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Volume 25, Number 12 539
Current Research
Iam a scientific bricklayer helping to build, throughnew information that my colleagues and I discover, asound foundation of knowledge about heaves (for-merly called chronic obstructive pulmonary disease)
in horses. I rely on colleagues at my own university andothers to provide the skills I lack. My labor is like that ofmasons building ancient cathedrals, who knew theymight not see the edifice completed in their lifetime butthat one day it would be complete, with a spire. My“spire” is a heaves susceptibility marker (HSM). WithHSM, foals could be managed to prevent heaves, an in-formed decision could be made about purchasing a horse,or selective breeding might eliminate the disease.
We have used many approaches to gain clues aboutHSM, which I suspect is a result of a gene mutation.Primarily, we have used a scientific process known as hy-pothesis testing to investigate the etiology, or cause, ofheaves. Many of these hypotheses were based on pub-lished research undertaken by other laboratories that wetrust had undertaken careful and skilled studies. We in-vestigated the effect of heaves on lung function, deter-mined the time course of inflammation, and asked whymuscle spasms occur around air passages and why excessmucus accumulates. Once it became clear that inflamma-tion is the basis of the lung dysfunction in heaves, weneeded to find the signaling molecules involved, whichrequired an understanding of the immune response. After20-plus years, we can say with confidence that exposureof susceptible horses to high particulate loads from hay
Reprinted from Lloyd’s Equine Disease Quarterly, October 2005.0737-0806/$ - see front matter© 2005 Elsevier Inc. All rights reserved.doi:10.1016/j.jevs.2005.11.004
Heaves Research at Michigan State UniversityDr N. Edward Robinson
and other sources activates signaling molecules in lungcells. This response initiates neutrophilic inflammation,which is associated with increased activity of nerves andcauses the muscle around airways to contract.Simultaneously, mucus accumulates as a consequence ofincreased activity of mucin genes and stiffening of themucus. As long as inflammation persists, mucus persists,and structural changes in the airway muscle and sur-rounding fibrous tissue develop. Because excessive in-flammation is at the core of the problem, HSM will mostlikely be a regulator of inflammation.
Our group has been able to generate this knowledgebecause of consistent funding (around $300,000 annually)for many years. A critical mass of faculty, graduate stu-dents, and technicians maintains the level of intellectualactivity and technical expertise. We have developed skillin studying heaves. If our funding had been intermittent,we would lack experienced personnel as we diverted ourresearch away from the horse to other endeavors.
As a horse person, you might say, “Heaves is nothreat to our industry, so do we really need HSM?” Thatis a valid criticism, but instead of heaves, think about theemergence of a “new” infectious disease or a syndromesuch as mare reproductive loss syndrome. When a newproblem occurs for which a foundation of knowledgemust be built, you need skilled “masons” in that field,with all their tools. These problems cannot be solved witha short-term financial fix using individuals with little ex-perience or knowledge in the relevant disciplines.
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