Equine laminitis: loss of hemidesmosomes in hoof secondary epidermal lamellae correlates to dose in an oligofructose induction model: an ultrastructural study

French, K. R.; Pollitt, C. C.

doi:10.2746/0425164044877125

Cited by 79 publications

(73 citation statements)

References 11 publications

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“…Laminitis is considered as a systemic disease with clinical signs localized in the foot. Even where mitochondrial dysfunction has not been demonstrated in the foot, energy deficiency has been suggested as an explanation for the disruption of the hemidesmosomes leading to the failure of the dermal-epidermal interface [32].…”

Section: Discussionmentioning

confidence: 99%

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

et al. 2014

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Laminitis is a common and debilitating disease affecting horses and ponies. It often leads to the demise of the animal. Energy deficiency is suspected to entrain the disruption of the hemidesmosomes leading to the failure of the dermal-epidermal interface. The aim of this study was to measure the muscle mitochondrial function by high resolution respirometry. Muscle micro-biopsies were obtained from 11 horses affected by acute metabolic laminitis, 6 horses affected by acute laminitis resulting from a systemic inflammation response syndrome and 28 healthy horses distributed in 2 control groups: 17 horses with a body condition score [BSC, ranging from 0 (emaciated) to 5 (obese)] of 2 to 3 and 11 horses with a BSC of 4 to 5. During the acute phase of laminitis, a significant reduction of the muscle mitochondrial respiration was observed. The muscle mitochondrial dysfunction occurred independently of the etiology (metabolic disorder or systemic inflammation) leading to laminitis. The reduction of the oxidative phosphorylation and of the maximal respiratory capacity (after uncoupling) may induce depletion of the cell's ATP content. If the same mitochondrial alteration occurs in the foot lamina, mitochondria targeting should be considered for the future, not only to better understand the physiopathology of the disease but also to maintain and to support the mitochondrial function before reaching the « mitochondrial dysfunction threshold » that may lead to the failure of the dermal-epidermal interface.

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Section: Discussionmentioning

confidence: 99%

Muscle Mitochondrial Dysfunction in Horses Affected by Acute Laminitis

et al. 2014

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“…Most studies using an equine laminitis model performed euthanasia to obtain the lamellar samples (French et al 2004, Hurley et al 2006). This methodology is advantageous because numerous hoof lamellae, other tissues, and organ samples are available for each horse.…”

Section: Discussionmentioning

confidence: 99%

Histologic and inflammatory lamellar changes in horses with oligofructose-induced laminitis treated with a CXCR1/2 antagonist

et al. 2016

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RESUMO.-[Alterações histológicas e inflamatórias no tecido laminar de equinos submetidos ao modelo de laminite por oligofrutose e tratados com um antagonista para CXCR1/2.] A expressão de quimiocinas e a infiltração de leucócitos no tecido laminar são característicos de laminite aguda de equinos. O presente estudo avaliou o efeito terapêutico da administração intravenosa de DF1681B , um antagonista seletivo para CXCR1 e CXCR2 (receptores de quimiocinas), em um modelo de laminite equina por oligofrutose. Utilizaram-se doze cavalos sem raça definida, compreendendo quatro machos e oito fêmeas não gestantes, com idade (média ±SD) 7±3,5 anos, pesando 305±35kg e com uma pontuação média de condição corporal de 5±1/9. Os indivíduos elegíveis eram clinicamente saudáveis, sem história prévia de claudicação relacionados ao casco. Após administração de oligofrutose (10g/kg por sonda nasogás-trica), os animais foram divididos em dois grupos: tratado (30mg/kg de DF1681B intravenosa, 6, 12, 18 e 24h após a oligofrutose) e não tratado, que recebeu placebo. Bióp-sias laminares foram realizadas antes e 12, 36 e 72h após a administração de oligofrutose. As amostras foram coradas com ácido periódico de Schiff (PAS) e classificadas de 0-6 de acordo com alterações nas células epidérmicas e na membrana basal. Também determinaram-se as expressões gênicas de IL-1β, CXCL1 e IL-6 por RT-PCR. Testes paramé-tricos e não paramétricos foram utilizados para comparar os momentos em cada grupo (P<0,05). Estatisticamente, os graus PAS e as expressões de IL-1β e IL-6 se elevaram após a indução no grupo não tratado, mas se mantiveram cons- With the hypothesis that blocking chemokine signaling can ameliorate acute laminitis, the aim was to evaluate the therapeutic effect of intravenous DF1681B, a selective antagonist for CXCR1 and CXCR2 (chemokine receptors), in an oligofructose equine laminitis model. To twelve mixed breed clinically healthy hoses with no previous history of hoof-related lameness was administered oligofructose (10g/kg given by nasogastric tube) and divided into two groups: treated (intravenous DF1681B at 30mg/kg 6, 12, 18, and 24h after oligofructose) and non-treated groups. Laminar biopsies were performed before and 12, 36, and 72h after administering oligofructose. Samples were stained with periodic acid-Schiff (PAS) and scored from 0 to 6 according to epidermal cell and basal membrane changes. The IL-1β, IL-6, and CXCL1 RNA expressions were determined by RT-PCR. Parametric and non--parametric tests were used to compare times within each group (P<0.05). The PAS grades and IL-1β and IL-6 RNA expression increased in the non-treated group, but remained constant in the treated horses. In conclusion, DF1681B therapy reduced laminar inflammation and epidermal deterioration in treated horses. CXCR1/2 blockage should be considered therapeutically for equine acute laminitis. tantes nos cavalos tratados. Em conclusão, a terapia por DF1681B reduziu a inflamação laminar e a deterioração epidérmica em equinos submetidos ao modelo de intoxicaç...

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“…There are two distinct gelatinases of the MMPs family, MMP-2 and MMP-9, which are also found as proenzymes, produced by basal cells for physiologic control of hoof growth (FRENCH & POLLITT, 2004). It has been demonstrated that the concentration of these substances increases, substantially, 48 hours after laminitis induction through carbohydrate administration (KYAW-TANNER & POLLITT, 2004), and that MMP-9 seems to be better associated to inflammatory processes, since it is activated by proinflammatory cytokines and released by leukocytes, while MMP-2 is found in large quantities on normal tissues (KYAW-TANNER & POLLITT, 2004, LOFTUS et al, 2006.…”

Section: Introductionmentioning

confidence: 99%