Background: As a potent pro-inflammatory cytokine of the interleukin (IL)-1 family, IL-18 was elevated in early active progressive plaque-type psoriatic lesions and that serum or plasma levels of IL-18 correlated with...Background: As a potent pro-inflammatory cytokine of the interleukin (IL)-1 family, IL-18 was elevated in early active progressive plaque-type psoriatic lesions and that serum or plasma levels of IL-18 correlated with the Psoriasis Area and Severity Index (PASI). Although results from previous studies have established that IL-18 may aggravate psoriatic inflammation, the mechanisms of this process remain unknown. In this study, IL-18 knock out (KO) mice and wild-type (WT) mice were used to investigate the effects of IL-18 within a mouse model of psoriasis. Methods: WT and IL-18 KO mice were divided into four groups, including imiquimod (IMQ)-treated IL-18 KO group (w = 11) and WT group (n = 13) as well as their respectively gene-matched control mice (receiving vaseline;w = 12). PASI scores were used to evaluate psoriatic lesions in IMQ-treated mice. Pathological features and dermal cellular infiltration were investigated by hematoxylin and eosin staining. The levels of psoriasis-related cytokines including IL-23, IL-17, IL-12, IL-10, IFNγ, IL-15, IL-27, and IL-4 were tested by real-time polymerase chain reaction (PCR). The protein level of IL-1β, IL-27, CXCL1, and Ly6g were investigated by immunohistochemistry (IHC). Results: Acanthosis (98.46±14.12 vs. 222.68土71.10μm, P<0.01) and dermal cell infiltration (572.25±47.45 vs. 762.47土 59.59cells/field, P< 0.01) were significantly milder in IMQ-induced IL-18 KO mice compared with that in WT mice. IMQ-induced IL-18 KO mice manifested larger areas of Munro microabscesses (11,467.83±5112.09 vs. 4093.19±2591.88 pirn2, P< 0.01) and scales (100,935.24 ±41,167.77 vs. 41,604.41 ± 14,184.10 μm, P<0.01) as compared with WT mice. In skin lesions ot IL-18 KO mice, the expressions of IL-1β, IL-4, and IL-27 were all significantly upregulated but IL-17 was decreased. Histologically, strong positive signals of Ly6g were observed within the epidermis of IL-18 KO mice but expressions of CXCL1 were decreased. Conclusions: IL-18 may exacerbate prominent inflammation and influence pathological features in IMQ-induced mouse model of psoriasis. IL-18 may upregulate pro-inflammatory cytokines and reduce protective cytokines, thus aggravating psoriatic inflammation. In addition, IL-18 may be involved in the formation of Munro microabscesses and scales.展开更多
To the Editor:Malassezia and Staphylococcus epidermidis(S.epidermidis)are commensal organisms found on human skin,and both display an imbalance of colonization in individuals with seborrheic dermatitis/dandruff(SD/D)[...To the Editor:Malassezia and Staphylococcus epidermidis(S.epidermidis)are commensal organisms found on human skin,and both display an imbalance of colonization in individuals with seborrheic dermatitis/dandruff(SD/D)[1-3].Malassezia have been implicated in SD/D pathogenesis,as evidenced by an imbalance in the numbers of Malassezia that colonize the skin lesions of people with SD/D,and the fact that antifungal treatment exerts a modifying effect.[4].展开更多
To the Editor: A 10-year-old girl presented with an asymptomatic ulcerated tumor on her right forearm for 18 months [Figure 1a]. The minor initially was inconspicuous and then gradually enlarged with painless ulcerat...To the Editor: A 10-year-old girl presented with an asymptomatic ulcerated tumor on her right forearm for 18 months [Figure 1a]. The minor initially was inconspicuous and then gradually enlarged with painless ulceration in its center [Figure 1b]. Three months later, she developed three nontender new nodules on her right arm, proximal to the initial ulcerated nodule. Her general condition was good. Skin examination revealed a 4 cm × 4 cm tumor, with central ulceration and raised margins. Three diameters in 3-5 cm,展开更多
基金National Natural Science Foundation of China (Nos. 81673070, 81872538).
文摘Background: As a potent pro-inflammatory cytokine of the interleukin (IL)-1 family, IL-18 was elevated in early active progressive plaque-type psoriatic lesions and that serum or plasma levels of IL-18 correlated with the Psoriasis Area and Severity Index (PASI). Although results from previous studies have established that IL-18 may aggravate psoriatic inflammation, the mechanisms of this process remain unknown. In this study, IL-18 knock out (KO) mice and wild-type (WT) mice were used to investigate the effects of IL-18 within a mouse model of psoriasis. Methods: WT and IL-18 KO mice were divided into four groups, including imiquimod (IMQ)-treated IL-18 KO group (w = 11) and WT group (n = 13) as well as their respectively gene-matched control mice (receiving vaseline;w = 12). PASI scores were used to evaluate psoriatic lesions in IMQ-treated mice. Pathological features and dermal cellular infiltration were investigated by hematoxylin and eosin staining. The levels of psoriasis-related cytokines including IL-23, IL-17, IL-12, IL-10, IFNγ, IL-15, IL-27, and IL-4 were tested by real-time polymerase chain reaction (PCR). The protein level of IL-1β, IL-27, CXCL1, and Ly6g were investigated by immunohistochemistry (IHC). Results: Acanthosis (98.46±14.12 vs. 222.68土71.10μm, P<0.01) and dermal cell infiltration (572.25±47.45 vs. 762.47土 59.59cells/field, P< 0.01) were significantly milder in IMQ-induced IL-18 KO mice compared with that in WT mice. IMQ-induced IL-18 KO mice manifested larger areas of Munro microabscesses (11,467.83±5112.09 vs. 4093.19±2591.88 pirn2, P< 0.01) and scales (100,935.24 ±41,167.77 vs. 41,604.41 ± 14,184.10 μm, P<0.01) as compared with WT mice. In skin lesions ot IL-18 KO mice, the expressions of IL-1β, IL-4, and IL-27 were all significantly upregulated but IL-17 was decreased. Histologically, strong positive signals of Ly6g were observed within the epidermis of IL-18 KO mice but expressions of CXCL1 were decreased. Conclusions: IL-18 may exacerbate prominent inflammation and influence pathological features in IMQ-induced mouse model of psoriasis. IL-18 may upregulate pro-inflammatory cytokines and reduce protective cytokines, thus aggravating psoriatic inflammation. In addition, IL-18 may be involved in the formation of Munro microabscesses and scales.
文摘To the Editor:Malassezia and Staphylococcus epidermidis(S.epidermidis)are commensal organisms found on human skin,and both display an imbalance of colonization in individuals with seborrheic dermatitis/dandruff(SD/D)[1-3].Malassezia have been implicated in SD/D pathogenesis,as evidenced by an imbalance in the numbers of Malassezia that colonize the skin lesions of people with SD/D,and the fact that antifungal treatment exerts a modifying effect.[4].
文摘To the Editor: A 10-year-old girl presented with an asymptomatic ulcerated tumor on her right forearm for 18 months [Figure 1a]. The minor initially was inconspicuous and then gradually enlarged with painless ulceration in its center [Figure 1b]. Three months later, she developed three nontender new nodules on her right arm, proximal to the initial ulcerated nodule. Her general condition was good. Skin examination revealed a 4 cm × 4 cm tumor, with central ulceration and raised margins. Three diameters in 3-5 cm,