Papel das Yops secretadas por Yersinia sobre a resposta imune do hospedeiro / Role of Yops secreted by Yersinia in the host immune response

O gênero Yersinia compreende três espécies patogênicas para humanos: Y. pestis, Y. enterocolitica e Y. pseudotuberculosis. A patogenicidade de Yersinia está ligada à presença do plasmideo de 70-kb (pYV) que é comum às três espécies e codifica um sistema de secreção do tipo III e um conjunto de proteínas de virulência, incluindo aquelas conhecidas como Yops (Yersinia outer proteins), que são exportadas por este sistema quando as células do hospedeiro são infectadas pela bactéria. Duas Yops translocadoras (YopB e YopD) se inserem na membrana plasmática e funcionam no transporte de seis efetoras (YopO, YopH, YopM, YopJ e YopT) para o citosol da célula do hospedeiro. As Yops efetoras funcionam interferindo em múltiplas vias de sinalização da célula infectada. Como consequência, a resposta imune inata e adaptativa do hospedeiro fica afetada. Este trabalho enfoca o papel das Yops na modulação da resposta imune do hospedeiro

Histopathological and ultrastructural alterations of induced Yersinia enterocolitica infection in mice.

Yersinia enterocolitica is an enteric bacterium and infections by this organism are mostly foodborne. It has been implicated to cause enterocolitis, terminal ilitis. diarrhoea, mesenteric lymphadenitis and arthritis in man. Due to paucity of information regarding histopathological and specially ultrastructural alterations in tissues affected, this study was planned with mice as the experimental model. Nine pathogenic Y.enterocoliticaisolates were used to infect 80 albino mice by oral and intraperitoneal route. Pathological alterations were studied by light and electron microscopy. Histopathological examination of intestines showed severe edema, purulent enteritis, goblet cell hyperplasia infiltration of mononuclear cells, thickening of mucosa and necrosis of the tips of villi. Liver showed congestion, hepatocellular degeneration and necrosis, atrophy of hepatocytes and microabcesses. The lungs revealed congestion, edema, haemorrhage and purulent ronchopneumonia, while kidneys showed mild necrotic changes and bacterial emboli in glomeruli. Ultrastructural changes were indicative of mitochondrial degeneration and their loss in kidneys, membranous degeneration with formation of myelin figures in lungs and disorganization, disruption and bleb formation of microvilli in intestines. Y.enterocolitica caused significant histopathological and ultrastructural alterations in experimentally infected mice. Variation in pathogenicity of different strains of Y.enterocolitica was also observed.