I just wanted to share this French article about new research with regards to COPD. The research is done by the french INSERM institute. I've put the original article in French through Google translate to post it in English so I'am sorry if some of the translation is approximate but it's always good to read about some the work being done in the field.
The original article dates back to November 2015 and can be found here:
Inserm researchers are working to develop a drug that could finally help avoid the inevitable worsening of chronic obstructive pulmonary disease. By identifying a mechanism associated with exacerbations of this chronic inflammatory disease of the airways, researchers have discovered a directly exploitable therapeutic target.
This is a therapeutic path that could "revolutionize" the treatment of chronic obstructive pulmonary disease (or COPD). Professor Patrick Berger * does not beat around the bush to describe the potential of the discovery that has just completed his team at the University Hospital of Bordeaux. Currently, this chronic disease of the bronchi can not be cured. The available treatments are symptomatic, easing only transiently patients with moderate efficiency. Yet COPD is a highly prevalent disease whose main risk factor is smoking. "In France, 75% of adults are smokers or former smokers. Of these, half of the individuals have the same COPD if they still ignore. By 2030, it will be the fourth leading cause of death worldwide, "explains Patrick Berger. This means if the issue is size.
COPD is characterized by inflammation and bronchial remodeling thereof. It causes progressive airway obstruction and breathing difficulties. Exacerbations, ie a sudden worsening of symptoms occur in 80% of patients and often lead to hospitalization and an excess risk of death in the months and years following. It is this problem that the researchers wanted to target.
In two other respiratory diseases, asthma and pulmonary fibrosis, there is an elevation of the concentration of fibrocytes, stem cells of the bone marrow and enter the blood come to colonize the inflamed regions, contributing to the aggravation of these diseases. In the case of asthma, these cells differentiate into smooth muscle cells (myocytes) to increase the contractions of the bronchi. In case of pulmonary fibrosis, fibrocytes differentiate into fibroblasts (the tissue supporting cells) and accentuate fibrosis. The researchers asked whether fibrocytes were also involved in COPD exacerbations, contributing to their severity.
Atypical fibrocytes to target:
Pneumonia is an inflammation of the lungs usually caused most often by a virus or a bacterium.
To have the heart net, they analyzed the concentration of fibrocytes in the blood of 65 patients affected by bronchial exacerbation and monitoring their breathing capacity for at least two months. They have done the same in individuals showing stable COPD without exacerbation, and in non-affected individuals with COPD. Thus they found a massive increase in the concentration fibrocytes during exacerbations associated with COPD. In fact, "more fibrocytes the high concentration, the greater the patient's prognosis is poor, constituting a mortality index in three years. In addition, over the concentration of fibrocytes remains high in the two months following the episode, more breath is corrupt, "says Patrick Berger.
Looking more closely at these fibrocytes, the authors found that they were two specific receptors in certain chemokines, substances produced by the body capable of attracting cells in the blood. "These fibrocytes appear to be hypersensitive to two chemokines that cause their migration into the airways at the time of exacerbation," explains the researcher. The mechanisms of this migration are being considered. The authors also try whether, once arrived in the bronchi, these cells differentiate into myofibroblasts contribute to the remodeling of the bronchi and the worsening of the disease.
A drug test:
Pending clarification of these points, the association between the migration of fibrocytes in the blood of patients with COPD and prognosis of the disease is clear enough to try to stop this phenomenon. The authors tested a molecule already on the market in the context of haematological indication (the plerixafor). It works by blocking a chemokine receptor identified on the surface of fibrocytes (CXCR4). The in vitro results are promising and have led researchers to apply for a patent to protect this work. A first clinical trial could start soon. "Blocking this migration may in fact, for the first time, change the history of the disease," concludes the researcher.