<p>IL-33/13 Axis and IL-4/31 Axis Play Distinct Roles in Inflammatory Process and Itch in Psoriasis and Atopic Dermatitis</p>

Abstract

Background: Pruritus is the most common symptom in patients with skin disease. Psoriasis and atopic dermatitis are clinically distinct inflammatory diseases. Interleukins are cytokines which play key roles in inflammatory signaling pathways. Materials and Methods: Cross-sectional study was conducted among patients with psoriasis and atopic dermatitis: 59 psoriatic patients, 56 AD patients, and 49 matched healthy controls. Interleukins 4, 13, 31, 33 serum levels were assayed by ELISA and results were compared using SPSS. Itch severity and disease severity were measured and correlation with interleukin levels was determined using SPSS. Results: The serum levels of IL-4,-13,-31,-33 were elevated in atopic dermatitis patients compared to controls. Itch and disease severity were not correlated with elevated serum levels of these interleukins. In psoriasis, the levels of IL-4 and-31 were elevated compared to controls, whereas the levels of IL-13 and-33 were lower than controls. The levels of measured interleukins in psoriasis did not correlate with itch and disease severity. Conclusion: IL-31 is the key mediator for pruritus in both AD and Ps patients. IL-4/31 axis and IL-33/13 axis play distinct roles in the pathogenesis of Atopic dermatitis and Psoriasis. Interleukin serum levels were not correlated with itch and disease severity in both conditions.

Involvement of Neuro-Immune Interactions in Pruritus With Special Focus on Receptor Expressions

“…IL-31/IL-31RA interaction activates signal transduction pathways leading to expression and release of various chemokines, proinflammatory cytokines, regulation of cell proliferation and stimulation of DRG neurons that play important role in pruritus induction and inflammatory diseases ( 72 – 74 ). A number of researchers observed an association between IL-31 and inflammatory skin diseases with severe pruritus including AD ( 61 , 75 ), bullous pemphigoid ( 76 ), cutaneous T-cell lymphoma ( 77 ), CSU ( 78 ) and psoriasis ( 79 ). Regarding treatment approaches, a successful therapy of urticaria using omalizumab led to decreased serum levels of IL-31 ( 80 ).…”

Molecular Aspects of Pruritus Pathogenesis in Psoriasis

“…Among the tested cytokines (IFN-ɣ, TNF-α, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12) only IL-2, a SP-induced cytokine that triggers the maturation of T cells, was significantly increased in pruritic psoriatic skin [ 7 ]. Other cytokines, such as IL-4, IL-13, IL-31 and IL-33 play a key role in the pro-inflammatory and anti-inflammatory signaling pathways in patients suffering from inflammatory skin diseases such as psoriasis or atopic dermatitis [ 19 ]. In 2020, Badoor et al published results of a study evaluating the correlation between serum concentration of IL-4, IL-13, IL-31 and IL-33 and intensity of pruritus in psoriasis and atopic dermatitis.…”

“…In 2020, Badoor et al published results of a study evaluating the correlation between serum concentration of IL-4, IL-13, IL-31 and IL-33 and intensity of pruritus in psoriasis and atopic dermatitis. In patients with psoriasis, similarly to atopic dermatitis, the levels of IL-4 and IL-31 were significantly elevated in comparison to healthy controls [ 19 ]. These findings were compatible with the results of another study in which elevated levels of IL-31 in the skin or serum of patients with psoriasis were demonstrated [ 46 , 47 ].…”

“…These findings were compatible with the results of another study in which elevated levels of IL-31 in the skin or serum of patients with psoriasis were demonstrated [ 46 , 47 ]. However, these elevated concentrations did not correlate with the intensity of itch [ 19 ]. Interestingly, Narbutt et al proved significant reduction in both, serum IL-31 levels and severity of pruritus after narrowband ultraviolet B (UVB) phototherapy [ 47 ].…”

Bone mineral density, osteopenia, osteoporosis, and fracture risk in patients with atopic dermatitis: a systematic review and meta- analysis

“…There is also growing knowledge regarding the immune-mediated pathomechanism of AD, and the osteoimmunology has highlighted the cross-regulation of bone and the immune system, which involving various cell types, signaling pathways, cytokines, and chemokines, under both homeostatic and pathogenic conditions (31)(32)(33). Since many cytokines and immune cell types have been found to be active in AD and play a role in bone remodeling, which may help to elaborate on how immuneassociated diseases affect osteoimmunology and lead to bone loss (32)(33)(34)(35)(36)(37)(38). Besides, a number of studies have found that Vitamin D deficiency is more prevalent in patients with AD and correlated with the severity of the disease, and extra supplementation of Vitamin D could result in a clinically meaningful AD severity reduction (39).…”