IMPACT OF THE VIRULENCE FACTOR YopP ON THE DEVELOPMENT OF IMMUNE RESPONSE AGAINST YERSINIA ENTEROCOLITICA

JUAN EDUARDO SILVA ; ROBERTO CARLOS DAVICINO; MARÍA SILVIA DI GENARO

Buenos Aires

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

SOCIEDADES DE BIOCIENCIAS

Yersinia enterocolitica (Ye) are Gram-negative enteropathogenicbacteria. Ye inject the effector proteins called Yersinia outer proteins(Yops) into host target cells. YopP induces apoptosis in macrophagesand dendritic cells (DC). Here, we aimed to compare the invasionproperties and immune response induced by YopP-deficient(Ye DYopP) and wild type (Ye wt) strains. Therefore, C57BL/6 micewere oragastrically infected with 1-5 x 108 or 5 x 1010 Ye DYopP, Yewt or Ye wt-GFP. After 30, 60, 120 min and 5 days after infection,Peyer?s patches (PP), mesenteric lymph node (MLN) and spleen(S) were obtained. Colony forming units (CFU) were evaluated inthe organs at 60 min and 5 days after infection. Cytokines and NFkβwere measured by ELISA, and cell infiltration by flow cytometry.Mice infected with Ye DYopP showed increased CFU in PP at 60min (p≤ 0.05), and in MLN and S after 5 days post-infection (p≤0.01). Besides, higher amount of pro-inflammatory cytokines (IL-1β,IFN-g, TNF, IL-6, and IL-17) (p≤ 0.05), and increased translocationof NF-kβ (p≤ 0.05) was detected in PP of mice infected with YeDYopP compared to those infected with Ye wt. However, IL-10 decreasedafter Ye DYopP infection (p≤ 0.01). At 5 days after Ye DYopPinfection, it was found increased frequency and absolute numberof macrophage (CD11b+ F4/80+) in PP and MLN (p≤ 0.001), and ofneutrophils (CD11b+, Ly6G+) in PP (p≤ 0.01). However, we did notobserve differences in the absolute number of macrophages, dendriticcells (CD11c+) and CD11cint CD11b+ inflammatory cells in S at60 min post-infection. Because we did not found early differences incell recruitment, we evaluated cells involving on immediate disseminationof Ye. We observed an increased number of CD11c+ CD11b+CD103+ GFP+ at 60 and 120 min post-infection in S from Ye wt-GFPinfected mice (p≤ 0.05). We concluded that YopP could be playinga critical role in Ye infection, controlling the immune response atmucosal entry sites.