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.