A1 Refereed original research article in a scientific journal
Leptin and fractalkine: novel subcutaneous cytokines in burn injury
Authors: Friston D, Junttila S, Lemes JBP, Laycock H, Torres-Perez JV, Want E, Gyenesei A, Nagy I
Publisher: Company of Biologists
Publication year: 2020
Journal: Disease Models and Mechanisms
Journal name in source: DISEASE MODELS & MECHANISMS
Journal acronym: DIS MODEL MECH
Article number: ARTN dmm042713
Volume: 13
Issue: 4
Number of pages: 10
ISSN: 1754-8403
DOI: https://doi.org/10.1242/dmm.042713
Abstract
Burn injury is a pathology underpinned by progressive and aberrant inflammation. It is a major clinical challenge to survival and quality of life. Although the complex local and disseminating pathological processes of a burn injury ultimately stem from local tissue damage, to date relatively few studies have attempted to characterise the local inflammatory mediator profile. Here, cytokine content and associated transcriptional changes were measured in rat skin for three hours immediately following induction of a scald-type (60 degrees C, 2 min) bum injury model. Leptin (P=0.0002) and fractalkine (P=0.0478) concentrations were significantly elevated post-bum above pre-bum and control site values, coinciding with the development of bum site oedema and differential expression of leptin mRNA (P=0.0004). Further, gene sequencing enrichment analysis indicated cytokine-cytokine receptor interaction (P=1.45 x 10(-6)). Subsequent behavioural studies demonstrated that, following subcutaneous injection into the dorsum of the paw, both leptin and fractalkine induced mechanical allodynia, heat hyperalgesia and the recruitment of macrophages. This is the first report of leptin elevation specifically at the bum site, and the first report of fractalkine elevation in any tissue post-bum which, together with the functional findings, calls for exploration of the influence of these cytokines on pain, inflammation and burn wound progression. In addition, targeting these signalling molecules represents a therapeutic potential as early formative mediators of these pathological processes.
Burn injury is a pathology underpinned by progressive and aberrant inflammation. It is a major clinical challenge to survival and quality of life. Although the complex local and disseminating pathological processes of a burn injury ultimately stem from local tissue damage, to date relatively few studies have attempted to characterise the local inflammatory mediator profile. Here, cytokine content and associated transcriptional changes were measured in rat skin for three hours immediately following induction of a scald-type (60 degrees C, 2 min) bum injury model. Leptin (P=0.0002) and fractalkine (P=0.0478) concentrations were significantly elevated post-bum above pre-bum and control site values, coinciding with the development of bum site oedema and differential expression of leptin mRNA (P=0.0004). Further, gene sequencing enrichment analysis indicated cytokine-cytokine receptor interaction (P=1.45 x 10(-6)). Subsequent behavioural studies demonstrated that, following subcutaneous injection into the dorsum of the paw, both leptin and fractalkine induced mechanical allodynia, heat hyperalgesia and the recruitment of macrophages. This is the first report of leptin elevation specifically at the bum site, and the first report of fractalkine elevation in any tissue post-bum which, together with the functional findings, calls for exploration of the influence of these cytokines on pain, inflammation and burn wound progression. In addition, targeting these signalling molecules represents a therapeutic potential as early formative mediators of these pathological processes.
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