Evaluation of cytokine production by equine alveolar macrophages exposed to lipopolysaccharide, Aspergillus fumigatus, and a suspension of hay dust.
OBJECTIVE
To evaluate cytokine production by equine alveolar macrophages after exposure to lipopolysaccharide (LPS), Aspergillus fumigatus, and hay dust, and determine the effect of clenbuterol on the cytokine response.


METHODS
6 horses.


METHODS
Alveolar macrophages were exposed to PBS solution (negative control), LPS, hyphae and conidia of Aspergillus fumigatus (AF), or a suspension of hay dust (HDS) and incubated for 24 hours at 37 degrees C. Concentrations of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta were measured in the supernatant. The procedure was repeated with cells that were concurrently incubated with 0.5 microM clenbuterol.


RESULTS
Exposure to HDS and AF significantly increased production of TNF-alpha by equine alveolar macrophages. The increase in TNF-alpha produced in response to HDS and AF was 5 and 7 times as great, respectively, as the increase measured in response to LPS. The concentration of IL-1beta in the supernatant was significantly increased after exposure of cells to AF. Clenbuterol was effective at inhibiting TNF-alpha production by cells exposed to LPS, HDS, or AF.


CONCLUSIONS
Increased production of TNF-alpha and IL-1 indicated that the pro-inflammatory cytokines produced by alveolar macrophages in response to allergens may play a role in recurrent airway obstruction (RAO) in horses. Equine alveolar macrophages are not only a primary pulmonary defense mechanism but may also influence the pathogenesis of equine RAO. The beta2-adrenoceptor agonist clenbuterol, a drug that is commonly used for treatment of equine RAO, promotes immediate bronchodilation and may also contribute to downward modulation of the inflammatory response.
Laan
Tamarinde T J M
TT
Department of Equine Science, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 12-16, 3508 TD Utrecht, The Netherlands.
Bull
Sarah
S
Pirie
R Scott
RS
Fink-Gremmels
Johanna
J
D000402:Airway Obstruction / Q000139:chemically induced / Q000276:immunology / Q000662:veterinary*; D000704:Analysis of Variance; D000818:Animals; D001232:Aspergillus fumigatus / Q000276:immunology / Q000472:pathogenicity; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D004391:Dust / Q000276:immunology; D006734:Horse Diseases / Q000276:immunology*; D006736:Horses; D007375:Interleukin-1 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology / Q000633:toxicity; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000276:immunology*; D006109:Poaceae / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D004391:Dust; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha