Amicrobial pustulosis of the folds is a chronic relapsing neutrophilic dermatosis characterized by sterile pustules compromising skin folds, scalp, face and periorificial regions. It predominantly affects women. Demodicosis is an inflammatory disease associated with cutaneous overpopulation of the mite Demodex spp., the pathogenesis of which is not completely established, but is frequently related to local immunodeficiency. A case of a young woman with amicrobial pustulosis of the folds, and isolated worsening of facial lesions, is reported; investigation revealed overlapping demodicosis. There was complete regression of lesions with acaricide and cyclin treatment. This case warns of a poorly diagnosed but disfiguring and stigmatizing disease, often associated with underlying dermatoses or inadvertent treatments on the face.

Myiasis is a temporary infection of the skin or other organs with fly larvae.1The larvae develop into boil-like lesions. Creeping sensations and pain are usually described by patients. Following the maturation of the larvae, spontaneous exiting and healing is experienced. Herein we present a case of a traveler returning from Central African Republic. She does not recall insect bites. She never took off her clothing for recreational bathing, nor did she visit any rural areas. The lesions appeared on unexposed skin. The specific diagnosis was performed by morphologic characterization of the larvae, resulting in Cordylobia anthropophaga, the dominant form of myiasis in Africa. To our knowledge, this is the first reported case of C. anthropophaga in Latin America.

Human leukocyte antigen (HLA)-G is an immune checkpoint molecule that plays critical roles in immune response and in triggering inhibitory signaling to immune cells such as T cells, natural killer cells, and antigen-presenting cells. Thus, the application of HLA-G can be considered for treating immune response-related inflammatory disorders. We have previously reported that treatment with HLA-G1 and HLA-G2 ameliorates the joint swelling associated with collagen-induced arthritis of DBA/1 mice, an animal model for rheumatoid arthritis. In this study, we further investigated the effects of HLA-G1 on atopic dermatitis (AD), the most common inflammatory skin disorder. AD-like lesions were induced with the extract of the house dust mite Dermatophagoides farinae in NC/Nga mice. Continuous administration of HLA-G1 ameliorated the AD-like skin lesions in the mice. Furthermore, production of immunoglobulin E, interleukin (IL)-13, and IL-17A was significantly reduced in HLA-G1-treated mice, suggesting a Th2/Th17-mediated immune-inhibitory function of HLA-G1 in vivo. Our studies shed light on novel therapeutic strategies with recombinant HLA-G proteins for immune reaction-mediated chronic inflammatory disorders.

Atopic dermatitis (AD) is a common chronic inflammatory skin disease, affecting 10-20% of individuals worldwide. Therefore, the discovery of drugs for treating AD is an attractive subject and important to human health. Diospyros kaki and Diospyros kaki (D. kaki) folium exert beneficial effects on allergic inflammation. However, the effect of D. kaki calyx on AD remains elusive. The present study evaluated the effects of an aqueous extract of D. kaki calyx (AEDKC) on AD-like skin lesions using mouse and keratinocyte models. We used a mouse AD model by the repeated skin exposure of house dust mite extract [Dermatophagoides farinae extract (DFE)] and 2,4-dinitrochlorobenzene (DNCB) to the ears. In addition, to determine the underlying mechanism of its operation, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)-activated keratinocytes (HaCaT) were used. Oral administration of AEDKC decreased AD-like skin lesions, as demonstrated by the reduced ear thickness, serum immunoglobulin E (IgE), DFE-specific IgE, IgG2a, histamine level and inflammatory cell infiltration. AEDKC inhibited the expression of pro-inflammatory cytokines and a chemokine via downregulation of nuclear factor-κB and signal transducer and activator of transcription 1 in HaCaT cells. On examination of the AD-related factors in vivo and in vitro, it was confirmed that AEDKC decreased AD-like skin lesions. Taken together, the results suggest that AEDKC is a potential drug candidate for the treatment of AD.