Showing posts with label Cholera. Show all posts
Showing posts with label Cholera. Show all posts

Friday, May 24, 2019

How to lurk: Droosphila used in study related to attachment of the cholera-causing bacteria Vibrio cholerae to arthropod intestines

Kamareddine L, Wong ACN, Vanhove AS, Hang S, Purdy AE, Kierek-Pearson K, Asara JM, Ali A, Morris JG Jr, Watnick PI. Activation of Vibrio cholerae quorum sensing promotes survival of an arthropod host. Nat Microbiol. 2018 Feb;3(2):243-252. PMID: 29180725; PMCID: PMC6260827.

Abstract: "Vibrio cholerae colonizes the human terminal ileum to cause cholera, and the arthropod intestine and exoskeleton to persist in the aquatic environment. Attachment to these surfaces is regulated by the bacterial quorum-sensing signal transduction cascade, which allows bacteria to assess the density of microbial neighbours. Intestinal colonization with V. cholerae results in expenditure of host lipid stores in the model arthropod Drosophila melanogaster. Here we report that activation of quorum sensing in the Drosophila intestine retards this process by repressing V. cholerae succinate uptake. Increased host access to intestinal succinate mitigates infection-induced lipid wasting to extend survival of V. cholerae-infected flies. Therefore, quorum sensing promotes a more favourable interaction between V. cholerae and an arthropod host by reducing the nutritional burden of intestinal colonization."

Asking yourself, "Um, what?" Here's an interpretation by your blog author: 
Bacteria called Vibrio cholerae cause cholera in humans. When they're not doing that, they lurk inside the guts (and on the outsides) of arthropods that live in the water. This study uses fruit flies as a lab-friendly system in which to look at a specific aspect of the interaction between a host arthropod's gut and Vibrio bacteria. Turns out that confusing the bacteria about how many of themselves are around stops them from taking up a molecule called succinate, leaving more of the succinate around for the fly. With more succinate available, the fly uses up less of its fat reserves than it usually would when infected. This helps the infected fly survive longer.

Monday, August 27, 2018

Fly Study Points to Bacterial Regulation of Acetate as Factor in Vibrio cholera virulence

Liimatta K, Flaherty E, Ro G, Nguyen DK, Prado C, Purdy AE. A putative acetylation system in Vibrio cholerae modulates virulence in arthropod hosts. Appl Environ Microbiol. 2018 Aug 24. PMID: 30143508.

From the abstract: "Acetylation is a broadly conserved mechanism of covalently modifying the proteome to precisely control protein activity. In bacteria, central metabolic enzymes and regulatory proteins, including those involved in virulence, can be targeted for acetylation. In this study, we directly link a putative acetylation system to metabolite-dependent virulence in the pathogen Vibrio cholerae ... The Drosophila model of Vibrio cholerae infection has revealed that bacterial regulation of acetate and other small metabolites from within the fly gastrointestinal tract is crucial to its virulence. Here, we demonstrate that genes that may modify the proteome of V. cholerae affect virulence towards Drosophila ... These findings further highlight the many layers of regulation that tune bacterial metabolism to alter the trajectory of interactions between bacteria and their hosts."

Friday, July 27, 2018

Using fruit flies and house flies to study cholera

Purdy AE. Fly Models of Vibrio cholerae Infection and Colonization. Methods Mol Biol. 2018;1839:77-96. doi: 10.1007/978-1-4939-8685-9_8. PubMed PMID: 30047056.

From the abstract: "Studies of Vibrio cholerae pathogenesis in the context of novel eukaryotic model systems have expanded our understanding of genes that underlie V. cholerae interactions with humans, as well as host organisms in the environment. ... The Drosophila model for V. cholerae infection is a powerful tool for discovering new genetic pathways that govern bacterial physiology and colonization in the arthropod gastrointestinal tract. Assays to measure both virulence and colonization have been established and are easily adopted in labs unfamiliar with Drosophila work. Experiments to compare survival of flies colonized with different bacterial mutants are simple to perform and can be completed in less than a week, allowing colonization to be quantified and localized easily. The availability of molecular and genetic tools for the fly enables further exploration of host factors that restrict V. cholerae colonization and invasive infection. Based on the Drosophila system, a house fly (Musca domestica) model of V. cholerae colonization has also been developed. The new house fly model may prove a useful tool for examining V. cholerae infection dynamics in the context of a host carrying a complex microbial community, with a fundamentally different ecology that may increase its chances of acting as a vector for cholera disease."

Wednesday, July 11, 2018

Fly model of cholera used to explore cellular mechanisms of disease

Fast D, Kostiuk B, Foley E, Pukatzki S. Commensal pathogen competition impacts host viability. Proc Natl Acad Sci U S A. 2018 Jul 3;115(27):7099-7104. PMID: 29915049.

From the abstract: "While the structure and regulatory networks that govern type-six secretion system (T6SS) activity of Vibrio cholerae are becoming increasingly clear, we know less about the role of T6SS in disease. Under laboratory conditions, V. cholerae uses T6SS to outcompete many Gram-negative species, including other V. cholerae strains and human commensal bacteria. ... We used the Drosophila melanogaster model of cholera to define the contribution of T6SS to V. cholerae pathogenesis. ... interactions between T6SS and host commensals impact pathogenesis. Inactivation of T6SS, or removal of commensal bacteria, attenuates disease severity. Reintroduction of the commensal, Acetobacter pasteurianus, into a germ-free host is sufficient to restore T6SS-dependent pathogenesis in which T6SS and host immune responses regulate viability. Together, our data demonstrate that T6SS acts on commensal bacteria to promote the pathogenesis of V. cholerae."

Tuesday, April 1, 2014

Cholera and Notch signaling--study includes fly assays

Guichard A, Cruz-Moreno B, Aguilar B, van Sorge NM, Kuang J, Kurkciyan AA, Wang Z, Hang S, Pineton de Chambrun GP, McCole DF, Watnick P, Nizet V, Bier E. Cholera toxin disrupts barrier function by inhibiting exocyst-mediated trafficking of host proteins to intestinal cell junctions. Cell Host Microbe. 2013 Sep 11;14(3):294-305. PMID: 24034615; PMCID: PMC3786442.

Tuesday, January 28, 2014

Review: study of infectious pathogens in the fly model

Panayidou S, Ioannidou E, Apidianakis Y. Human pathogenic bacteria, fungi, and viruses in Drosophila: Disease modeling, lessons, and shortcomings. Virulence. 2014 Jan 7;5(2). PMID: 24398387.