Cited by 284Redox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative MechanismsBacterial Genetics and Biotechnology

The DOI matches its Crossref record; 92 of the 92 references it cites were found in a registry or an index.

Reactive Oxygen Species in Pathogen Clearance: The Killing Mechanisms, the Adaption Response, and the Side Effects

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Li, Hao, Zhou, Xuedong, Huang, Yuyao, Liao, Binyou, Cheng, Lei, Ren, Biao·2021·Frontiers in Microbiology

Abstract

Reactive oxygen species (ROS) are attractive weapons in both antibiotic-mediated killing and host-mediated killing. However, the involvement of ROS in antibiotic-mediated killing and complexities in host environments challenge the paradigm. In the case of bacterial pathogens, the examples of some certain pathogens thriving under ROS conditions prompt us to focus on the adaption mechanism that pathogens evolve to cope with ROS. Based on these, we here summarized the mechanisms of ROS-mediated killing of either antibiotics or the host, the examples of bacterial adaption that successful pathogens evolved to defend or thrive under ROS conditions, and the potential side effects of ROS in pathogen clearance. A brief section for new antibacterial strategies centered around ROS was also addressed.

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Crossref · 10.3389/fmicb.2020.622534

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FIGURE 1 Metabolic remodeling designed to reduce oxidative damage. In antibiotic treatments, dysfunction of TCA cycle and hyperactivation of cell respiration lead to ROS accumulation in bacteria. Defense against ROS can be achieved by metabolic remodeling. Reduced endogenous ROS formation can be achieved by upregulation of the glyoxylate shunt, which bypasses two NADH-generating steps. Replenishment of antioxidants can be achieved by rerouting metabolism toward the pentose phosphate pathway and enhancing production of cofactor NADPH. Also, ketoacids, including pyruvate and α-ketoglutarate, can mitigate oxidative damage via non-enzymatic decarboxylation in the presence of numerous carbon sources. G6P, glucose 6-phosphate; G6DPH, glucose-6-phosphate dehydrogenase.
FIGURE 1 Metabolic remodeling designed to reduce oxidative damage. In antibiotic treatments, dysfunction of TCA cycle and hyperactivation of cell respiration lead to ROS accumulation in bacteria. Defense against ROS can be achieved by metabolic remodeling. Reduced endogenous ROS formation can be achieved by upregulation of the glyoxylate shunt, which bypasses two NADH-generating steps. Replenishment of antioxidants can be achieved by rerouting metabolism toward the pentose phosphate pathway and enhancing production of cofactor NADPH. Also, ketoacids, including pyruvate and α-ketoglutarate, can mitigate oxidative damage via non-enzymatic decarboxylation in the presence of numerous carbon sources. G6P, glucose 6-phosphate; G6DPH, glucose-6-phosphate dehydrogenase.CC BY · PubMed Central
FIGURE 2 Promoting antibiotic resistance and tolerance as potential side effects of ROS. (A) ROS promote resistance by directly damaging DNA and leading to mutagenesis. (B) ROS act as a signal for gene transformation, by promoting the transformation of antibiotic resistance genes (ARGs) and eDNA in certain species. (C) Host-derived ROS promote antibiotic tolerance by targeting TCA cycle and retarding cellular respiration in S. aureus. (D) Host-derived ROS promote antibiotic tolerance by increased production of MDR efflux pump via activation of redox regulon SoxRS.
FIGURE 2 Promoting antibiotic resistance and tolerance as potential side effects of ROS. (A) ROS promote resistance by directly damaging DNA and leading to mutagenesis. (B) ROS act as a signal for gene transformation, by promoting the transformation of antibiotic resistance genes (ARGs) and eDNA in certain species. (C) Host-derived ROS promote antibiotic tolerance by targeting TCA cycle and retarding cellular respiration in S. aureus. (D) Host-derived ROS promote antibiotic tolerance by increased production of MDR efflux pump via activation of redox regulon SoxRS.CC BY · PubMed Central

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Metadata

Authors
Li, H., Zhou, X., Huang, Y., Liao, B., Cheng, L., & Ren, B.
Affiliations
Sichuan University (CN)
Corresponding author
  • Cheng, Lei
  • Ren, Biao
Venue
Frontiers in Microbiology
Published
2021-02-04
Volume
11
Pages
622534-622534
ISSN
1664-302X (ISSN-L)
OpenAlex
W4206764679
Cited by
284
References
92
Citations by year
2026: 39 · 2025: 79 · 2024: 65 · 2023: 52 · 2022: 41 · 2021: 8
FWCI
4.35
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Microbiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China
  • Applied Basic Research Program of Sichuan Province
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords
reactive oxygen species, pathogen clearance, antibacterial strategies, pathogenic bacteria

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