ArticleInfection and immunity2014
Serratia marcescens ShlA pore-forming toxin is responsible for early induction of autophagy in host cells and is transcriptionally regulated by RcsB.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Antibiotic-induced stress responses in Gram-negative bacteria and their role in antibiotic resistance.The Journal of antimicrobial chemotherapy · 2025Review
- Article
- Making a Pathogen? Evaluating the Impact of Protist Predation on the Evolution of Virulence in Serratia marcescens.Genome biology and evolution · 2024Article
- Increased Proteolytic Activity ofPolish journal of microbiology · 2024Article
- Article
- PtrA regulates prodigiosin synthesis and biological functions inFrontiers in microbiology · 2023Article
- Autophagy in the normal and diseased cornea.Experimental eye research · 2022Review
- IgaA Protein, GumB, Has a Global Impact on the Transcriptome and Surface Proteome of Serratia marcescens.Infection and immunity · 2022Article
- Bacterial pore-forming toxins.Microbiology (Reading, England) · 2022Article
- PsrA is a novel regulator contributes to antibiotic synthesis, bacterial virulence, cell motility and extracellular polysaccharides production in Serratia marcescens.Nucleic acids research · 2022Article
- Article
- Antibiotics Used in Empiric Treatment of Ocular Infections Trigger the Bacterial Rcs Stress Response System Independent of Antibiotic Susceptibility.Antibiotics (Basel, Switzerland) · 2021Article
- The Rcs Stress Response System Regulator GumB Modulates Serratia marcescens-Induced Inflammation and Bacterial Proliferation in a Rabbit Keratitis Model and CytotoxicityInfection and immunity · 2021Article
- Serratia marcescens RamA Expression Is under PhoP-Dependent Control and Modulates Lipid A-Related Gene Transcription and Antibiotic Resistance Phenotypes.Journal of bacteriology · 2021Article
- Sotolon is a natural virulence mitigating agent in Serratia marcescens.Archives of microbiology · 2021Article
- Differential susceptibility of airway and ocular surface cell lines to FlhDC-mediated virulence factors PhlA and ShlA fromJournal of medical microbiology · 2021Article
- Regulator RcsB Controls Prodigiosin Synthesis and Various Cellular Processes in Serratia marcescens JNB5-1.Applied and environmental microbiology · 2021Article
- Urethral Catheter Biofilms Reveal Plasticity in Bacterial Composition and Metabolism and Withstand Host Immune Defenses in Hypoxic Environment.Frontiers in medicine · 2021Article
- The Rcs System inFrontiers in microbiology · 2021Review
- Biologically active pigment and ShlA cytolysin of Serratia marcescens induce autophagy in a human ocular surface cell line.BMC ophthalmology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serratia marcescens is a Gram-negative bacterium that thrives in a wide variety of ambient niches and interacts with an ample range of hosts. As an opportunistic human pathogen, it has increased its clinical incidence in recent years, being responsible for life-threatening nosocomial infections. S. marcescens produces numerous exoproteins with toxic effects, including the ShlA pore-forming toxin, which has been catalogued as its most potent cytotoxin. However, the regulatory mechanisms that govern ShlA expression, as well as its action toward the host, have remained unclear. We have shown that S. marcescens elicits an autophagic response in host nonphagocytic cells. In this work, we determine that the expression of ShlA is responsible for the autophagic response that is promoted prior to bacterial internalization in epithelial cells. We show that a strain unable to express ShlA is no longer able to induce this autophagic mechanism, while heterologous expression of ShlA/ShlB suffices to confer on noninvasive Escherichia coli the capacity to trigger autophagy. We also demonstrate that shlBA harbors a binding motif for the RcsB regulator in its promoter region. RcsB-dependent control of shlBA constitutes a feed-forward regulatory mechanism that allows interplay with flagellar-biogenesis regulation. At the top of the circuit, activated RcsB downregulates expression of flagella by binding to the flhDC promoter region, preventing FliA-activated transcription of shlBA. Simultaneously, RcsB interaction within the shlBA promoter represses ShlA expression. This circuit offers multiple access points to fine-tune ShlA production. These findings also strengthen the case for an RcsB role in orchestrating the expression of Serratia virulence factors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.