A metatranscriptomic approach to explore longitudinal tissue specimens from non-healing diabetes related foot ulcers

Michael Radzieta; Timothy J. Peters; Hugh G. Dickson; Allison J. Cowin; Lawrence A. Lavery; Saskia Schwarzer; Tara Roberts; Slade O. Jensen; Matthew Malone

doi:10.1111/apm.13226

A metatranscriptomic approach to explore longitudinal tissue specimens from non-healing diabetes related foot ulcers

Michael Radzieta, Timothy J. Peters, Hugh G. Dickson, Allison J. Cowin, Lawrence A. Lavery, Saskia Schwarzer, Tara Roberts, Slade O. Jensen, Matthew Malone

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

Cellular mechanisms and/or microbiological interactions which contribute to chronic diabetes related foot ulcers (DRFUs) were explored using serially collected tissue specimens from chronic DRFUs and control healthy foot skin. Total RNA was isolated for next-generation sequencing. We found differentially expressed genes (DEGs) and enriched hallmark gene ontology biological processes upregulated in chronic DRFUs which primarily functioned in the host immune response including: (i) Inflammatory response; (ii) TNF signalling via NFKB; (iii) IL6 JAK-STAT3 signalling; (iv) IL2 STAT5 signalling and (v) Reactive oxygen species. A temporal analysis identified RN7SL1 signal recognition protein and IGHG4 immunoglobulin protein coding genes as being the most upregulated genes after the onset of treatment. Testing relative temporal changes between healing and non-healing DRFUs identified progressive upregulation in healed wounds of CXCR5 and MS4A1 (CD20), both canonical markers of lymphocytes (follicular B cells/follicular T helper cells and B cells, respectively). Collectively, our RNA-seq data provides insights into chronic DRFU pathogenesis.

Original language	English
Pages (from-to)	383-396
Number of pages	14
Journal	APMIS: Journal of Pathology, Microbiology and Immunology
Volume	130
Issue number	7
DOIs	https://doi.org/10.1111/apm.13226
Publication status	Published - Jul 2022

Bibliographical note

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© 2022 The Authors. APMIS published by John Wiley & Sons Ltd on behalf of Scandinavian Societies for Medical Microbiology and Pathology.

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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10.1111/apm.13226

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@article{1788857a25af4fea9a1c53727341427d,

title = "A metatranscriptomic approach to explore longitudinal tissue specimens from non-healing diabetes related foot ulcers",

abstract = "Cellular mechanisms and/or microbiological interactions which contribute to chronic diabetes related foot ulcers (DRFUs) were explored using serially collected tissue specimens from chronic DRFUs and control healthy foot skin. Total RNA was isolated for next-generation sequencing. We found differentially expressed genes (DEGs) and enriched hallmark gene ontology biological processes upregulated in chronic DRFUs which primarily functioned in the host immune response including: (i) Inflammatory response; (ii) TNF signalling via NFKB; (iii) IL6 JAK-STAT3 signalling; (iv) IL2 STAT5 signalling and (v) Reactive oxygen species. A temporal analysis identified RN7SL1 signal recognition protein and IGHG4 immunoglobulin protein coding genes as being the most upregulated genes after the onset of treatment. Testing relative temporal changes between healing and non-healing DRFUs identified progressive upregulation in healed wounds of CXCR5 and MS4A1 (CD20), both canonical markers of lymphocytes (follicular B cells/follicular T helper cells and B cells, respectively). Collectively, our RNA-seq data provides insights into chronic DRFU pathogenesis.",

author = "Michael Radzieta and Peters, {Timothy J.} and Dickson, {Hugh G.} and Cowin, {Allison J.} and Lavery, {Lawrence A.} and Saskia Schwarzer and Tara Roberts and Jensen, {Slade O.} and Matthew Malone",

note = "Publisher Copyright: {\textcopyright} 2022 The Authors. APMIS published by John Wiley & Sons Ltd on behalf of Scandinavian Societies for Medical Microbiology and Pathology.",

year = "2022",

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doi = "10.1111/apm.13226",

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AU - Radzieta, Michael

AU - Peters, Timothy J.

AU - Dickson, Hugh G.

AU - Cowin, Allison J.

AU - Lavery, Lawrence A.

AU - Schwarzer, Saskia

AU - Roberts, Tara

AU - Jensen, Slade O.

AU - Malone, Matthew

PY - 2022/7

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N2 - Cellular mechanisms and/or microbiological interactions which contribute to chronic diabetes related foot ulcers (DRFUs) were explored using serially collected tissue specimens from chronic DRFUs and control healthy foot skin. Total RNA was isolated for next-generation sequencing. We found differentially expressed genes (DEGs) and enriched hallmark gene ontology biological processes upregulated in chronic DRFUs which primarily functioned in the host immune response including: (i) Inflammatory response; (ii) TNF signalling via NFKB; (iii) IL6 JAK-STAT3 signalling; (iv) IL2 STAT5 signalling and (v) Reactive oxygen species. A temporal analysis identified RN7SL1 signal recognition protein and IGHG4 immunoglobulin protein coding genes as being the most upregulated genes after the onset of treatment. Testing relative temporal changes between healing and non-healing DRFUs identified progressive upregulation in healed wounds of CXCR5 and MS4A1 (CD20), both canonical markers of lymphocytes (follicular B cells/follicular T helper cells and B cells, respectively). Collectively, our RNA-seq data provides insights into chronic DRFU pathogenesis.

AB - Cellular mechanisms and/or microbiological interactions which contribute to chronic diabetes related foot ulcers (DRFUs) were explored using serially collected tissue specimens from chronic DRFUs and control healthy foot skin. Total RNA was isolated for next-generation sequencing. We found differentially expressed genes (DEGs) and enriched hallmark gene ontology biological processes upregulated in chronic DRFUs which primarily functioned in the host immune response including: (i) Inflammatory response; (ii) TNF signalling via NFKB; (iii) IL6 JAK-STAT3 signalling; (iv) IL2 STAT5 signalling and (v) Reactive oxygen species. A temporal analysis identified RN7SL1 signal recognition protein and IGHG4 immunoglobulin protein coding genes as being the most upregulated genes after the onset of treatment. Testing relative temporal changes between healing and non-healing DRFUs identified progressive upregulation in healed wounds of CXCR5 and MS4A1 (CD20), both canonical markers of lymphocytes (follicular B cells/follicular T helper cells and B cells, respectively). Collectively, our RNA-seq data provides insights into chronic DRFU pathogenesis.

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JO - APMIS: Journal of Pathology, Microbiology and Immunology

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A metatranscriptomic approach to explore longitudinal tissue specimens from non-healing diabetes related foot ulcers

Abstract

Bibliographical note

Open Access - Access Right Statement

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