Cholera Toxin Production Induced upon Anaerobic Respiration is Suppressed by Glucose Fermentation in Vibrio cholerae

Oh, Young Taek; Lee, Kang-Mu; Bari, Wasimul; Kim, Hwa Young; Kim, Hye Jin; Yoon, Sang Sun

doi:10.4014/jmb.1512.12039

Cited by 9 publications

(6 citation statements)

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“…For example, tetrathionate respiration provides Salmonella enterica serovar Typhimurium with advantage to colonize the inflamed intestines [27,28]. Cholera toxin production by Vibrio cholerae is also enhanced by anaerobic respiration [29,30]. Recently, it was demonstrated that the ability of L. monocytogenes to perform extracellular electron transfer conferred a clear fitness advantage in vivo [31].…”

Section: Discussionmentioning

confidence: 99%

Stimulating Respiratory Activity Primes Anaerobically Grown Listeria monocytogenes for Subsequent Intracellular Infections

2018

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Listeria monocytogenes (L. monocytogenes) is a Gram-positive, enteric pathogen and the causative agent of listeriosis. During transition through the gastrointestinal tract, L. monocytogenes routinely encounters suboxic conditions. However, how the exposure to the low oxygen environment affects subsequent pathogenesis is not completely understood. Our lab previously reported that anaerobically grown L. monocytogenes exhibited an intracellular growth defect in macrophages even though the infection took place under aerobic conditions. This phenotype suggests that prior growth conditions have a prolonged effect on the outcome of subsequent intracellular infection. In this study, to further investigate the mechanisms that contribute to the compromised intracellular growth after anaerobic exposure, we hypothesized that the lack of respiratory activity under anaerobic conditions prevented anaerobically grown L. monocytogenes to establish subsequent intracellular growth under aerobic conditions. To test this hypothesis, respiratory activity in anaerobically grown L. monocytogenes was stimulated by exogenous fumarate and subsequent intracellular pathogenesis was assessed. The results showed that fumarate supplementation significantly increased the respiratory activity of anaerobically grown L. monocytogenes and rescued the subsequent intracellular growth defect, likely through promoting the production of listeriolysin O, phagosomal escape, and cell-cell spread. This study highlights the importance of respiratory activity in L. monocytogenes in modulating the outcome of subsequent intracellular infections.

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Section: Discussionmentioning

confidence: 99%

Stimulating Respiratory Activity Primes Anaerobically Grown Listeria monocytogenes for Subsequent Intracellular Infections

2018

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“…Stringent response stimulated by the accumulation of guanosine pentaphosphate/tetraphosphate (p)ppGpp under stress conditions play an important role in the growth and virulence of V. cholerae . Administration of glucose, which is present in the oral rehydartion solution might reduce (p)ppGpp-mediated CT-production and growth of the pathogen under the influence of anaerobic glucose metabolism (Oh et al, 2016 ). Genome-wide screening has revealed that flagellin FlaC is involved in flagellum function and toxin production at higher (p)ppGpp levels (Kim et al, 2018 ).…”

Section: Flagellar Regulatory Systemmentioning

confidence: 99%

Virulence Regulation and Innate Host Response in the Pathogenicity of Vibrio cholerae

Ramamurthy

Nandy

Mukhopadhyay

et al. 2020

Front. Cell. Infect. Microbiol.

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The human pathogen Vibrio cholerae is the causative agent of severe diarrheal disease known as cholera. Of the more than 200 "O" serogroups of this pathogen, O1 and O139 cause cholera outbreaks and epidemics. The rest of the serogroups, collectively known as non-O1/non-O139 cause sporadic moderate or mild diarrhea and also systemic infections. Pathogenic V. cholerae circulates between nutrient-rich human gut and nutrient-deprived aquatic environment. As an autochthonous bacterium in the environment and as a human pathogen, V. cholerae maintains its survival and proliferation in these two niches. Growth in the gastrointestinal tract involves expression of several genes that provide bacterial resistance against host factors. An intricate regulatory program involving extracellular signaling inputs is also controlling this function. On the other hand, the ability to store carbon as glycogen facilitates bacterial fitness in the aquatic environment. To initiate the infection, V. cholerae must colonize the small intestine after successfully passing through the acid barrier in the stomach and survive in the presence of bile and antimicrobial peptides in the intestinal lumen and mucus, respectively. In V. cholerae, virulence is a multilocus phenomenon with a large functionally associated network. More than 200 proteins have been identified that are functionally linked to the virulence-associated genes of the pathogen. Several of these genes have a role to play in virulence and/or in functions that have importance in the human host or the environment. A total of 524 genes are differentially expressed in classical and El Tor strains, the two biotypes of V. cholerae serogroup O1. Within the host, many immune and biological factors are able to induce genes that are responsible for survival, colonization, and virulence. The innate host immune response to V. cholerae infection includes activation of several immune protein complexes, receptor-mediated signaling pathways, and other bactericidal proteins. This article presents an overview of regulation of important virulence factors in V. cholerae and host response in the context of pathogenesis.

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“…In addition to TorSR, TMAO respiration in V. cholerae is also governed by the catabolite repression protein (CRP), impairing TMAO reduction when glucose is available under anaerobic conditions. It has been proposed that the depletion of intracellular cAMP under high glucose concentrations leads to the inactivation of CRP and, as a consequence, expression of the TMAO reductase TorA is abrogated (Oh et al, 2015).…”

Section: Anaerobic Tmao Respirationmentioning

confidence: 99%

Adaptation of Vibrio cholerae to Hypoxic Environments

2020

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Bacteria can colonize virtually any environment on Earth due to their remarkable capacity to detect and respond quickly and adequately to environmental stressors. Vibrio cholerae is a cosmopolitan bacterium that inhabits a vast range of environments. The V. cholerae life cycle comprises diverse environmental and infective stages. The bacterium is found in aquatic ecosystems both under free-living conditions or associated with a wide range of aquatic organisms, and some strains are also capable of causing epidemics in humans. In order to adapt between environments, V. cholerae possesses a versatile metabolism characterized by the rapid cross-regulation of energyproducing pathways. Low oxygen concentration is a key environmental factor that governs V. cholerae physiology. This article reviews the metabolic plasticity that enables V. cholerae to thrive on low oxygen concentrations and its role in environmental and host adaptation.

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Cholera Toxin Production Induced upon Anaerobic Respiration is Suppressed by Glucose Fermentation in Vibrio cholerae

Cited by 9 publications

References 0 publications

Stimulating Respiratory Activity Primes Anaerobically Grown Listeria monocytogenes for Subsequent Intracellular Infections

Stimulating Respiratory Activity Primes Anaerobically Grown Listeria monocytogenes for Subsequent Intracellular Infections

Virulence Regulation and Innate Host Response in the Pathogenicity of Vibrio cholerae

Adaptation of Vibrio cholerae to Hypoxic Environments

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