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Cells
Special Issues
Microbe–Heavy Metal Interactions
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Microbe–Heavy Metal Interactions

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 March 2025 | Viewed by 2490

Special Issue Editor

Prof. Dr. Timothy E. Ford

E-Mail Website
Guest Editor
Biomedical and Nutritional Sciences, Center for Pathogen Research & Training (CPRT), University of Massachusetts Lowell, Lowell, MA, USA
Interests: environmental microbiology; community-based participatory research; water and health; waterborne disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The multitude of ways in which microbes adapt to the presence of heavy metals have been extensively described in the literature. Today’s current focus on “omics” approaches to understand how microbes adapt to harsh environments, such as the presence of heavy metals, is yielding vast amounts of data. However, there are still many unanswered questions, such as what the main adaptive mechanism itself is. The three likely drivers—natural selection, horizontal gene transfer and gene duplication—still need to be defined for specific systems and stressors. There is no doubt that metal resistance in bacteria has significant implications for the fate and transport of heavy metals in the environment, for bioextraction, for bioremediation and for detoxification. In addition to this list, we now add the link between metal resistance and antibiotic resistance that remains to be clearly explained. 

This Special Issue will examine the current and anticipated advances in the field, as well as encourage contributions from the cutting-edge omics research that is emerging from many laboratories around the world and advancing, for example, our understanding of the co-selection for antibiotic resistance. We also encourage submissions from the translational research that is driving the fields of bioextraction and bioremediation, in addition to advancing our understanding of the fate of heavy metals in the environment.

Prof. Dr. Timothy E. Ford
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • horizontal gene transfer (HGT)
  • gene duplication
  • natural selection
  • mutation
  • heavy metal resistance genes (MRGs)
  • antibiotic resistance genes (ARGs)
  • acid mine drainage (AMD)
  • heavy metals
  • plasmids
  • mobile genetic elements (MGEs)
  • transposons
  • extreme environments
  • bioremediation

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Published Papers (1 paper)

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Research

19 pages, 2948 KiB  
Article
Heat-Stable Enterotoxin Secretions Assessed via ICP-MS Reveal Iron-Mediated Regulation of Virulence in CFA/I- and CS6-Expressing ETEC Isolates
by Ian E. Hollifield, Natalya I. Motyka, Sydney R. Stewart, Michelle D. Blyth, Kaylynn A. Fernando, Kristen L. Clement and Jacob P. Bitoun
Cells 2023, 12(4), 567; https://doi.org/10.3390/cells12040567 - 10 Feb 2023
Cited by 2 | Viewed by 1861
Abstract
Enterotoxigenic Escherichia coli (ETEC) are a significant cause of childhood diarrhea in low-resource settings. ETEC are defined by the production of heat-stable enterotoxin (ST) and/or heat-labile enterotoxin (LT), which alter intracellular cyclic nucleotide signaling and cause the secretion of water and electrolytes into [...] Read more.
Enterotoxigenic Escherichia coli (ETEC) are a significant cause of childhood diarrhea in low-resource settings. ETEC are defined by the production of heat-stable enterotoxin (ST) and/or heat-labile enterotoxin (LT), which alter intracellular cyclic nucleotide signaling and cause the secretion of water and electrolytes into the intestinal lumen. ETEC take cues from chemicals (e.g., glycans, bile salts, and solutes) that may be liberated following enterotoxin activity to recognize entrance into the host. ETEC then alter the expression of surface adhesins called colonization factors (CFs) to attach to the intestinal epithelium, proliferate, and cause disease. Here, we used an in vivo model of oral ST intoxication to determine its impact on luminal ion concentrations via ICP-MS. We also used functional assays, including Western blots, qPCR, and toxin activity assays, to assess the impact of luminal ion flux on CF and toxin expression. Finally, we assessed ETEC strains with CFs CFA/I or CS6 in a streptomycin mouse model of ETEC colonization. ST causes rapid and significant increases in luminal chloride but significant decreases in luminal magnesium and iron. We confirmed that increased sodium chloride suppresses CFA/I production in ETEC H10407 but does not affect CS6 production in ETEC 214-4. CFA/I production in ETEC H10407 is increased when magnesium becomes limiting, although it does not affect CS6 production in ETEC 214-4. Iron restriction via deferoxamine induces CFA/I expression in ETEC H10407 but not CS6 expression in ETEC 214-4. We demonstrate that ST production is suppressed via iron restriction in H10407, 214-4, and over 50 other ETEC clinical isolates. Lastly, we demonstrate that the iron restriction of mice using oral deferoxamine pre-treatment extends the duration of ETEC H10407 (CFA/I+) fecal shedding while accelerating ETEC 214-4 (CS6+) fecal shedding. Combined, these data suggest that enterotoxins modulate luminal ion flux to influence ETEC virulence including toxin and CF production. Full article
(This article belongs to the Special Issue Microbe–Heavy Metal Interactions)
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