I’ve never been a big fan of mice. After a particularly traumatic experience with a Norwegian rat while living in Northern Germany, I’ve just had a kind of rodent phobia. Thus, it’s ironic that my future health is inextricably tied to colonies of little furry mice, passing their lives away in sterile little cages and tucked away in various labs across the world.
While at the American Thoracic Society meeting in San Diego, the lives, and thus benefits, of these little creatures were a major topic of consideration.
My very uneducated, and completely non-medical understanding of the debate is something like this. Scientists need mice to study potential therapies for pulmonary fibrosis, but as of yet, there seems to be no perfect mouse model. The thing about mice is they don’t live very long. Many genetic causes of pulmonary fibrosis develop over time, and mice that might have the genes to develop fibrosis typically die before it ever happens. Living in those nice little sterile cages, free from the toxins and intrusions of the world, probably doesn’t help either.
So, researchers studying treatments for pulmonary fibrosis have to find a way to speed up the fibrosis process. Right now the most accepted way to do this is to expose mice to bleomycin, a drug used to treat cancer that is known to cause pulmonary fibrosis a side effect.
The trouble is no one seems to be able to say for sure if when treating fibrosis in mice caused by bleomycin exposure, scientists are actually treating the underlying disease process, or simply repairing a lung injury.
Another alternative some scientists use is to expose mice to asbestos – which seems like even more of a problem to my uneducated mind, but what do I know?
Donna and I sat in several sessions as various mouse models were discussed. We scratched our heads. Why aren’t more scientists using the HPS mouse model? There’s no doubt that HPS mice (bred with two types of HPS) develop fibrosis – it’s a clear genetic cause – no guess work there about lung injury.
Why is the majority of the research community stuck on this bleomycin model? Sure, the HPS model has its faults too – but if none of the models are perfect, then why is the majority of research occurring with the bleomycin treated mice? Why don’t they at least mix it up a bit? Is it just that they don't know about HPS? Or, is there a better reason?
There are a few other reasons I think the HPS mouse model should get more consideration as an alternative mouse model – but I’ll comment more on those after Dr. Lisa Young publishes her research on this. She’s got some very interesting findings, and is already in a race to get them published.
If there’s some researcher out there who might stumble across this blog, and be able to explain it to me better, I’d appreciate some help understanding this; but it seems to me more use of the HPS mouse model would benefit research into idiopathic pulmonary fibrosis as well as research into Hermansky-Pudlak Syndrome.
Someone please explain to me the flaws in my logic? I’m definitely not a scientist. I’m just a patient scratching my head trying to figure this all out.
While at the American Thoracic Society meeting in San Diego, the lives, and thus benefits, of these little creatures were a major topic of consideration.
My very uneducated, and completely non-medical understanding of the debate is something like this. Scientists need mice to study potential therapies for pulmonary fibrosis, but as of yet, there seems to be no perfect mouse model. The thing about mice is they don’t live very long. Many genetic causes of pulmonary fibrosis develop over time, and mice that might have the genes to develop fibrosis typically die before it ever happens. Living in those nice little sterile cages, free from the toxins and intrusions of the world, probably doesn’t help either.
So, researchers studying treatments for pulmonary fibrosis have to find a way to speed up the fibrosis process. Right now the most accepted way to do this is to expose mice to bleomycin, a drug used to treat cancer that is known to cause pulmonary fibrosis a side effect.
The trouble is no one seems to be able to say for sure if when treating fibrosis in mice caused by bleomycin exposure, scientists are actually treating the underlying disease process, or simply repairing a lung injury.
Another alternative some scientists use is to expose mice to asbestos – which seems like even more of a problem to my uneducated mind, but what do I know?
Donna and I sat in several sessions as various mouse models were discussed. We scratched our heads. Why aren’t more scientists using the HPS mouse model? There’s no doubt that HPS mice (bred with two types of HPS) develop fibrosis – it’s a clear genetic cause – no guess work there about lung injury.
Why is the majority of the research community stuck on this bleomycin model? Sure, the HPS model has its faults too – but if none of the models are perfect, then why is the majority of research occurring with the bleomycin treated mice? Why don’t they at least mix it up a bit? Is it just that they don't know about HPS? Or, is there a better reason?
There are a few other reasons I think the HPS mouse model should get more consideration as an alternative mouse model – but I’ll comment more on those after Dr. Lisa Young publishes her research on this. She’s got some very interesting findings, and is already in a race to get them published.
If there’s some researcher out there who might stumble across this blog, and be able to explain it to me better, I’d appreciate some help understanding this; but it seems to me more use of the HPS mouse model would benefit research into idiopathic pulmonary fibrosis as well as research into Hermansky-Pudlak Syndrome.
Someone please explain to me the flaws in my logic? I’m definitely not a scientist. I’m just a patient scratching my head trying to figure this all out.
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