Laminar inflammatory gene expression in the carbohydrate overload model of equine laminitis

Leise, Britta S.; Faleiros, Rafael Resende; Watts, M.; Johnson, Philip J.; Black, Samuel J.; Belknap, James K.

doi:10.1111/j.2042-3306.2010.00122.x

Cited by 87 publications

(143 citation statements)

References 49 publications

(159 reference statements)

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“…Additionally, evidence of marked inflammation in NON‐CRYO limbs in the current study is provided by comparison of lamellar mRNA concentrations of inflammatory mediators in NON‐CRYO limbs from the current study with mRNA concentrations of inflammatory mediators in archived lamellar tissue from nonseptic control animals 4, 7. These data indicate that NON‐CRYO limbs in the current study exhibited up to 90‐fold increases ( P < .05) in lamellar mRNA concentrations of several classes of inflammatory molecules (E‐selectin, CXCL‐1, IL‐8, IL‐6, and Cox‐2) when compared to the low mRNA concentrations of these same molecules in nonseptic control samples (Table S1).…”

Section: Discussionmentioning

confidence: 86%

“…Each sample was run in duplicate. To determine whether the time of lamellar tissue harvest affected the inflammatory profile in limbs maintained at ambient temperature, RT‐qPCR was conducted (as described above) on cDNA obtained from lamellar tissue samples from this study (OG3), from nonseptic archived control lamellar tissue,4 and from lamellar tissue harvested at OG17 (both from previous studies). These RT‐qPCRs were run in identical fashion to those described above, with the exception that, because of limited quantity of cDNA from previous studies, these samples were not analyzed for mRNA concentrations of CXCL‐6, IL‐10, MCP‐1, or MCP‐2.…”

Section: Methodsmentioning

confidence: 99%

“…The fold changes for each inflammatory mediator of interest were determined by comparing the copy numbers of the hypothermic (CRYO) limb with the ambient control (NON‐CRYO) limb from the same horse. For the analysis of the inflammatory profile of the ambient limbs, fold changes were determined by comparing the copy number from the OG17 and OG3 limbs (respectively) to the nonseptic archived control (CON) 4…”

Section: Methodsmentioning

confidence: 99%

“…In study subjects in which laminitis was induced using various models of SRL, marked increases in a wide range of proinflammatory mediators were detected when compared to nonseptic control horses 4, 5, 6, 7, 8. Similar to the reports from the use of moderate regional hypothermia (approximately 30°C) in human patients to limit damage to vital organs in cases of inflammatory injury, continuous marked digital hypothermia (5–10°C) limited the structural failure of the lamellae both in horses with clinical sepsis and in experimentally induced laminitis 7, 9, 10, 11, 12.…”

mentioning

confidence: 99%

“…Lamellar samples from the same study demonstrating the protective effect of hypothermia initiated at the onset of lameness were used to determine the gene expression of proinflammatory cytokines, chemokines, endothelial cell adhesion molecules, and COX‐2 13. As a result of finding a minimal effect of hypothermia on inflammatory signaling in this study, lamellar mRNA concentrations from the current study were compared to those of previous SRL studies in which lamellae were harvested at earlier time points to determine whether the lack of an anti‐inflammatory effect of hypothermia in this study was due to a lack of hypothermia‐induced inhibition of inflammatory mediators or simply the result of a generalized decrease in gene expression of inflammatory mediators in late‐stage laminitis 2, 4, 7…”

mentioning

confidence: 99%

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Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model

Dern

Watts

Werle

et al. 2017

Veterinary Internal Medicne

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BackgroundIn the oligofructose (OF) model of sepsis‐related laminitis (SRL), digital hypothermia (“cryotherapy”) initiated before the onset of clinical signs is reported not only to limit lamellar injury, but also to cause marked inhibition of lamellar inflammatory signaling.Hypothesis/ObjectivesBecause hypothermia also has been reported to be protective when not initiated until the onset of lameness in the OF model of SRL, we hypothesized that the lamellar protection conferred by hypothermia is caused by local lamellar inhibition of inflammatory signaling as described when hypothermia was initiated earlier in the disease process.AnimalsEight Standardbred geldings aged 3–11 years with no lameness and no abnormalities of the feet detectable by gross or radiographic examination.MethodsUsing the OF model of SRL, lamellar mRNA concentrations of proinflammatory cytokines, chemokines, and endothelial adhesion proteins were compared between samples from treated limbs (CRYO, submerged in ice water for 36 hour starting at the onset of lameness), untreated limbs (NON‐CRYO, opposite limb from CRYO limbs maintained at ambient temperature), and untreated limbs from normal horses in which laminitis was not induced (CON).ResultsAlthough OF administration resulted in increases in lamellar mRNA concentrations of several inflammatory mediators in NON‐CRYO limbs (vs CON), digital hypothermia had no significant effect on these increases.Conclusions and Clinical ImportanceThe lack of inflammatory inhibition in lamellar tissue samples in our study indicates that the protective effects of digital hypothermia instituted at the onset of clinical signs of laminitis do not arise from inhibition of inflammatory pathways.

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Section: Discussionmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%