The Effect of Race Training on the Basal Gene Expression of Alveolar Macrophages Derived From Standardbred Racehorses

赛马训练对标准赛马肺泡巨噬细胞基础基因表达的影响

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作者:Anna E Karagianni, Kim M Summers, Anne Couroucé, Marianne Depecker, Bruce C McGorum, David A Hume, R Scott Pirie

Abstract

Mild-to-moderate equine asthma is prevalent in young racehorses, particularly early in their training period. Although the precise etiopathogenesis remains undetermined, it is possible that the susceptibility of this population might partly reflect an exercise-associated immune derangement at the level of the airway. We performed a genome-wide basal gene expression scan on alveolar macrophages (AMs) isolated from Standardbred racehorses before and after commencement of competition race training with a view to identifying any exercise-associated gene expression modulation consistent with functional alterations, which might reflect training-associated immunological derangement. Microarray technology was used to analyze the basal gene expression profiles of bronchoalveolar fluid-derived AMs, harvested from six systemically healthy Standardbred racehorses before (T0) and after (T1) entry into training. In addition, AM lipopolysaccharide (LPS)-induced TNF-α and IL-10 release at T0 and T1 was assessed. Although the data revealed significant interhorse heterogeneity in relation to the magnitude of individual gene expression at each timepoint, within each horse, several inflammatory-related genes [e.g., chemokine ligands, interferons, and nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB)] declined in expression from T0 to T1. Entry into training did not significantly alter AM LPS-induced TNF-α or IL-10 release. The data support a direct effect of training on AM basal gene expression, particularly with respect to immune-related genes. The pattern of training-associated differential gene expression may indicate relative downregulation of inflammatory-related genes, consistent with an immunosuppressive effect of training and an increased susceptibility to opportunistic pathogens.

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