Estudo da resposta imune, colonização e invasão de aves (Gallus gallus domesticus) por estirpes de Salmonella Enteritidis e Salmonella Typhimurium contendo deleções nos genes clpp e flid
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Data
2020-03-02
Autores
Barbosa, Fernanda de Oliveira [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
Salmonella Enteritidis e Salmonella Typhimurium causam infecções em seres humanos e animais que são frequentemente associadas à extensa colonização intestinal e excreção fecal. A presença de estrutura flagelar no patógeno está relacionada à indução de inflamação intestinal e atenuação de infecção sistêmica no hospedeiro. Por outro lado, a infecção por estirpes aflageladas resulta em pouca inflamação e consequente infecção sistêmica grave. No presente estudo, foi avaliada a hipótese de que a síntese de maior quantidade de flagelina em estirpes de Salmonella geneticamente modificadas poderia levar a infecção sistêmica menos intensa em aves. Para investigar as conseqüências da superprodução de flagelina, foram construídas estirpes de Salmonella Enteritidis e Typhimurium contendo deleções nos genes clpP e fliD (que levam à superexpressão de flagelina) e patogenicidade e imunogenicidade foram comparadas com as respectivas estirpes selvagens em aves infectadas. Os resultados indicaram que o aumento da síntese de flagelina por SE ΔclpPΔfliD e STM ΔclpPΔfliD culmina em déficit da taxa de multiplicação bacteriana. Porém, tais alterações não interferiram na capacidade de colonização cecal e excreção fecal das estirpes mutantes. O mesmo foi observado em fígado e baço, mas após 14 dpi as estirpes mutantes tendem a serem eliminadas destes órgãos. Mesmo com síntese mais elevada de flagelina, as estirpes mutantes recrutaram quantidades semelhantes de linfócitos e macrófagos em tonsila cecal, baço e fígado que as estirpes selvagens. Infecções por STM ΔclpPΔfliD produziram sinais clínicos mais brandos em comparação à STM, e alta produção de IL22 em 7 dpi. Enquanto que SE ΔclpPΔfliD desencadeou sinais clínicos semelhantes aos induzidos por SE, porém, com níveis mais elevados de IL22 e IL18, porém com repressçao de CCl4, CXCLi2 e IL17 em no intestino no início da infecção. Ao que tudo indica a maior produção de flagelina por ambas as estirpes mutantes alteraram a patogenicidade, possivelmente por alterarem a ativação e modulação do sistema imune da ave.
Salmonella Enteritidis and Salmonella Typhimurium cause infections in humans and animals that are often associated with extensive intestinal colonization and faecal shedding. The presence of flagellar structure in the pathogen is related to the induction of intestinal inflammation and attenuation of systemic infection in the host. On the other hand, the absence of flagellin results in severe systemic infection as a result of mild inflammatory intestinal responses provoked by aflagellated strains. The hypothesis that higher flagellin production by Salmonella strains could induce immunogenic response during infection in chickens was evaluated in the present study. To investigate the consequences of flagellin overproduction, strains of Salmonella Enteritidis and Typhimurium containing clpP and fliD deletions (which lead to flagellin overexpression) were constructed, and pathogenicity and immunogenicity were compared with their respective wild-type strains in infected chickens. The results suggested that the increase in flagellin synthesis by SE ΔclpPΔfliD and STM ΔclpPΔfliD culminates in a deficit in the bacterial multiplication rate. However, that changes did not interfere with the capacity for caecal colonization and faecal excretion of mutant strains. The same was observed in the liver and spleen, but after 14 dpi, mutant strains tend to be eliminated from these organs. Even with higher flagellin synthesis, the mutant strains recruited similar amounts of lymphocytes and macrophages in the caecal tonsil, spleen and liver than wild-type strains. and high IL22 production at 7 dpi. While SE ΔclpPΔfliD triggered clinical signs similar to those induced by SE, but with higher levels of IL22 and IL18, but with repression of CCl4, CXCLi2 and IL17 in the intestine at the beginning of the infection. Apparently, the higher production of flagellin by both mutant strains altered the pathogenicity, possibly by altering the activation and modulation of the chicken's immune system.
Salmonella Enteritidis and Salmonella Typhimurium cause infections in humans and animals that are often associated with extensive intestinal colonization and faecal shedding. The presence of flagellar structure in the pathogen is related to the induction of intestinal inflammation and attenuation of systemic infection in the host. On the other hand, the absence of flagellin results in severe systemic infection as a result of mild inflammatory intestinal responses provoked by aflagellated strains. The hypothesis that higher flagellin production by Salmonella strains could induce immunogenic response during infection in chickens was evaluated in the present study. To investigate the consequences of flagellin overproduction, strains of Salmonella Enteritidis and Typhimurium containing clpP and fliD deletions (which lead to flagellin overexpression) were constructed, and pathogenicity and immunogenicity were compared with their respective wild-type strains in infected chickens. The results suggested that the increase in flagellin synthesis by SE ΔclpPΔfliD and STM ΔclpPΔfliD culminates in a deficit in the bacterial multiplication rate. However, that changes did not interfere with the capacity for caecal colonization and faecal excretion of mutant strains. The same was observed in the liver and spleen, but after 14 dpi, mutant strains tend to be eliminated from these organs. Even with higher flagellin synthesis, the mutant strains recruited similar amounts of lymphocytes and macrophages in the caecal tonsil, spleen and liver than wild-type strains. and high IL22 production at 7 dpi. While SE ΔclpPΔfliD triggered clinical signs similar to those induced by SE, but with higher levels of IL22 and IL18, but with repression of CCl4, CXCLi2 and IL17 in the intestine at the beginning of the infection. Apparently, the higher production of flagellin by both mutant strains altered the pathogenicity, possibly by altering the activation and modulation of the chicken's immune system.
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Palavras-chave
Aves, Flagelo, Mutagênese, Paratifo, Salmonelose, Birds, Flagellum, Fowl paratyphoid, Mutagenesis, Salmonellosis