Phentotypic, gentotypic antimicrobial resistance and pathogenicity of Salmonella enterica serovars Typimurium and Enteriditis in poultry and poultry products

Khan, Sher Bahadar; Khan, Mumtaz Ali; Ahmad, Irshad; Rehman, Tayyab; Ullah, Shahid; Dad, Rahim; Sultan, Asad; Memon, Ashraf

doi:10.1016/j.micpath.2019.01.046

Cited by 27 publications

(13 citation statements)

References 34 publications

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“…In addition, outbreak strains also showed resistance to NAL. These five antibiotics were the most common antibiotics for which S. Typhimurium exhibited resistance, especially in China Liang et al, 2018;Khan et al, 2019;Mellor et al, 2019). NAL belongs to the first generation of quinolone antibiotics, and many intestinal infecting bacteria have developed resistance to it.…”

Section: Discussionmentioning

confidence: 99%

Investigation of a Salmonellosis Outbreak Caused by Multidrug Resistant Salmonella Typhimurium in China

Xiang

Li²,

Dong

et al. 2020

Front. Microbiol.

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Section: Discussionmentioning

confidence: 99%

Investigation of a Salmonellosis Outbreak Caused by Multidrug Resistant Salmonella Typhimurium in China

Xiang

Li²,

Dong

et al. 2020

Front. Microbiol.

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“…The existing research tends to use Salmonella Typhimurium to study the interaction between host autophagic activity and bacterial invasion. However, Salmonella Enteritidis, which belongs to another Salmonella serotype, could be much difference from Salmonella Typhimurium in host-adaptability, virulence, intracellular survival and so on (47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

Salmonella Enteritidis Effector AvrA Suppresses Autophagy by Reducing Beclin-1 Protein

et al. 2020

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Autophagy is a cellular process to clear pathogens. Salmonella enterica serovar Enteritidis (S.E) has emerged as one of the most important food-borne pathogens. However, major studies still focus on Salmonella enterica serovar Typhimurium. Here, we reported that AvrA, a S. Enteritidis effector, inhibited autophagy to promote bacterial survival in the host. We found that AvrA regulates the conversion of LC3 I into LC3 II and the enrichment of lysosomes. Beclin-1, a key molecular regulator of autophagy, was decreased after AvrA expressed strain colonization. In S.E-AvrA − -infected cells, we found the increases of protein levels of p-JNK and p-c-Jun and the transcription level of AP-1. AvrA-reduction of Beclin-1 protein expression is through the JNK pathway. The JNK inhibitor abolished the AvrA-reduced Beclin-1 protein expression. Moreover, we identified that the AvrA mutation C186A abolished its regulation of Beclin-1 expression. In addition AvrA protein was found interacted with Beclin-1. In organoids and infected mice, we explored the physiologically related effects and mechanism of AvrA in reducing Beclin-1 through the JNK pathway, thus attenuating autophagic responses. This finding not only indicates an important role of S. Enteritidis effector in reducing host protein as a strategy to suppress autophagy, but also suggests manipulating autophagy as a new strategy to treat infectious diseases.

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Section: Discussionmentioning

confidence: 99%

SalmonellaEnteritidis Effector AvrA suppresses autophagy by reducing Beclin-1 protein

Jiao

Zhang

Lin

et al. 2020

Preprint

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Autophagy is a cellular process to clear pathogens. Salmonella enterica serovar Enteritidis (S.E) has emerged as one of the most important food-borne pathogens.However, major studies still focus on Salmonella enterica serovar Typhimurium. Here, we reported that AvrA, a S. Enteritidis effector, inhibited autophagy to promote bacterial survival in the host. We found that AvrA regulates the conversion of LC3 I into LC3 II and the enrichment of lysosomes. Beclin-1, a key molecular regulator of autophagy, was decreased after AvrA expressed strain colonization. In S.E-AvrA--infected cells, we found the increases of protein levels of p-JNK and p-c-Jun and the transcription level of AP-1. AvrA-reduction of Beclin-1 protein expression is through the JNK pathway. The JNK inhibitor abolished the AvrA-reduced Beclin-1 protein expression. Moreover, we identified that the AvrA mutation C186A abolished its regulation of Beclin-1 expression.In addition, AvrA protein interacted with Beclin-1. In organoids and infected mice, we explored the physiologically related effects and mechanism of AvrA in reducing Beclin-1 through the JNK pathway, thus attenuating autophagic responses. Importance:Salmonella Enteritidis is an important pathogen with a public health concern and farm production risk, yet the host-pathogen interactions that govern the survival of S.Enteritidis infections are incompletely understood. Anti-bacterial autophagy provides potent cell-autonomous immunity against bacterial colonization. Here, we report that a new role for effector AvrA of S. Enteritidis in the reduction of Beclin-1 protein expression through the JNK pathway and the attenuation of the autophagic response in intestinal epithelial cells. This finding not only indicates an important role of S. Enteritidis effector in reducing host protein as a strategy to suppress autophagy, but also suggests manipulating autophagy as a new strategy to treat infectious diseases.3

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Phentotypic, gentotypic antimicrobial resistance and pathogenicity of Salmonella enterica serovars Typimurium and Enteriditis in poultry and poultry products

Cited by 27 publications

References 34 publications

Investigation of a Salmonellosis Outbreak Caused by Multidrug Resistant Salmonella Typhimurium in China

Investigation of a Salmonellosis Outbreak Caused by Multidrug Resistant Salmonella Typhimurium in China

Salmonella Enteritidis Effector AvrA Suppresses Autophagy by Reducing Beclin-1 Protein

SalmonellaEnteritidis Effector AvrA suppresses autophagy by reducing Beclin-1 protein

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