, funded by BSAVA PetSavers, has been an incredible journey of learning and growth. The experience was both academically and personally challenging, pushing me to expand my skills, knowledge, and resilience. It offered me invaluable opportunities to delve deeply into my area of research and develop professionally. I am profoundly grateful for this opportunity and for the unwavering support of everyone who made it possible, including my project supervisors, colleagues, and BSAVA PetSavers. This experience has been transformative, shaping me into a more capable and confident researcher, and I am excited to progress my career further in the field of scientific research.

Biographies

Abigail Campbell

Abigail graduated from Scotland’s Rural College in 2023 with BSc (Hons) in Applied Animal Science. She developed a strong passion for scientific research during her undergraduate studies, particularly while undertaking her dissertation. Her final year project focused on investigating the effect of feeding practices on parasite prevalence in domestic dogs. Upon graduation, Abigail was awarded the BSAVA PetSavers postgraduate opportunity, enabling her to pursue and successfully complete a Master of Science by Research degree at the University of Edinburgh.

Francesca Soutter

Francesca Soutter graduated from the University of Glasgow in 2008. She completed a small animal rotating internship at the Royal Veterinary College (RVC) and two years in small animal general practice before returning to the RVC to undertake a PhD investigating Leishmaniasis in dogs. She then worked on vaccines for pigs and poultry as a postdoctoral researcher. She joined Scotland’s Rural College in 2021 where she is a lecturer on the Applied Animal Science degree. Her research interests are focussed on the interface between the host immune system and pathogens and how this can be utilised to develop novel therapeutics.

Tim Nuttall

Tim Nuttall graduated from the University of Bristol in 1992. He trained in dermatology at the University of Edinburgh, where he later completed a PhD in canine atopic dermatitis. He then spent 12 years at the University of Liverpool before returning to the Royal (Dick) School of Veterinary Studies as Head of Dermatology. His clinical and research interests include atopic dermatitis, otitis, pododermatitis, and antimicrobial stewardship.

Victoria Robinson

Victoria Robinson graduated from the Royal (Dick) School of Veterinary Studies in 2008. After several years in mixed and companion animal practice she completed a rotating internship at The University of Liverpool. She completed her ECVD residency in 2020 at The Dermatology Referral Service in Glasgow and boarded the same year. She returned to her alma mater in August 2022 as Senior Lecturer in Veterinary Dermatology. Her research interests include antimicrobial resistant and biofilm-producing infections.

References

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Blubaugh, A., Hoover, K., Kim, S. J., Fogle, J. E., Sow, F. B. and Banovic, F. (2024) ‘Characterization of the Pro-Inflammatory and Pruritogenic Transcriptome in Skin Lesions of the Experimental Canine Atopic Acute IgE-Mediated Late Phase Reactions Model and Correlation to Acute Skin Lesions of Human Atopic Dermatitis’, Vet Sci, 11(3).

Conrey, P. E., Denu, L., O’Boyle, K. C., Rozich, I., Green, J., Maslanka, J., Lubin, J. B., Duranova, T., Haltzman, B. L., Gianchetti, L., Oldridge, D. A., De Luna, N., Vella, L. A., Allman, D., Spergel, J. M., Tanes, C., Bittinger, K., Henrickson, S. E. and Silverman, M. A. (2023) ‘IgA deficiency destabilizes homeostasis toward intestinal microbes and increases systemic immune dysregulation’, Sci Immunol, 8(83), pp. eade2335.

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Wood, S. H., Ke, X., Nuttall, T., McEwan, N., Ollier, W. E. and Carter, S. D. (2009) ‘Genome-wide association analysis of canine atopic dermatitis and identification of disease related SNPs’, Immunogenetics, 61(11-12), pp. 765-72.

 

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