Staphylococcal Biofilms in Atopic Dermatitis

Abstract

Purpose of Review Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder that is a major public health burden worldwide. AD lesions are often colonized by Staphylococcus aureus and Staphylococcus epidermidis. An important aspect of Staphylococcus spp. is their propensity to form biofilms, adhesive surface-attached colonies that become highly resistant to antibiotics and immune responses, and recent studies have found that clinical isolates colonizing AD skin are often biofilm-positive. Biofilm formation results in complex bacterial communities that have unique effects on keratinocytes and host immunity. This review will summarize recent studies exploring the role of staphyloccocal biofilms in atopic dermatitis and the implications for treatment. Recent Findings Recent studies suggest an important role for biofilms in the pathogenesis of numerous dermatologic diseases including AD. S. aureus biofilms have been found to colonize the eccrine ducts of AD skin, and these biofilms influence secretion of keratinocyte cytokines and trigger differentiation and apoptosis of keratinocytes. These activities may act to disrupt barrier function and promote disease pathogenesis as well as allergen sensitization. Summary Formation of biofilm is a successful strategy that protects the bacteria from environmental danger, antibiotics, and phagocytosis, enabling chronic persistence in the host. An increasing number of S. aureus skin isolates are resistant to conventional antibiotics, and staphylococcal biofilm communities are prevalent on the skin of individuals with AD. Staphylococcal colonization of the skin impacts skin barrier function and plays multiple important roles in AD pathogenesis.

Staphylococcus pseudintermedius Surface Protein L (SpsL) Is Required for Abscess Formation in a Murine Model of Cutaneous Infection

“…Experiments performed over a longer period could determine if S. pseudintermedius is able to persist and avoid clearance in the SpsL-dependent abscesses in comparison to the cellulitis pathology. Additionally, bacterial aggregation could be beneficial to S. pseudintermedius in other types of infection, and particularly in the initial stages of biofilm formation, which may promote colonization and persistence on indwelling devices or atopic skin ( 41 , 42 ).…”

Revealing the secret life of skin ‐ with the microbiome you never walk alone

“…S. epidermidis and S. aureus , for example, have at least 18 and 29 genes, respectively, coding for surface binding proteins . If the skin conditions are permissive−for instance in case of skin disorders such as acne or atopic dermatitis or in case of a wound − after firm attachment bacteria start to proliferate to form entire colonies and stick to each other by producing extracellular matrix leading to the formation of bacterial biofilms . However, even though many bacteria have virtually the ability to form biofilms, it is important to note that under normal physiological conditions the human skin does not allow the formation of biofilms as the requirements for their formation (e.g.…”

“…S. epidermidis and S. aureus, for example, have at least 18 and 29 genes, respectively, coding for surface binding proteins [50]. If the skin conditions are permissiveÀfor instance in case of skin disorders such as acne [51,52] or atopic dermatitis [53] or in case of a wound [54] À after firm attachment bacteria start to proliferate…”

Biotherapeutic Approaches in Atopic Dermatitis

“…S. aureus also expresses various virulence factors such as α‐toxin [ 33 ] (a potent cytolysin responsible for keratinocyte cell death), protein A (SpA), [ 34 ] lipotechoic acid (LTA), [ 35 ] phenol soluble modulin (PSM)‐α, [ 36 ] and proteases. [ 37 ] The pathogen can also form biofilms, [ 38 ] which disrupt the skin barrier and promote inflammation. [ 32 ] S. aureus may also induce glucocorticoid resistance in humans, [ 39 ] rendering topical steroid therapy inefficacious in severe AD in colonized patients, and thereby requiring more potent immunomodulators such as pimecrolimus and cyclosporin for treatment.…”