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Thread: Putting the brakes on lung disease

  1. #1
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    Default Putting the brakes on lung disease

    Lung disease is truly out of control. I think we are finally seeing some serious research that can significantly impact those affected with it. I sure hope so.

    https://pursuit.unimelb.edu.au/artic...n-lung-disease

    Researchers have uncovered a molecular pathway that can be blocked to potentially prevent the destructive inflammation of chronic obstructive pulmonary disease, a major worldwide killer

    By Andrew Trounson, University of Melbourne

    Sometimes you can have too much of a good thing – even infection-fighting white blood cells.

    People with emphysema, or Chronic Obstructive Pulmonary Disease (COPD), have their lung tissues slowly eaten away by chronic inflammation, and the major culprits are specialised white blood cells called neutrophils and macrophages. While adept at combating lung infections, these cells can also attack the elastic fibres of the lungs leaving people struggling for breath and prone to chest infections.

    A scanning electron micrograph of the lining of a bronchus, or airway passage, inside a healthy lung. Picture: David Gregory & Debbie Marshall/Wellcome Collections
    There is no cure, and while abnormally high levels of white blood cells have long been associated with emphysema, scientists have struggled to find an underlying cause that drugs could effectively target.

    But a team of Australian scientists from Monash University and the University of Melbourne have discovered that COPD – and the co-associated medical problems that afflict patients – can be stopped by directly “blocking” a critical protein known as G-CSF that ordinarily works to stimulate the production of white blood cells.

    TREATMENT POTENTIAL

    The study, published in The Journal of Clinical Investigation, https://www.jci.org/articles/view/98224 opens the way for what could be the first treatment that actually prevents the disease from progressing, as well as providing a new ‘biomarker’ to screen people for much earlier diagnosis.

    “We found elevated levels of G-CSF in mice with COPD, and when it was eliminated, the excessive numbers of white blood cells in their lungs were markedly reduced and the lungs themselves no longer became diseased,” says senior author of the study, immunologist Associate Professor Margaret Hibbs from Monash University.

    “Nothing previously has proved to be effective in treating patients with COPD, which is why this finding is so exciting. We can now attempt to target this protein.”

    The genesis of the research goes back to a major international study, published in 2012, that highlighted a strong association between COPD and elevated numbers of white blood cells. When they looked at the results, Associate Professor Hibbs and her long-time friend and collaborator Professor Gary Anderson, director of the Lung Health Research Centre at the University of Melbourne, were intrigued.

    When follow up studies found that high white blood cell counts were also associated with the damage COPD does to other tissues, like the heart, muscles and bones, they decided to investigate.

    “That really cemented in our minds that the white blood cells were a fundamental clue to follow,” says Professor Anderson.

    They formed a team of medical researchers with diverse expertise, including study lead author and immunologist Dr Evelyn Tsantikos from Monash University, and carefully evaluated the effects of blocking G-CSF using mice genetically modified to be prone to COPD symptoms.

    OVER 250 MILLION CASES WORLDWIDE

    “When we blocked G-CSF, the effect was absolutely striking,” says Professor Anderson. “It prevented not only the emphysema, but also the wider medical problems, whether it be the heart, muscles or bone. We realised we had uncovered a potential pathway for treatments.”

    COPD kills about 3 million people each year, making it the third most common cause of death worldwide behind heart disease and stroke. Globally there were an estimated 251 million cases of COPD in 2016, while in Australia over 1.45 million people have some form of COPD.

    But narrowing down an apparent cause of COPD in mice to G-CSF doesn’t mean it works the same way in humans. Before they could contemplate moving into clinical trials the team needed to know if the elevated levels of G-CSF in mice with COPD was replicated in patients suffering from COPD.

    To investigate this critical point, they presented their findings to clinical respiratory researcher and director of clinical training at the Royal Melbourne Hospital, Associate Professor Lou Irving.

    He immediately appreciated the implications and facilitated access to a cohort of respiratory patients, with and without COPD, who volunteered to be sampled as a normal part of their care. As the team suspected, they found that COPD in humans was correlated with high levels of G-CSF.

    CLINICAL TRIALS NEEDED

    “We now have a very good case that we have indeed found a mechanism not just for preventing emphysema and chronic bronchitis in the lungs, but also for preventing the damaging medical conditions associated with it,” says Professor Anderson.

    “There are several safe ways to reduce G-CSF in people and this concept can now be tested in human clinical trials.”

    G-CSF can be blocked using already established antibodies. By simply adjusting the dose of any eventual therapeutic, Professor Anderson says clinicians could be able to maintain the infection-fighting ability of these white blood cells while preventing the collateral damage that leads to COPD.

    “We aren’t proposing to eliminate G-CSF but to keep it at levels within the normal range. That way we can preserve the normal defence function of these white blood cells but stop them from becoming over-aggressive to lung tissue and other body tissues.”

    According to Professor Hibbs, “this would be the first ever strategy that would not only treat the lung disease but the co-associated medical conditions at the same time.

    “If successful, this has the potential to benefit the millions of people who suffer this terrible disease.”
    First treatment in 2007. Pioneering ever since.

    Barbara

  2. #2
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    Default German doctors also might have way to stop emphysema

    Barb; here is another article to stop COPD (https://copdnewstoday.com/2018/05/08...tudy-suggests/) I am happy to see at least some research. God bless

  3. #3
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    Default

    Thanks jgp - There does seem to be a flurry of research lately.

    Here's the article you posted the link for -

    Blocking Cholesterol Derivative May Offer Way to Treat COPD, Study Suggests
    MAY 8, 2018 Jose Marques Lopes, PhD

    Blocking Cholesterol Derivative May Offer Way to Treat COPD, Study Suggests

    Blocking a cellular pathway related to cholesterol metabolism shows early promise in treating chronic obstructive pulmonary disease (COPD), a German study in mice reports.

    The research, “Cholesterol metabolism promotes B-cell positioning during immune pathogenesis of chronic obstructive pulmonary disease,” was published in the journal EMBO Molecular Medicine.

    Cigarette smoking and environmental pollution are the major risk factors for COPD development, causing an inflammatory reaction in the airways and lung that progressively impairs breathing.

    Although the underlying processes of COPD remain largely unknown, increasing evidence supports a key role for inducible bronchus-associated lymphoid tissue (iBALT), a type of lung lymphoid tissue that develops after pulmonary infection or inflammation. iBALTs are tertiary lymphoid organs, which form near sites of inflammation.

    The processes driving iBALT generation, especially during chronic exposure to cigarette smoke, are also unknown. To address this gap, scientists analyzed known processes in other lymphoid tissues, in particular the metabolism of oxysterols, which are derivatives of cholesterol with an important role in various biological processes. One such process is the positioning of immune cells in lymphoid tissue.

    “We wanted to find out whether that is also the case around the lungs and specifically in cigarette-smoke-induced COPD,” Ali Önder Yildirim, PhD, a researcher at the Helmholtz Zentrum München, and one of the study’s senior authors, said in a news release.

    “We focused on tertiary lymphoid organs in the bronchi. It is believed that the development of iBALT plays a key role in the deterioration of COPD but until now it was unclear exactly how iBALT forms,” Yildirim added.

    Results revealed that airway cells taken from the lungs of COPD patients and cigarette smoke-exposed mice had higher-than-usual levels of metabolic enzymes involved in oxysterol metabolism, and in regulating cigarette smoke-induced migration of B-cells (a type of immune cell) and iBALT formation.

    Additional mice experiments showed that the absence of these enzymes reduced iBALT generation, and lessened evidence of cigarette smoke-caused emphysema, immune cell migration and lung damage.

    Blocking oxysterol’s molecular pathway with clotrimazole, an approved treatment, prevented immune cell migration and iBALT formation, and reduced emphysema.

    Overall, the findings “identify a novel therapeutic target for the treatment of COPD and potentially other diseases driven by the generation of tertiary lymphoid organs,” the researchers wrote.

    “Our future goal is to transfer the results from the model to humans with a view to intervening in the development of COPD,” Yildirim said. “There is still a lot of work to do, however we are very much looking forward to it.”
    First treatment in 2007. Pioneering ever since.

    Barbara

  4. #4
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    Default About the putting the brakes on article

    Barb; There are two things that bother me about the article and a lot of other COPD research is they only do it on mice, we are not mice!!!!!!!! Secondly the article says white blood cells are the culprit for eating away our lungs in emphysema, well the thing that really increases white blood cells in our system is prednisone??????

  5. #5
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    Default

    You are right. It's time to put the mice on ice. Prednisone is handed out by some doctors like candy. It sounds like it just adds fuel to the fire. I did read an article last week that patients who were given only antibiotics and no prednisone for an exacerbation did better than those who were also given prednisone as far as not damaging their lungs further.

    I have to wonder about a lot of research. In the article I posted to start this thread, it stated, "But narrowing down an apparent cause of COPD in mice to G-CSF doesn’t mean it works the same way in humans. Before they could contemplate moving into clinical trials the team needed to know if the elevated levels of G-CSF in mice with COPD was replicated in patients suffering from COPD."
    I have had treatments where I was given injections of G-CSF to stimulate the release of stem cells and in fact one of the best treatments I ever had involved 4 injections prior to stem cell harvest and infusion. It is confusing to say the least, but I think Trounson is on to something. COPD is a complicated disease to say the least.
    First treatment in 2007. Pioneering ever since.

    Barbara

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