HS is fundamentally an inflammatory disease. Inflammation in HS is dysregulated: it is triggered by relatively minor stimuli (a blocked hair follicle), but the normal signals that tell the immune system to stand down are not working properly. The result is a self-sustaining inflammatory cycle that damages tissue, creates abscesses and tunnels, and drives the chronic, recurring nature of the condition. Key inflammatory molecules elevated in HS include TNF-alpha, IL-17, IL-23, IL-1, and IL-36.
Why HS is an inflammatory condition, not an infection
HS lesions contain bacteria. But bacteria do not cause HS. In HS, the skin's immune cells overreact to the normal bacterial presence on the skin, mounting an inflammatory response that is disproportionate and difficult to resolve.
This is why antibiotics alone do not cure HS. They can reduce bacterial load and the inflammatory stimulus it provides, but they do not address the underlying immune dysregulation. It also explains why the most effective treatments for moderate-to-severe HS are biologics — drugs that specifically target the cytokines driving inflammation.
The HS Foundation puts it clearly: "Your immune system is overactive, not defective." The immune system in HS is not failing to respond. It is responding too much, and failing to stop.
The role of cytokines in HS
Cytokines are signalling proteins produced by immune cells. In HS, multiple cytokines are chronically elevated in lesional skin and in the bloodstream.
TNF-alpha: One of the primary drivers of HS inflammation. Adalimumab (Humira), the first FDA-approved biologic for HS, is a TNF inhibitor. Infliximab also targets TNF.
IL-17: The target of secukinumab (Cosentyx) and bimekizumab (Bimzelx). A 2026 mechanistic study found that in HS, IL-17 signals primarily through dermal fibroblasts rather than keratinocytes, which has clinical implications for treatment.
IL-23: Part of the Th17 inflammatory axis. IL-23 inhibitors are in active clinical development for HS.
IL-1 and IL-36: Additional cytokines implicated in HS inflammation and explored as therapeutic targets.
The follicular occlusion cascade: where it starts
In HS, the trigger is follicular occlusion: the blocking of a hair follicle. When keratinocytes accumulate and block the follicular opening, the follicle becomes distended and eventually ruptures, releasing follicular contents into the surrounding dermis. The immune system treats this as a threat.
In people who do not have HS, this response is proportionate. The follicle heals. In people with HS, the immune system's response is dysregulated. The inflammatory cascade does not resolve. Instead, it recruits more immune cells, drives more cytokine production, and creates the nodule, abscess, or tunnel that characterises the condition.
Genetics explain an estimated 70% of HS susceptibility, according to HS Foundation research.
Why HS inflammation is systemic, not just local
Blood tests in HS patients consistently show elevated inflammatory markers, including C-reactive protein (CRP), throughout the body. This systemic inflammation helps explain why HS is associated with metabolic syndrome, type 2 diabetes, inflammatory bowel disease, arthritis, and cardiovascular risk. These comorbidities share inflammatory drivers. They are not coincidental.
Managing HS is about managing systemic inflammatory load, not just treating individual lesions. Lifestyle factors, nutritional status, sleep, stress, and metabolic health all influence the overall inflammatory environment in which the condition operates.
How anti-inflammatory approaches relate to HS
Biologics interrupt the inflammatory cascade by targeting TNF-alpha, IL-17, or IL-23 directly. Anti-inflammatory lifestyle and nutritional approaches operate on the same principle, at a different scale of effect.
A Mediterranean-style diet, adequate zinc and vitamin D status, and stress management all influence the same inflammatory pathways that drive HS. The effect size is smaller and less predictable than biologic therapy. But for people with mild HS, or as an adjunct to medical treatment at any stage, reducing overall inflammatory load is a legitimate and evidence-supported goal.
Zinc inhibits NF-kB signalling, reducing downstream cytokine production. Vitamin D regulates the immune cells driving HS inflammation. Curcumin phytosome targets similar cytokine pathways through a different mechanism. These ingredients do not replace biologic therapy at Stage 2 or 3. Understanding the shared inflammatory mechanism helps clarify why they are biologically relevant.
For more on how specific supplements have been studied in HS contexts, see our post on does zinc help hidradenitis suppurativa (add URL once Post #2 is live) and our overview of what supplements actually help HS (add URL when Post #10 publishes)
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Frequently asked questions
Is HS an autoimmune disease?
No. HS is classified as autoinflammatory, not autoimmune. Autoimmune diseases involve the immune system producing antibodies that attack the body's own tissues. In HS, the immune system mounts a dysregulated inflammatory response to follicular rupture, driven by innate immune activation and cytokine overproduction rather than autoantibodies.
What makes HS inflammation different from normal skin inflammation?
Normal inflammation is self-limiting: it resolves once the trigger is removed and the tissue heals. HS inflammation is dysregulated in two ways: it is triggered by stimuli that would not cause significant inflammation in most people, and it fails to resolve once it starts.
Why do biologics work for HS?
Biologics target specific cytokines driving the inflammatory cascade. Adalimumab inhibits TNF-alpha. Secukinumab and bimekizumab inhibit IL-17. By blocking these signalling molecules, biologics interrupt the inflammatory cascade before it creates lesions.
Does reducing inflammation stop HS from progressing?
Effective inflammation control is the primary mechanism by which all HS treatments reduce progression. Biologics are the most potent tools. Lifestyle modifications, nutritional support, and metabolic health optimisation all contribute to reducing inflammatory load, which is associated with reduced disease activity over time.
Can CRP levels indicate HS activity?
CRP is a systemic inflammatory marker elevated in HS patients, reflecting overall inflammatory burden. It is not HS-specific, but monitoring it over time can indicate whether inflammatory load is increasing or decreasing. Your dermatologist may include it in routine blood panels.
This article is for educational purposes only. It is not a substitute for medical advice. If you have hidradenitis suppurativa, work with a board-certified dermatologist to build a treatment plan.
References
- HS Foundation. HS causes: inflammation, not infection. https://www.hs-foundation.org/hs-causes
- HS Foundation Patient Guide. Chapter 3: HS Genetics and Inflammation. December 2024.
- Cavagnero KJ, et al. Disease context dictates the cellular targets of IL-17 in inflammatory skin disease. bioRxiv. Mar 2026. PMID: 41929214. https://pubmed.ncbi.nlm.nih.gov/41929214/
- Best Practice in the Management of HS Lesions. Journal of Wound Care. July 2025.
Published by HS Daily.
