Assessing fitness in endurance horses.

A field test and a standardized treadmill test were used to assess fitness in endurance horses. These tests discriminated horses of different race levels: horses participating in races of 120 km and more showed higher values of VLA4 (velocity at which blood lactate reached 4 mmol/L) and V200 (velocity at which heart rates reached 200 beats per min) than horses of lower race levels.

Determination of muscle mitochondrial respiratory capacity in Standardbred racehorses as an aid to predicting exertional rhabdomyolysis.

This prospective cohort study evaluated the potential of high-resolution respirometry applied to permeabilized muscle fibers for fitness evaluation in French Standardbred racehorses. Fitness evaluation by means of respirometric parameters did not correlate with racing performance registered over the following racing season. However, altered mitochondrial energy metabolism was associated with higher risk of developing exertional rhabdomyolysis, a common cause of exercise intolerance in racehorses. These data represent a first step towards establishing reference values for muscle OXPHOS capacity in this breed.

Expression microarray as a tool to identify differentially expressed genes in horses suffering from inflammatory airway disease.

BACKGROUND: Inflammatory airway disease (IAD) affects performance and well-being of horses. Diagnosis is primarily reached by bronchoalveolar lavage (BAL) cytology which is invasive and requires sedation. OBJECTIVES: The purpose of this study was to identify differential gene expression in peripheral blood of horses with IAD using species-specific expression microarrays. METHODS: Equine gene expression microarrays were used to investigate global mRNA expression in circulating leukocytes from healthy, IAD-affected, and low-performing Standardbred and endurance horses. RESULTS: Nine genes in Standardbred and 61 genes in endurance horses were significantly differentially regulated (P < .001). These genes were related to inflammation (eg, ALOX15B, PLA2G12B, and PENK), oxidant/antioxidant balance (eg, DUOXA2 and GSTO1-1), and stress (eg, V1aR, GRLF1, Homer-2, and MAOB). All these genes were up-regulated, except down-regulated Homer-2 and MAOB. DUOXA2, ALOX15B, PLA2G12B, MAOB, and GRLF1 expression was further validated by RT-qPCR. An increase in glutathione peroxidase (GPx) activity in heparinized whole blood of IAD-affected Standardbred (P = .0025) and endurance horses (P = .0028) also suggests a deregulation of the oxidant/antioxidant balance. There was good correlation (r = .7354) between BAL neutrophil percentage and whole blood GPx activity in all horses. CONCLUSIONS: This study showed that circulating blood cell gene expression reflects inflammatory responses in tissues. Whether any of the genes have potential for diagnostic applications in the future remains to be investigated. Although not specific for IAD, whole blood GPx activity appears to be correlated with BAL neutrophil percentage. This finding should be further assessed by testing a larger number of horses.

Characterization of pentraxin 3 in the horse and its expression in airways.

The long pentraxin 3 (PTX3) plays an important role in host defence and its over-expression may contribute to airway injury. The aim of the present study was therefore to characterize in more detail PTX3 and its expression in the horses' airway. Six healthy horses and six horses affected by recurrent airway obstruction (R.A.O.) were submitted to a dusty environment challenge. PTX3 DNA and cDNA were cloned and sequenced. PTX3 expression was evaluated by RT-qPCR, Western blotting and immunohistochemistry in bronchoalveolar lavage fluid (BALF) cells, BALF supernatant and bronchial epithelial cells. An alternative splicing of the second exon of PTX3 occurred, resulting in two forms of the protein: "spliced" (32 kDa) and "full length" (42 kDa). PTX3 was detected in BALF macrophages, neutrophils and bronchial epithelial cells. It was over-expressed in the BALF supernatant from R.A.O.-affected horses in crisis. However, dust was unable to induce PTX3 in BALF cells ex vivo, indicating that dust is an indirect inducer of PTX3. Dust exposure in-vivo induced PTX3 in BALF macrophages but there was no significant difference between healthy and R.A.O.-affected horses. Conversely, PTX3 was over-expressed in the bronchial epithelial cells from R.A.O.-affected horses in crisis. These data indicate a differential regulatory mechanism in inflammatory and bronchial epithelial cells and offer therapeutically interesting perspectives.