
HS Pathophysiology: Follicular Occlusion, Biofilm, and Innate Inflammation
Follicular occlusion, anaerobic biofilm, and innate immune activation combine to drive tissue destruction. The panel explains why tunnels sustain inflammation and mark the transition from acute disease to irreversible scarring.
Episodes in this series
"HS Pathophysiology: Follicular Occlusion, Biofilm, and Innate Inflammation" takes up the question of what drives tissue destruction in HS and why tunnels behave differently from nodules.
The panel is asked to describe the pathophysiology of HS and what drives the changes seen in patients. The panel identifies follicular occlusion and hyperproliferation of the epithelium as the primary events. Under the microscope, the tunnels resemble a very angry, inflamed psoriasis, although they do not behave identically because the tunnel is a sequestered anaerobic environment. Secretions, dead keratinocytes, and skin oils serve as a food source for anaerobic bacteria, which leads to biofilm formation. The resulting inflammation is driven largely by the innate immune system, which is fast and vicious by design. When it misfunctions in this way, cytokines such as TNF-alpha, IL-1 beta, IL-17, and IL-36 rise, creating a perfect storm that destroys tissue. The panel also stresses that the disease is multifactorial. Neutrophils and B cell inflammation within the follicular epithelium of the tunnels are part of the picture, and the panel suggests the field is only scratching the surface of what is still to come.
The discussion then moves to what makes tunnels different from an isolated nodule. The panel explains that a biofilm will always be present in a tunnel for as long as it remains inflamed, because the hyperproliferative epithelium produces too much food for bacteria to go unnoticed. Biofilms resist both the immune system and antimicrobial agents. The anaerobic environment also explains why enteric pathogens grow out of tunnels, a finding that can surprise clinicians early in their careers. These pathogens are highly immunostimulatory, so inflammation keeps accelerating and damages native tissue. Structural damage then becomes irreversible, marking the shift from an acute inflammatory disease to a chronic, scarring one.
Up next, in "HS Draining Tunnels: Severity Markers, Scarring, and Unmet Needs," the experts discuss what draining tunnels signal about severity and progression.
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