Ozone Therapy Attenuates NF-κB-Mediated Local Inflammatory Response and Activation of Th17 Cells in Treatment for Psoriasis

Background: psoriasis, NF-κB and Th17 inflammation

Psoriasis is a chronic, immune-mediated skin disease in which patches of skin become thickened, red and scaly. Much of that inflammation is driven by an over-active immune signalling pathway called NF-κB and by a subset of immune cells known as Th17 cells, which release inflammatory messengers such as interleukin-17 (IL-17). Standard treatments can help control the disease but may lose effect over time or carry side effects, so researchers continue to look for approaches that calm this inflammatory cascade. Ozone therapy has been studied for its ability to modulate oxidative stress and inflammation, which prompted this group to ask whether it could influence the specific pathways that drive psoriasis.

Study design: patients, a mouse model and cell work

This was a translational study combining several strands of evidence rather than a large controlled trial. The human component involved a small group of 10 people with psoriasis vulgaris, whose disease severity was tracked using the Psoriasis Area and Severity Index (PASI) and whose skin was assessed for inflammatory cytokines. Alongside this, the researchers used an imiquimod-induced mouse model, a well-established laboratory model that produces psoriasis-like skin lesions in BALB/c mice, together with laboratory cell work to examine the underlying signalling pathways. There was no randomised control group in the human arm, so the patient data should be read as an early clinical observation supported by mechanistic experiments.

Findings: reduced severity scores and lower inflammatory signals

In the patients, topical ozone treatment was associated with lower PASI scores and reduced expression of inflammatory cytokines, including IL-17a, IL-6 and TNF-α. In the mouse model, ozone treatment reduced the formation of psoriasis-like lesions and appeared to work by inhibiting the TLR2/NF-κB signalling pathway and dampening the activation of Th17 cells. Taken together, the clinical and laboratory results pointed in the same direction: ozone appeared to attenuate the local inflammatory response that characterises psoriasis.

What the authors concluded

The authors concluded that ozone therapy can attenuate local inflammatory reactions and the activation of Th17 cells in psoriasis by inhibiting the NF-κB pathway. They framed this as a mechanistic rationale for exploring ozone in skin inflammation, and stated that the approach warrants further evaluation before any conclusions can be drawn about its place in routine clinical care.

Limitations of this study

The clinical portion of this work was small and uncontrolled, involving just 10 patients with no comparison group, so it cannot establish how well ozone performs against existing treatments or placebo. Much of the mechanistic evidence comes from a mouse model and cell experiments, which do not always translate directly to people. The authors also noted the absence of long-term efficacy and recurrence-rate data, and pointed out that questions about ozone's effects on skin-cell proliferation and blood-vessel behaviour remain unanswered. Larger randomised controlled trials would be needed to confirm whether these promising early signals hold up in practice.