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- Bacterial Crosstalk via Antimicrobial Peptides on the Human Skin: Therapeutics from a Sustainable Perspective
- Seon Mi Lee , Hye Lim Keum , Woo Jun Sul
- J. Microbiol. 2023;61(1):1-11. Published online January 31, 2023
- DOI: https://doi.org/10.1007/s12275-022-00002-8
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- 0 Download
- 3 Web of Science
- 5 Crossref
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Abstract
- The skin’s epidermis is an essential barrier as the first guard against invading pathogens, and physical protector from external injury. The skin microbiome, which consists of numerous bacteria, fungi, viruses, and archaea on the epidermis, play a key role in skin homeostasis. Antibiotics are a fast-acting and effective treatment method, however, antibiotic use is a nuisance that can disrupt skin homeostasis by eradicating beneficial bacteria along with the intended pathogens and cause antibioticresistant bacteria spread. Increased numbers of antimicrobial peptides (AMPs) derived from humans and bacteria have been reported, and their roles have been well defined. Recently, modulation of the skin microbiome with AMPs rather than artificially synthesized antibiotics has attracted the attention of researchers as many antibiotic-resistant strains make treatment mediation difficult in the context of ecological problems. Herein, we discuss the overall insights into the skin microbiome, including its regulation by different AMPs, as well as their composition and role in health and disease.
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Citations
Citations to this article as recorded by
- The epidermal lipid-microbiome loop and immunity: Important players in atopic dermatitis
Junchao Wu, Lisha Li, Tingrui Zhang, Jiaye Lu, Zongguang Tai, Quangang Zhu, Zhongjian Chen
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Journal Article
- Soft sweep development of resistance in Escherichia coli under fluoroquinolone stress
- Xianxing Xie , Ruichen Lv , Chao Yang , Yajun Song , Yanfeng Yan , Yujun Cui , Ruifu Yang
- J. Microbiol. 2019;57(12):1056-1064. Published online September 25, 2019
- DOI: https://doi.org/10.1007/s12275-019-9177-5
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- 1 Web of Science
- 1 Crossref
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Abstract
- We employed a stepwise selection model for investigating the dynamics of antibiotic-resistant variants in Escherichia coli K-12 treated with increasing concentrations of ciprofloxacin (CIP). Firstly, we used Sanger sequencing to screen the variations in the fluoquinolone target genes, then, employed Illumina NGS sequencing for amplicons targeted regions with variations. The results demonstrated that variations G81C in gyrA and K276N and K277L in parC are standing resistance variations (SRVs), while S83A and S83L in gyrA and G78C in parC were emerging resistance variations (ERVs). The variants containing SRVs and/or ERVs were selected successively based on their sensitivities to CIP. Variant strain 1, containing substitution G81C in gyrA, was immediately selected following ciprofloxacin exposure, with obvious increases in the parC SRV, and parC and gyrA ERV allele frequencies. Variant strain 2, containing the SRVs, then dominated the population following a 20× increase in ciprofloxacin concentration, with other associated allele frequencies also elevated. Variant strains 3 and 4, containing ERVs in gyrA and parC, respectively, were then selected at 40× and 160× antibiotic concentrations. Two variants, strains 5 and 6, generated in the selection procedure, were lost because of higher fitness costs or a lower level of resistance compared with variants 3 and 4. For the second induction, all variations/indels were already present as SRVs and selected out step by step at different passages. Whatever the first induction or second induction, our results confirmed the soft selective sweep hypothesis and provided critical information for guiding clinical treatment of pathogens containing SRVs.
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Citations
Citations to this article as recorded by-
Could traces of fluoroquinolones in food induce ciprofloxacin resistance in
Escherichia coli
and
Klebsiella pneumoniae
? An
in vivo
study in
Galleria mellonel
Zina Gestels, Yuliia Baranchyk, Dorien Van den Bossche, Jolein Laumen, Said Abdellati, Basil Britto Xavier, Sheeba Santhini Manoharan-Basil, Chris Kenyon, Sadjia Bekal, Mustafa Sadek
Microbiology Spectrum.2024;[Epub] CrossRef
-
Could traces of fluoroquinolones in food induce ciprofloxacin resistance in
Escherichia coli
and
Klebsiella pneumoniae
? An
in vivo
study in
Galleria mellonel
Review
- REVIEW] The development of fluconazole resistance in Candida albicans – an example of microevolution of a fungal pathogen
- Joachim Morschhäuser
- J. Microbiol. 2016;54(3):192-201. Published online February 27, 2016
- DOI: https://doi.org/10.1007/s12275-016-5628-4
- 58 View
- 0 Download
- 81 Crossref
-
Abstract
- The yeast Candida albicans is a member of the microbiota in the gastrointestinal and urogenital tracts of most healthy persons, but it can also cause symptomatic infections, especially in immunocompromised patients. During the life-long association with its human host, C. albicans generates genetically altered variants that are better adapted to changes in their environment. A prime example of this microevolution is the development of resistance to the commonly used drug fluconazole, which inhibits ergosterol biosynthesis, during antimycotic therapy. Fluconazole resistance can be caused by mutations in the drug target, by changes in the sterol biosynthesis pathway, and by gain-of-function mutations in transcription factors that result in the constitutive upregulation of ergosterol biosynthesis genes and multidrug efflux pumps. Fluconazole also induces genomic rearrangements that result in gene amplification and loss of heterozygosity for resistance mutations, which further increases drug resistance. These genome alterations may affect extended chromosomal regions and have additional phenotypic consequences. A striking case is the loss of heterozygosity for the mating type locus MTL in many fluconazole-resistant clinical isolates, which allows the cells to switch to the mating-competent opaque phenotype. This, in turn, raises the possibility that sexual recombination between different variants of an originally clonal, drug-susceptible population may contribute to the generation of highly fluconazole-resistant strains with multiple resistance mechanisms. The gain-of-function mutations in transcription factors, which result in deregulated gene expression, also cause reduced fitness. In spite of this, many clinical isolates that contain such mutations do not exhibit fitness defects, indicating that they have overcome the costs of drug resistance with further evolution by still unknown mechanisms.
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Histone Acetyltransferase Encoded by
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Future Microbiology.2017; 12(16): 1497. CrossRef - Human fungal pathogens: Why should we learn?
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