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Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds
In burn patients Pseudomonas aeruginosa infection is a major cause of morbidity. Analysis of the pathogen’s gene expression as it transitions from colonization to acute and then biofilm wound infection may provide strategies for infection control. Toward this goal, we seeded log-phase P. aeruginosa...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8526614/ https://www.ncbi.nlm.nih.gov/pubmed/34667187 http://dx.doi.org/10.1038/s41598-021-00073-4 |
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author | D’Arpa, Peter Karna, S. L. Rajasekhar Chen, Tsute Leung, Kai P. |
author_facet | D’Arpa, Peter Karna, S. L. Rajasekhar Chen, Tsute Leung, Kai P. |
author_sort | D’Arpa, Peter |
collection | PubMed |
description | In burn patients Pseudomonas aeruginosa infection is a major cause of morbidity. Analysis of the pathogen’s gene expression as it transitions from colonization to acute and then biofilm wound infection may provide strategies for infection control. Toward this goal, we seeded log-phase P. aeruginosa (PAO1) into 3-day-old, full-thickness excision wounds (rabbit ear) and harvested the bacteria during colonization (Hrs 2 and 6), acute infection (Hr 24), and biofilm infection (Days 5 and 9) for transcriptome analysis (RNA-Seq). After 2–6 h in the wound, genes for metabolism and cell replication were down-regulated while wound-adaptation genes were up-regulated (vs. expression in log-phase culture). As the infection progressed from acute to biofilm infection, more genes became up-regulated than down-regulated, but the down-regulated genes enriched in more pathways, likely because the genes and pathways that bacteria already colonizing wounds up-regulate to establish biofilm infection are less known. Across the stages of infection, carbon-utilization pathways shifted. During acute infection, itaconate produced by myeloid cells appears to have been a carbon source because myeloid cell infiltration and the expression of the host gene, ACOD1, for itaconate production peaked coincidently with the expression of the PAO1 genes for itaconate transport and catabolism. Additionally, branched-chain amino acids are suggested to be a carbon source in acute infection and in biofilm infection. In biofilm infection, fatty acid degradation was also up-regulated. These carbon sources feed into the glyoxylate cycle that was coincidently up-regulated, suggesting it provided the precursors for P. aeruginosa to synthesize macromolecules in establishing wound infection. |
format | Online Article Text |
id | pubmed-8526614 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-85266142021-10-20 Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds D’Arpa, Peter Karna, S. L. Rajasekhar Chen, Tsute Leung, Kai P. Sci Rep Article In burn patients Pseudomonas aeruginosa infection is a major cause of morbidity. Analysis of the pathogen’s gene expression as it transitions from colonization to acute and then biofilm wound infection may provide strategies for infection control. Toward this goal, we seeded log-phase P. aeruginosa (PAO1) into 3-day-old, full-thickness excision wounds (rabbit ear) and harvested the bacteria during colonization (Hrs 2 and 6), acute infection (Hr 24), and biofilm infection (Days 5 and 9) for transcriptome analysis (RNA-Seq). After 2–6 h in the wound, genes for metabolism and cell replication were down-regulated while wound-adaptation genes were up-regulated (vs. expression in log-phase culture). As the infection progressed from acute to biofilm infection, more genes became up-regulated than down-regulated, but the down-regulated genes enriched in more pathways, likely because the genes and pathways that bacteria already colonizing wounds up-regulate to establish biofilm infection are less known. Across the stages of infection, carbon-utilization pathways shifted. During acute infection, itaconate produced by myeloid cells appears to have been a carbon source because myeloid cell infiltration and the expression of the host gene, ACOD1, for itaconate production peaked coincidently with the expression of the PAO1 genes for itaconate transport and catabolism. Additionally, branched-chain amino acids are suggested to be a carbon source in acute infection and in biofilm infection. In biofilm infection, fatty acid degradation was also up-regulated. These carbon sources feed into the glyoxylate cycle that was coincidently up-regulated, suggesting it provided the precursors for P. aeruginosa to synthesize macromolecules in establishing wound infection. Nature Publishing Group UK 2021-10-19 /pmc/articles/PMC8526614/ /pubmed/34667187 http://dx.doi.org/10.1038/s41598-021-00073-4 Text en © This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article D’Arpa, Peter Karna, S. L. Rajasekhar Chen, Tsute Leung, Kai P. Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title | Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title_full | Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title_fullStr | Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title_full_unstemmed | Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title_short | Pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
title_sort | pseudomonas aeruginosa transcriptome adaptations from colonization to biofilm infection of skin wounds |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8526614/ https://www.ncbi.nlm.nih.gov/pubmed/34667187 http://dx.doi.org/10.1038/s41598-021-00073-4 |
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