CONICET | Buscador de Institutos y Recursos Humanos

JAHN GRACIELA A; SÁNCHEZ MARÍA BELÉN; INNOCENTI BADANO, ALICIA CAROLINA ; MACKERN OBERTI, JUAN PABLO; PENNACCHIO GISELA E; YUDICA SEDANO, FLORENCIA; VALDEZ SUSANA R; NEIRA FLAVIA J; PIETROBON ELISA O; SOAJE MARTA; MORENO-SOSA MARÍA TAMARA

Lugar:

Buenos Aires

Reunión:

Congreso; LXII Reunión Anual de la Sociedad de Investigación Clínica; 2017

Institución organizadora:

SAIC, SAIB, SAI, SAFE, SAA, SAB, SAFIS, SAA, SAP.

Resumen:

It is known that desmogleins areinvolved in cell adhesion mechanisms and are crucial in keeping structural integrityof different tissues, including skin. They also play important roles indifferentiation, cell activation and migration. Keratinocytes (KC) produceseveral inflammatory factors that modulate leukocytes. Psoriasis is a chronicinflammatory skin disease, characterized by KC hyperproliferation, vasculaturegrowth, and leukocyte infiltration into the dermis and epidermis. Imiquimod(IMQ) is an immunomodulator used in mice to induce lesions closely resemblinghuman psoriasis. The aim of our work was to assess the impact of desmoglein-4deficiency in the amount of skin leukocyte infiltration in an IMQ inducedpsoriasis model in rats. To this end, OFA hr/hr rats, which are mutant for thedesmoglein-4 gene and Sprague-Dawley (SD) wild type rats were used. IMQ wasadministered to both strains in shaved skin for four days to generatepsoriasis-like lesions. Skin biopsies from treated and untreated OFA and SDrats were weighed and minced to obtain cell suspensions that were stained withmonoclonal antibodies against CD45 (panleukocytary lineage) and CD3 (T celllineage) conjugated with fluorochromes and analyzed by flow cytometry.Interestingly, we found that IMQ treatment to both groups increased CD45+ CD3+cells in OFA skin compared to controls, but this difference was much greaterand significant in OFA rats (SD 0.79±0.24 vs OFA 4.12±0.75, p<0.05) thatcorrelated with increased inflammatory area and histopathologic changes in OFArats. These results suggest that desmoglein-4 absence contributes to psoriasis progress,promoting expansion of leukocyte population in skin. Although further researchis needed, these results could have a potential impact on the design ofclinical therapies for psoriasis progression.