Candida albicans is the most common pathogen causing clinical Candida infections. Neutrophils are a key member of the host innate immunity that plays an essential role in clearing invading C. albicans. In addition to the well-known defensive approaches such as phagocytosis, degranulation, and reactive oxygen species production, the formation of neutrophil extracellular traps (NETs) has also become an important way for neutrophils to defend against various pathogens. C. albicans has been reported to be capable of activating neutrophils to release NETs that subsequently kill fungi. The induction of NETs is affected by both the morphology and virulence factors of C. albicans, which also develops specific strategies to respond to the attack by NETs. Our review specifically focuses on the mechanisms by which C. albicans triggers NET formation and their subsequent interactions, which might provide meaningful insight into the innate immunity against C. albicans infection.

Psoriasis is a chronic, inflammatory skin disease, frequently associated with dyslipidemia. Lipid disturbance in psoriasis affects both circulatory system and cutaneous tissue. Epidermal Langerhans cells (LCs) are tissue-resident DCs that maintain skin immune surveillance and mediate various cutaneous disorders, including psoriasis. However, the role of LCs in psoriasis development and their lipid metabolic alternation remains unclear. Here, we demonstrate that epidermal LCs of psoriasis patients enlarge with longer dendrites and possess elevated IL-23p19 mRNA and a higher level of neutral lipids when compared with normal LCs of healthy individuals. Accordantly, epidermal LCs from imiquimod-induced psoriasis-like dermatitis in mice display overmaturation, enhanced phagocytosis, and excessive secretion of IL-23. Remarkably, these altered immune properties in lesional LCs are tightly correlated with elevated neutral lipid levels. Moreover, the increased lipid content of psoriatic LCs might result from impaired autophagy of lipids. Bulk RNA-Seq analysis identifies dysregulated genes involved in lipid metabolism, autophagy, and immunofunctions in murine LCs. Overall, our data suggest that dysregulated lipid metabolism influences LC immunofunction, which contributes to the development of psoriasis, and therapeutic manipulation of this metabolic process might provide an effective measurement for psoriasis.

Background: Stomolophus meleagris envenomation causes severe cutaneous symptoms known as jellyfish dermatitis. The potential molecule mechanisms and treatment efficiency of dermatitis remain elusive because of the complicated venom components. The biological activity and molecular regulation mechanism of Troxerutin (TRX) was firstly examined as a potential treatment for jellyfish dermatitis. Methods: We examined the inhibit effects of the TRX on tentacle extract (TE) obtained from S. meleagris in vivo and in vitro using the mice paw swelling models and corresponding assays for Enzyme-Linked Immunosorbent Assay (ELISA) Analysis, cell counting kit-8 assay, flow cytometry, respectively. The mechanism of TRX on HaCaT cells probed the altered activity of relevant signaling pathways by RNA sequencing and verified by RT-qPCR, Western blot to further confirm protective effects of TRX against the inflammation and oxidative damage caused by TE. Results: TE significantly induced the mice paw skin toxicity and accumulation of inflammatory cytokines and reactive oxygen species in vivo and vitro. Moreover, a robust increase in the phosphorylation of mitogen-activated protein kinase (MAPKs) and nuclear factor-kappa B (NF-κB) signaling pathways was observed. While, the acute cutaneous inflammation and oxidative stress induced by TE were significantly ameliorated by TRX treatment. Notablly, TRX suppressed the phosphorylation of MAPK and NF-κB by initiating the nuclear factor erythroid 2-related factor 2 signaling pathway, which result in decreasing inflammatory cytokine release. Conclusion: TRX inhibits the major signaling pathway responsible for inducing inflammatory and oxidative damage of jellyfish dermatitis, offering a novel therapy in clinical applications.

Background: Myeloid sarcoma (MS), which represents a rare malignancy that comprises of myeloid blasts occurring at extra-medullary sites, closely correlates with the onset and relapse of acute myeloid leukemia (AML) and other hemopoietic neoplasm. Female genital system is an uncommon location of MS, with the vulvar MS being even rarer that only eight cases have been reported in English-written literature.Case presentation: A 47-year-old woman presented with chronic ulceration on her vulva for one and a half month. Microscopic examination of incisional biopsy revealed dermal infiltration of myeloid precursor cells, which were positive for MPO, lysozyme, CD43, CD68, CD38 and CD117. Bone marrow flowcytometric analysis showed myeloblast count of 74%, which expressed CD13, CD33, CD117 and HLA-DR. A diagnosis of AML (M2 type) was made and vulvar MS was the earliest symptom. The patient achieved complete remission after chemotherapy with no evidence of recurrence in a 27-month follow-up. We reviewed the literature and identified 54 cases of Chinese patients with gynecological MS between 1999 and 2018, and discovered that in Chinese population, MS most frequently involved uterine cervix followed by the ovary and vulva, and ovarian MS onset much earlier than other sites. Remarkably, vulvar MS exhibited a high rate of concurrent AML and secondary myeloid leukemia within a short time of its occurrence. Despite its limited distribution, MS should be tackled aggressively with chemotherapy followed by allogeneic hematopoietic stem cell transplantation if the appropriate donor is available.Conclusions: Female genital MS, especially vulvar MS, should be included in the differential diagnosis of gynecological neoplasm, which will facilitate its early diagnosis and prompt management.

Background. Crisaborole has been considered a promising alternative for topical treatment of atopic dermatitis (AD), mainly supported by AD‐301 and AD‐302. However, critical insights into these two studies have previously been proposed. Objective. To make a comprehensive assessment of the application of crisaborole in mild to moderate AD. Methods. A systematic review and meta‐analysis were conducted, in which only randomized controlled trials comparing the application of crisaborole twice daily to vehicle or other active treatment in patients with mild to moderate AD were included. The selection of outcomes was based on the recommendation of the HOME initiative. Patient‐reported symptoms, clinician‐reported signs, health‐related quality of life, and the safety of crisaborole were all assessed using appropriate measurement instruments. Results. Eight RCTs with 2266 patients were included in the pooled analysis. Compared to those treated with vehicle, patients on crisaborole experienced a greater improvement in NRS (MD −0.70; 95% CI −0.94 to −0.47), POEM (MD −3.50; 95% CI −4.34 to −2.66), EASI (MD −14.49%; 95% CI −18.24% to −10.73%), ISGA (RR 1.45; 95% CI 1.28 to 1.63), DLQI (MD −1.54; 95% CI −2.17 to −0.92), and DFI (MD −1.16; 95% CI −1.72 to −0.59) during the 4‐week treatment. More patients achieved EASI 75 (RR 1.71; 95% CI 1.43 to 2.04) with crisaborole administration. There was no significant difference between two interventions in the incidence of AEs (RR 1.12; 95% CI 0.98 to 1.29), SAEs (RR 1.89; 95% CI 0.47 to 7.60), or AE‐related withdrawal (RR 0.87; 95% CI 0.47 to 1.60). One RCT also made comparison between crisaborole and pimecrolimus, suggesting that no significant difference was detected in the improvement of EASI or NRS at most time points. Conclusion. High‐quality evidence was provided to demonstrate that the short‐term application of crisaborole is safe and efficacious for the treatment of mild to moderate AD. The practical efficacy of crisaborole is similar to that of pimecrolimus.