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Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis

(2023) PLOS ONE. 18(7).
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Abstract
This study is the first to investigate the transcriptomic changes occurring in severe udder cleft dermatitis lesions (UCD) in Holstein-Friesian cows. An examination of the gene expression levels in natural UCD lesions and healthy udder skin through RNA Seq-Technology provided a deeper insight into the inflammatory pathways associated with this disease. A clear distinction between the gene expression patterns of UCD lesions and healthy skin was shown in the principal component analysis. Genes coding for inflammatory molecules were upregulated such as the chemokines C-X-C motif ligand 2 (CXCL2), 5 (CXCL5) and 8 (CXCL8), and C-C motif ligand 11 (CCL11). Moreover, the genes coding for the multifunctional molecules ADAM12 and SLPI were amongst the highest upregulated ones, whereas the most downregulated genes included the ones coding for keratins and keratin-associated molecules. Predominantly inflammatory pathways such as the chemokine signaling, cytokine receptor interaction and IL-17 signaling pathway were significantly upregulated in the pathway analysis. These results point towards a fulminant, dysregulated inflammatory response concomitant with a disruption of the skin barrier integrity and a hampered wound repair mechanism in severe UCD lesions.
Keywords
Multidisciplinary, SERUM-AMYLOID-A, DIGITAL DERMATITIS, RISK-FACTORS, DAIRY, EXPRESSION, PREVALENCE, INDUCTION, MIGRATION, DISCOVERY, CYTOKINES

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Citation

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MLA
Vermeersch, Anne-Sofie, et al. “Severe Udder Cleft Dermatitis Lesion Transcriptomics Points to an Impaired Skin Barrier, Defective Wound Repair and a Dysregulated Inflammatory Response as Key Elements in the Pathogenesis.” PLOS ONE, edited by Christophe Egles, vol. 18, no. 7, Public Library of Science (PLoS), 2023, p. e0288347, doi:10.1371/journal.pone.0288347.
APA
Vermeersch, A.-S., Ali, M., Gansemans, Y., Van Nieuwerburgh, F., Geldhof, P., Ducatelle, R., … Opsomer, G. (2023). Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis. PLOS ONE, 18(7), e0288347. https://doi.org/10.1371/journal.pone.0288347
Chicago author-date
Vermeersch, Anne-Sofie, Mohsin Ali, Yannick Gansemans, Filip Van Nieuwerburgh, Peter Geldhof, Richard Ducatelle, Dieter Deforce, Jozefien Callens, and Geert Opsomer. 2023. “Severe Udder Cleft Dermatitis Lesion Transcriptomics Points to an Impaired Skin Barrier, Defective Wound Repair and a Dysregulated Inflammatory Response as Key Elements in the Pathogenesis.” Edited by Christophe Egles. PLOS ONE 18 (7): e0288347. https://doi.org/10.1371/journal.pone.0288347.
Chicago author-date (all authors)
Vermeersch, Anne-Sofie, Mohsin Ali, Yannick Gansemans, Filip Van Nieuwerburgh, Peter Geldhof, Richard Ducatelle, Dieter Deforce, Jozefien Callens, and Geert Opsomer. 2023. “Severe Udder Cleft Dermatitis Lesion Transcriptomics Points to an Impaired Skin Barrier, Defective Wound Repair and a Dysregulated Inflammatory Response as Key Elements in the Pathogenesis.” Ed by. Christophe Egles. PLOS ONE 18 (7): e0288347. doi:10.1371/journal.pone.0288347.
Vancouver
1.
Vermeersch A-S, Ali M, Gansemans Y, Van Nieuwerburgh F, Geldhof P, Ducatelle R, et al. Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis. Egles C, editor. PLOS ONE. 2023;18(7):e0288347.
IEEE
[1]
A.-S. Vermeersch et al., “Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis,” PLOS ONE, vol. 18, no. 7, p. e0288347, 2023.
@article{01H7ZEHSAHSJJT9Z6T2GMR1MDJ,
  abstract     = {{This study is the first to investigate the transcriptomic changes occurring in severe udder cleft dermatitis lesions (UCD) in Holstein-Friesian cows. An examination of the gene expression levels in natural UCD lesions and healthy udder skin through RNA Seq-Technology provided a deeper insight into the inflammatory pathways associated with this disease. A clear distinction between the gene expression patterns of UCD lesions and healthy skin was shown in the principal component analysis. Genes coding for inflammatory molecules were upregulated such as the chemokines C-X-C motif ligand 2 (CXCL2), 5 (CXCL5) and 8 (CXCL8), and C-C motif ligand 11 (CCL11). Moreover, the genes coding for the multifunctional molecules ADAM12 and SLPI were amongst the highest upregulated ones, whereas the most downregulated genes included the ones coding for keratins and keratin-associated molecules. Predominantly inflammatory pathways such as the chemokine signaling, cytokine receptor interaction and IL-17 signaling pathway were significantly upregulated in the pathway analysis. These results point towards a fulminant, dysregulated inflammatory response concomitant with a disruption of the skin barrier integrity and a hampered wound repair mechanism in severe UCD lesions.}},
  author       = {{Vermeersch, Anne-Sofie and Ali, Mohsin and Gansemans, Yannick and Van Nieuwerburgh, Filip and Geldhof, Peter and Ducatelle, Richard and Deforce, Dieter and Callens, Jozefien and Opsomer, Geert}},
  editor       = {{Egles, Christophe}},
  issn         = {{1932-6203}},
  journal      = {{PLOS ONE}},
  keywords     = {{Multidisciplinary,SERUM-AMYLOID-A,DIGITAL DERMATITIS,RISK-FACTORS,DAIRY,EXPRESSION,PREVALENCE,INDUCTION,MIGRATION,DISCOVERY,CYTOKINES}},
  language     = {{eng}},
  number       = {{7}},
  pages        = {{14}},
  publisher    = {{Public Library of Science (PLoS)}},
  title        = {{Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis}},
  url          = {{http://doi.org/10.1371/journal.pone.0288347}},
  volume       = {{18}},
  year         = {{2023}},
}

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