Dataset Information

Investigating the link between particulate exposure and airway inflammation in the horse.

ABSTRACT: Inhalant exposure to airborne irritants commonly encountered in horse stables is implicated in the pathogenesis of inflammatory airway disease (IAD) and recurrent airway obstruction (RAO), non-infectious, inflammatory pulmonary disorders that impact the health and performance of horses across all equine disciplines. IAD and RAO have overlapping clinical, cytological, and functional manifestations of the pulmonary response to organic dust and noxious gases encountered in the barn environment. Study of these diseases has provided important but incomplete understanding of the effect of air quality upon the respiratory health of horses. In this review, the principles of particulate exposure assessment, including health-related aerosol size fractions and size-selective sampling, the factors influencing air quality in equine environments, and the effect of air quality on the equine respiratory tract are discussed. The objective of this review is to provide the reader with a summary of the most common chronic inflammatory airway diseases in the horse and the principles of air sampling that are essential to the planning, interpretation, and assessment of equine respiratory health-related exposure studies.

SUBMITTER: Ivester KM

PROVIDER: S-EPMC4895611 | biostudies-literature | 2014 Nov-Dec

REPOSITORIES: biostudies-literature

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Investigating the link between particulate exposure and airway inflammation in the horse.

Ivester K M KM Couëtil L L LL Zimmerman N J NJ

Journal of veterinary internal medicine 20141001 6

Inhalant exposure to airborne irritants commonly encountered in horse stables is implicated in the pathogenesis of inflammatory airway disease (IAD) and recurrent airway obstruction (RAO), non-infectious, inflammatory pulmonary disorders that impact the health and performance of horses across all equine disciplines. IAD and RAO have overlapping clinical, cytological, and functional manifestations of the pulmonary response to organic dust and noxious gases encountered in the barn environment. Stu ...[more]

PMID: 25273818

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Project description:Particulate matter (PM) is able to induce airway epithelial injury, while the detailed mechanisms remain unclear. Here we demonstrated that PM exposure inactivated MTOR (mechanistic target of rapamycin kinase), enhanced macroautophagy/autophagy, and impaired lysosomal activity in HBE (human bronchial epithelial) cells and in mouse airway epithelium. Genetic or pharmaceutical inhibition of MTOR significantly enhanced, while inhibition of autophagy attenuated, PM-induced IL6 expression in HBE cells. Consistently, club-cell-specific deletion of Mtor aggravated, whereas loss of Atg5 in bronchial epithelium reduced, PM-induced airway inflammation. Interestingly, the augmented inflammatory responses caused by MTOR deficiency were markedly attenuated by blockage of downstream autophagy both in vitro and in vivo. Mechanistically, the dysregulation of MTOR-autophagy signaling was partially dependent on activation of upstream TSC2, and interacted with the TLR4-MYD88 to orchestrate the downstream NFKB activity and to regulate the production of inflammatory cytokines in airway epithelium. Moreover, inhibition of autophagy reduced the expression of EPS15 and the subsequent endocytosis of PM. Taken together, the present study provides a mechanistic explanation for how airway epithelium localized MTOR-autophagy axis regulates PM-induced airway injury, suggesting that activation of MTOR and/or suppression of autophagy in local airway might be effective therapeutic strategies for PM-related airway disorders.Abbreviations: ACTB: actin beta; AKT: AKT serine/threonine kinase; ALI: air liquid interface; AP2: adaptor related protein complex 2; ATG: autophagy related; BALF: bronchoalveolar lavage fluid; COPD: chronic obstructive pulmonary disease; CXCL: C-X-C motif chemokine ligand; DOX: doxycycline; EGF: epidermal growth factor; EGFR: epidermal growth factor receptor; EPS15: epidermal growth factor receptor pathway substrate 15; HBE: human bronchial epithelial; H&E: hematoxylin & eosin; IKK: IKB kinase; IL: interleukin; LAMP2: lysosomal-associated membrane protein 2; LPS: lipopolysaccharide; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTEC: mouse tracheal epithelial cells; MTOR: mechanistic target of rapamycin kinase; MYD88: MYD88 innate immune signal transduction adaptor; NFKB: nuclear factor of kappa B; NFKBIA: NFKB inhibitor alpha; PM: particulate matter; PtdIns3K: phosphatidylinositol 3-kinase; Rapa: rapamycin; RELA: RELA proto-oncogene, NFKB subunit; SCGB1A1: secretoglobin family 1A member 1; siRNA: small interfering RNAs; SQSTM1: sequestosome 1; TEM: transmission electronic microscopy; TLR4: toll like receptor 4; TSC2: TSC complex subunit 2.

Dataset Information

Investigating the link between particulate exposure and airway inflammation in the horse.

Publications

Investigating the link between particulate exposure and airway inflammation in the horse.

Similar Datasets

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