Clostridioides difficile Sporulation

Serrano, Mónica; Martins, Diogo; Henriques, Adriano O.

doi:10.1007/978-3-031-42108-2_13

Cited by 2 publications

(3 citation statements)

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“…The pathogenesis is primarily driven by the activity of toxins A and B, encoded in the pathogenicity locus of the C. difficile genome [ 25 , 26 ]. In the anaerobic colonic environment, C. difficile spores germinate into vegetative cells, which release toxins that are internalized by gut epithelial cells [ 9 , 10 , 20 , 27 ]. These toxins glucosylate small Rho proteins ( Figure 1 A), leading to actin-cytoskeleton dysregulation, impaired cellular signaling, and other detrimental cellular effects [ 20 , 28 , 29 ].…”

Section: Overview Of C Difficile ’S Toxinsmentioning

confidence: 99%

“…C. difficile infects the host through the fecal-oral transmission of endospores, mainly affecting patients whose gut microbiota is depleted due to broad-spectrum antibiotics [2,7,8]. This disruption of normal colonic microbiota creates an environment conducive to the germination of spores into vegetative cells, which release toxin A and toxin B (some strains also produce binary toxin), damaging the intestinal epithelium [6,9,10]. Intestinal damage elicits a robust immune response in the colon, leading to a spectrum of clinical Toxins 2024, 16, 241 2 of 13 manifestations ranging from mild to severe diarrhea [6,9].…”

Section: Introductionmentioning

confidence: 99%

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Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis

Alam,

Madan

2024

Toxins

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Clostridioides difficile, a Gram-positive anaerobic bacterium, is the leading cause of hospital-acquired antibiotic-associated diarrhea worldwide. The severity of C. difficile infection (CDI) varies, ranging from mild diarrhea to life-threatening conditions such as pseudomembranous colitis and toxic megacolon. Central to the pathogenesis of the infection are toxins produced by C. difficile, with toxin A (TcdA) and toxin B (TcdB) as the main virulence factors. Additionally, some strains produce a third toxin known as C. difficile transferase (CDT). Toxins damage the colonic epithelium, initiating a cascade of cellular events that lead to inflammation, fluid secretion, and further tissue damage within the colon. Mechanistically, the toxins bind to cell surface receptors, internalize, and then inactivate GTPase proteins, disrupting the organization of the cytoskeleton and affecting various Rho-dependent cellular processes. This results in a loss of epithelial barrier functions and the induction of cell death. The third toxin, CDT, however, functions as a binary actin-ADP-ribosylating toxin, causing actin depolymerization and inducing the formation of microtubule-based protrusions. In this review, we summarize our current understanding of the interaction between C. difficile toxins and host cells, elucidating the functional consequences of their actions. Furthermore, we will outline how this knowledge forms the basis for developing innovative, toxin-based strategies for treating and preventing CDI.

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Section: Overview Of C Difficile ’S Toxinsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis

Alam,

Madan

2024

Toxins

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“…Spores are ubiquitous, but their presence is not always welcome. For instance, strict procedures are followed in hospitals to avoid nosocomial infections by Clostridioides difficile spores ( Serrano et al 2024 ). Even nonpathogenic spore formers such as B. subtilis can cause food spoilage ( Wen et al 2022 ).…”

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Spore germination: Two ion channels are better than one

Eichenberger

2024

Genes Dev.

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Germination is the process by which spores emerge from dormancy. Although spores can remain dormant for decades, the study of germination is an active field of research. In this issue ofGenes & Development, Gao and colleagues (pp. XXX–XXX) address a perplexing question: How can a dormant spore initiate germination in response to environmental cues? Three distinct complexes are involved: GerA, a germinant-gated ion channel; 5AF/FigP, a second ion channel required for amplification; and SpoVA, a channel for dipicolinic acid (DPA). DPA release is followed by rehydration of the spore core, thus allowing the resumption of metabolic activity.

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Clostridioides difficile Sporulation

Cited by 2 publications

References 269 publications

Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis

Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis

Spore germination: Two ion channels are better than one

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