الفهرس 
PsoriasisOnly 14 pages are availabe for public view
 |  | from | 144 |  |  |
| | | from | 144 | | |
Abstract
Psoriasis is a chronic debilitating skin disease with an estimated prevalence reaching 2% of the worldwide population. It is a systemic disease with a genetic component, associated with several other metabolic syndromes and systemic inflammatory diseases.
Psoriatic disease is driven by the interactions among innate and adaptive immune systems with structural components of the skin. The interleukin (IL)-23/T-helper 17 axis is the main player in psoriasis pathogenesis and IL-22 is one of the final products of this cascade. Interleukin (IL)-22 mediates keratinocyte proliferation and epidermal hyperplasia.
Dysbiosis of the skin can cause S. aureus to predominate in the microbial population inhabiting the skin. One of the mechanisms found to exacerbate psoriasis was the secretion of superantigen molecules by S. aureus. These superantigens, including Staphylococcal enterotoxins (SEs) [types A to V] and toxic shock syndrome toxin-1 (TSST-1), induce polyclonal T-cells activation with a massive release of cytokines.
In our study we tested for the correlation between the serum levels of IL-22 and Staphylococcus aureus toxins (SEA, SEB, SEC, TSST-1) with disease activity in plaque psoriasis. The study was conducted during the period from May 2021 till November 2021 on 50 psoriasis patients from the dermatology outpatient clinics of Ain Shams University hospitals, from which 25 S. aureus isolates were isolated.
The patients were classified into mild, moderate, and severe psoriasis. The control group comprised 20 sex- and age-matched apparently healthy volunteers. IL-22 concentration was assessed in sera of the patients and the control group by using the ELISA technique. The serum levels of IL-22 in patients were higher than in the control group, but the difference was statistically insignificant (p= 0.413). Serum IL-22 levels were positively correlated with the Psoriasis Area and Severity Index (PASI) score of psoriasis patients (p= 0.0003). The IL-22 serum levels in patients colonized with toxigenic strains of S. aureus were significantly higher than in patients colonized with non-toxigenic strains (p= 0.028).
Patients colonized with S. aureus had higher PASI scores than the non-colonized patients (P value = 0.025). In addition, patients colonized with toxigenic strains had PASI scores higher than those colonized with non-toxigenic strains (P value=0.038).
Our results suggest that IL-22 plays a role in the pathogenesis of psoriasis, and its secretion can be triggered by the toxins produced by S. aureus colonizing the skin of patients. Although IL-22 blocking didn’t seem to be promising in the treatment of psoriasis, understanding how microbial flora can affect psoriasis disease progression may open the door for new treatment modalities to restore microbial flora to its normal composition.
Conclusion
The results of the present study suggest the role of S. aureus colonization in the immunopathogenesis of psoriasis. Staphylococcal toxins may trigger the production of IL-22 in psoriasis patients.
Recommendations
1. Using local expression analysis of this cytokine along with other pro-inflammatory cytokines inside the psoriatic lesions (e. g. mRNA expression quantification or immunohistochemistry analyses) would be more comprehensive to explain the contribution of these cytokines in the immunopathogenesis of psoriasis.
2. Test for different S. aureus superantigen genes
3. Test for the effect of local probiotics in restoring normal composition of skin flora