Practical part:
During infection, bacteria, such as Yersinia enterocolitica, can actively translocate anti-inflammatory proteins into the host cell cytoplasm to suppress the host immune response. These proteins can be produced recombinantly and are to be formulated as drugs for therapy. For this purpose, the mouse model of imiquimod-induced psoriasis-like skin inflammation was used, and the animals were treated with the bacterial compounds. After the efficacy has been proven based on the reduction in disease severity, the mechanism of action shall be analyzed in detail. For this purpose, the induction of apoptosis, the inflammasome activation, cytokine production and NF-B activation or the effect of the proteins on the integrity of the epithelial barrier will be analyzed within this research module. Methods such as multicolor immunofluorescence, multiplex assays for cytokine quantification and characterization of signaling cascades, RNA sequencing or kinome analysis will be used.

Theoretical part (seminar):
During the research module, the pathomechanisms of chronic inflammatory skin diseases will be discussed, with a specific focus on the involvement of the immune system in the development of psoriasis vulgaris. At the same time, various possibilities how bacterial pathogens evade host immune defenses will be presented. These possibilities include the production of cell-penetrating peptides (CPEs) with anti-inflammatory properties, which can be developed as agents for therapy (drugs-from-bugs concept).