Skin is a protective barrier that regulates body temperature and is the first line of defense against foreign pathogens, including bacteria and viruses.

Animal skin represents a complex biological system in which barrier function, immune response and microbiota interact to maintain physiological balance. Similarly to human skin, this equilibrium is regulated by a diverse microbial ecosystem composed of bacteria, fungi and viruses (Ross et al., 2019). Through interkingdom interactions, these microorganisms communicate with each other and with the host via biochemical and biophysical signaling pathways, contributing to immune modulation, barrier integrity and overall skin health (Hoffmann et al., 2014).

Disruption of this balance (dysbiosis) is increasingly recognized as a key factor in the development of inflammatory dermatoses in animals, including atopic dermatitis and other chronic skin conditions commonly observed in companion animals (Bradley et al., 2016). These conditions are often associated with microbial imbalance, impaired barrier function and recurrent inflammation, significantly impacting animal welfare and quality of life (Santoro et al., 2015).

Canine atopic dermatitis (CAD) is a chronic inflammatory skin disease characterized by a complex interplay between epidermal barrier impairment, immune dysregulation, and microbial imbalance. One of the earliest and most critical events in CAD is the disruption of the skin barrier. Structural and functional alterations, including reduced integrity of the stratum corneum and tight junction dysfunction, lead to increased transepidermal water loss (TEWL). This reflects a compromised barrier, resulting in decreased skin hydration and increased permeability to environmental allergens and microbial factors (Marsella et al., 2011).

Within this altered microenvironment, bacterial colonization is not merely a secondary event, but a key contributor to disease progression. In particular, Staphylococcus pseudintermedius, the predominant staphylococcal species in canine atopic dermatitis, exhibits an enhanced ability to adhere to skin corneocytes (Bhaduri et al., 2022). As a result, S. pseudintermedius establishes a more stable and persistent colonization, which contributes to the amplification of local inflammation. The bacterium releases enzymes and virulence factors that further damage the epidermis, exacerbating barrier dysfunction and sustaining the inflammatory response (Simou et al., 2005).

A self-reinforcing cycle is therefore established: barrier impairment leads to increased TEWL and facilitates bacterial adhesion, while bacterial colonization further worsens barrier integrity and inflammation. In this context, therapeutic strategies aimed at reducing bacterial adhesion and restoring barrier function, including normalization of TEWL, are essential to effectively control disease progression and promote long-term skin homeostasis (Pucheu-Haston et al., 2015).