Cross Talk between Proliferative, Angiogenic, and Cellular Mechanisms Orchestred by HIF-1α in Psoriasis.

Psoriasis is a chronic inflammatory skin disease where the altered regulation in angiogenesis, inflammation, and proliferation of keratinocytes are the possible causes of the disease, and the transcription factor "hypoxia-inducible factor 1-alpha" (HIF-1α) is involved in the homeostasis of these three biological phenomena. In this review, the role of HIF-1α in the cross talk between the cytokines and cells of the immunological system involved in the pathogenesis of psoriasis is discussed.

Heptapeptide HP3 acts as a potent inhibitor of experimental imiquimod­induced murine psoriasis and impedes the trans­endothelial migration of mononuclear cells.

During the progression of psoriatic lesions, abundant cellular infiltration of myeloid cells, such as macrophages and activated dendritic cells, occurs in the skin and the infiltrating cells interact with naive lymphoid cells to generate a T helper (Th)1 and Th17 environment. Therapies to treat psoriasis include phototherapy, non­steroidal and steroidal drugs, as well as antibodies to block tumor necrosis factor­α, interleukin (IL)­17­A and IL­12/IL­23, which all focus on decreasing the proinflammatory hallmark of psoriasis. The present study obtained the heptapeptide HP3 derived from phage display technology that blocks mononuclear cell adhesion to endothelial cells and inhibits trans­endothelial migration in vitro. The activity of the heptapeptide in a murine model of psoriasis was also assessed, which indicated that early administration inhibited the development of psoriatic lesions. Therefore, the results suggested that HP3 may serve as a potential therapeutic target for psoriasis.

D-Amino acids inhibit biofilm formation in Staphylococcus epidermidis strains from ocular infections.

Biofilm formation on medical and surgical devices is a major virulence determinant for Staphylococcus epidermidis. The bacterium S. epidermidis is able to produce biofilms on biotic and abiotic surfaces and is the cause of ocular infection (OI). Recent studies have shown that d-amino acids inhibit and disrupt biofilm formation in the prototype strains Bacillus subtilis NCBI3610 and Staphylococcus aureus SCO1. The effect of d-amino acids on S. epidermidis biofilm formation has yet to be tested for clinical or commensal isolates. S. epidermidis strains isolated from healthy skin (n = 3), conjunctiva (n = 9) and OI (n = 19) were treated with d-Leu, d-Tyr, d-Pro, d-Phe, d-Met or d-Ala and tested for biofilm formation. The presence of d-amino acids during biofilm formation resulted in a variety of patterns. Some strains were sensitive to all amino acids tested, while others were sensitive to one or more, and one strain was resistant to all of them when added individually; in this way d-Met inhibited most of the strains (26/31), followed by d-Phe (21/31). Additionally, the use of d-Met inhibited biofilm formation on a contact lens. The use of l-isomers caused no defect in biofilm formation in all strains tested. In contrast, when biofilms were already formed d-Met, d-Phe and d-Pro were able to disrupt it. In summary, here we demonstrated the inhibitory effect of d-amino acids on biofilm formation in S. epidermidis. Moreover, we showed, for the first time, that S. epidermidis clinical strains have a different sensitivity to these compounds during biofilm formation.