Psoriasis is a chronic autoimmune skin disease marked by inflammation, scaling, and impaired skin integrity. It stems from immune dysregulation, particularly involving Th17 cells and overexpression of IL-17A. One of the lesser-known facets of psoriasis is the disruption it causes in the skin’s microbial community. Patients frequently show significant differences in microbiota composition compared to healthy individuals. IL-17A plays a dual role—fueling inflammation but also aiding in microbial defense. This study explores how IL-17A inhibitors, such as Secukinumab, impact both the structure and function of the skin microbiome during psoriasis treatment.
Methods
This clinical study involved 26 patients with moderate-to-severe psoriasis and 15 healthy controls. Skin swab samples were taken from oily (scalp, ear, back) and dry areas (abdomen, limbs) both before treatment and at week 9 of IL-17A inhibitor therapy. Microbial profiles were generated using 16S rDNA sequencing, and analyses included alpha/beta diversity, LEfSe, and predicted microbial functions using tools like PICRUST2. This design enabled researchers to capture site-specific and time-based changes in both microbial diversity and functional capability.
Key Findings
- Psoriasis patients had varied and disrupted microbial communities compared to controls, with clear anatomical site differences.
- IL-17A inhibition increased alpha diversity, indicating a more balanced microbial ecosystem post-treatment.
- Taxonomic shifts were observed post-treatment, with Staphylococcus and Corynebacterium declining, and Propionibacterium and Burkholderia increasing.
- Functional microbiome profiles began to resemble those of healthy skin after treatment, especially in dry areas.
- Specific metabolic pathways linked to microbial biosynthesis and detoxification changed significantly following IL-17A blockade.
This study highlights that IL-17A inhibitors, while not drastically altering microbial composition, meaningfully restore microbial diversity and functional stability. The most significant insight is that improved microbial function—not just structure—correlates with clinical improvement. These findings support the idea that microbiome-targeted strategies could complement existing therapies for psoriasis. As microbiome diagnostics improve, changes in diversity and metabolic potential may help guide more personalized treatment plans. Long-term studies are needed to determine how lasting these ecological shifts are, especially through remission or relapse phases.
Link to the study: https://tinyurl.com/4x6a3bc8
