Producción CyT
Libro de resúmenes del congreso - HYPERVIRULENT Clostridioides difficile BI/NAP1/027 STRAIN REGULATES T CELLS RESPONSES IN AN IN VIVO MURINE MODEL.
Congreso
Autoría:
Hernandez Del Pino, R.E. ; Cajia, M.F ; Brabero, A.M ; Celano, J. ; Estermann,M.A ; ESPAÑOL, LAUREANO ANGEL ; Morro,L.S. ; Machain,M. ; Pasquinelli,V.Fecha:
2019Editorial y Lugar de Edición:
SAIResumen *
Clostridioides difficile, the etiologic agent of antibiotic-associated diarrhea, is a Grampositive, anaerobic, spore-forming bacterium. BI/NAP1/027 is a hypervirulent strain that has dramatically changed the epidemiology of C. difficile infection (CDI). Since antibiotic runs the risk of prolonged gut microbiota perturbation and so recurrence of infection, identification of key effector molecules of host immune response against CDI may provide new therapeutic targets and biomarkers to improve treatment and diagnosis. We used a murine model to study the adaptive immune response during CDI. Afterinduction of dysbiosis, mice were infected with spores from BI/NAP1/027 strain. Infected mice evidenced typical CDI symptoms such as diarrhea, hunched posture, and weight loss (p<0.01). Infected mice also showed an increase in bacterial shedding (p<0.05) and clinical score. Mesenteric lymph nodes (MLNs) and intestinal lamina propria mononuclear cells (LPMC) were isolated 8 days post-infection. C. difficile-infected mice evidenced a down-modulation of CD3+SLAM+ (p<0.01) and CD3+ICOS+ (p<0.01) on LPMC, compared to control mice as shown by Flow Cytometry. A negative modulation of CD3+CD4+IL-17A+ LPMC (p<0.05) and CD3+CD4-IL-17A+ MLNs cells (p<0.05) was observed in C. difficile infectedmice. Similar results were obtained on CD3+CD4+IFN-γ+IL-17A+ LPMC and MLNscells (p<0.05). Moreover, cecal contents from C. difficile-infected mice showed increased IL-10 mRNA levels.Our results suggest that C. difficile modulate T cells functions/activation by regulating pro and anti-inflammatory cytokines production and costimulatory molecules expression during infection. Información suministrada por el agente en SIGEVAPalabras Clave
InfeccionesInmunologiaClostridioides difficile