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1.
Int J Mol Sci ; 24(14)2023 Jul 14.
Artigo em Inglês | MEDLINE | ID: mdl-37511208

RESUMO

The high-pathogenicity island (HPI) was initially identified in Yersinia and can be horizontally transferred to Escherichia coli to produce yersiniabactin (Ybt), which enhances the pathogenicity of E. coli by competing with the host for Fe3+. Pyroptosis is gasdermin-induced necrotic cell death. It involves the permeabilization of the cell membrane and is accompanied by an inflammatory response. It is still unclear whether Ybt HPI can cause intestinal epithelial cells to undergo pyroptosis and contribute to gut inflammation during E. coli infection. In this study, we infected intestinal epithelial cells of mice with E. coli ZB-1 and the Ybt-deficient strain ZB-1Δirp2. Our findings demonstrate that Ybt-producing E. coli is more toxic and exacerbates gut inflammation during systemic infection. Mechanistically, our results suggest the involvement of the NLRP3/caspase-1/GSDMD pathway in E. coli infection. Ybt promotes the assembly and activation of the NLRP3 inflammasome, leading to GSDMD cleavage into GSDMD-N and promoting the pyroptosis of intestinal epithelial cells, ultimately aggravating gut inflammation. Notably, NLRP3 knockdown alleviated these phenomena, and the binding of free Ybt to NLRP3 may be the trigger. Overall, our results show that Ybt HPI enhances the pathogenicity of E. coli and induces pyroptosis via the NLRP3 pathway, which is a new mechanism through which E. coli promotes gut inflammation. Furthermore, we screened drugs targeting NLRP3 from an existing drug library, providing a list of potential drug candidates for the treatment of gut injury caused by E. coli.


Assuntos
Células Epiteliais , Infecções por Escherichia coli , Escherichia coli , Mucosa Intestinal , Proteína 3 que Contém Domínio de Pirina da Família NLR , Piroptose , Animais , Camundongos , Enterócitos/metabolismo , Enterócitos/microbiologia , Células Epiteliais/metabolismo , Células Epiteliais/microbiologia , Escherichia coli/metabolismo , Escherichia coli/patogenicidade , Infecções por Escherichia coli/metabolismo , Inflamassomos/metabolismo , Inflamação/metabolismo , Mucosa Intestinal/citologia , Mucosa Intestinal/metabolismo , Mucosa Intestinal/microbiologia , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Piroptose/fisiologia
2.
Vet Microbiol ; 138(3-4): 273-80, 2009 Sep 18.
Artigo em Inglês | MEDLINE | ID: mdl-19410387

RESUMO

The RNA genome sequence of the rabbit passage-attenuated strain of foot-and-mouth disease virus (FMDV) Asia 1, ZB/CHA/58(att), was determined to be 8165 nt in length excluding the poly(C) tract in the 5' UTR and the poly(A) tail at the 3' end. ZB/CHA/58(att) was most similar to the vaccine strain Asia 1/YNBS/58 in genome sequence and there were no deletions or insertions within the deduced polyprotein between ZB/CHA/58(att) and YNBS/58, but there were a total of 25 substitutions at the amino acid level and an extra 19-nt stretch in the 5' UTR was found in ZB/CHA/58(att). An infectious full-length cDNA clone of ZB/CHA/58(att) was developed. Infectious virus could be recovered in BHK-21 cells transfected with the synthetic viral RNA transcribed in vitro. The plaque morphology, growth kinetics and antigenic profile of the infectious clone-derived virus (termed tZB) were indistinguishable from those induced by the parental virus. Furthermore, the virulence properties of ZB/CHA/58(att) and tZB were found to be highly similar in the mouse model. The availability of genome sequence information and infectious cDNA clone of the FMDV ZB/CHA/58(att) lays a new ground for further investigation of FMDV virulence determinants and development of new potent vaccine to FMD.


Assuntos
DNA Complementar/genética , DNA Viral/genética , Vírus da Febre Aftosa/patogenicidade , Genoma Viral , Sequência de Aminoácidos , Animais , Sequência de Bases , Bovinos , Linhagem Celular , China/epidemiologia , Clonagem Molecular , Cricetinae , Febre Aftosa/epidemiologia , Febre Aftosa/virologia , Vírus da Febre Aftosa/classificação , Genes Virais , Filogenia , Proteínas Virais/química , Virulência
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