Allicin Reduced the Secretion of Inflammatory Factors and Immune Cells Infiltration in IMQ-Induced Mouse Model
Psoriasis and other inflammatory skin diseases are widely thought to result from abnormal cytokine expression. IL-17 mediates inflammatory cell recruitment via inducing inflammatory cytokines and chemokines by keratinocytes in psoriatic lesions(Nograles et al. , 2008; Harper et al. , 2009). We examined the mRNA expression levels of inflammatory cytokines in IMQ-induced psoriasis skin lesions. As seen in Figures 6A and 6C, allicin significantly suppressed the mRNA levels of IL-17A. Then the expression of IL-17A was further validated by IHC (Figure 6C). In addition, allicin reduced IL-12, IL-20, and IL-22 levels, which are involved in the immune response of psoriasis (Figure 6B). Various immune cell subsets create a self-sustaining cycle of inflammation during the development of psoriasis, including T cells, neutrophils, and macrophages(Singh et al. , 2013). Current evidence suggests that the number of CD3+cells is increased in the skin tissue of patients with psoriasis (He et al. , 2021). We next determined whether allicin affected the accumulation of immune cells in IMQ-induced psoriasis-like skin, including T cells, macrophages, and neutrophils. The immunohistochemistry results showed that allicin reduced the infiltration of CD3+, F4/80+, and MPO+ cells compared to the IMQ-treated group (Figure 6D, E, F). As a result, allicin treatment alleviated immune cell infiltration and pro-inflammatory factor secretion substantially.