Asthma-COPD Overlap Patients Exhibit Mitochondria Dysfunction Similar to COPD

Patricia Inacio, PhD avatar

by Patricia Inacio, PhD |

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Mitochondria dysfunction and COPD

Patients with asthma-COPD overlap syndrome (ACOS) are closer to chronic obstructive pulmonary disease (COPD) based on mitochondria dysfunction, according to a recent study titled “Analysis of mitochondrial DNA alteration in new phenotype ACOS,” published in the open access journal BMC Pulmonary Medicine.

Mitochondria are organelles within our cells responsible for the generation of energy for the body. Mitochondria are also involved in cell proliferation, apoptosis (cell death), and intracellular calcium homeostasis. Importantly, mitochondria contain their own DNA (mtDNA), which is especially susceptible to damage inflicted by reactive oxygen species.

Mitochondria oxidation and damage to mtDNA was previously reported as a common feature in the development of several lung diseases, including obstructive lung diseases, asthma, and COPD. It is still unknown whether mtDNA damage also occurs in ACOS.

A team of researchers tackled this question and analyzed ACOS patients with confirmed diagnosis according to two international guidelines for ACOS, the Spanish one and the Global Initiative for Asthma (GINA)/Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. In total, 10 ACOS patients (according to Spanish guidelines), 13 ACOS patients (according to GINA/GOLD guidelines), 13 patients with COPD, 14 asthmatic patients, and 10 healthy controls were assessed. The team collected participants’ blood, induced sputum, and exhaled nitric oxide. MtDNA and nuclear DNA (nDNA) were quantified from participants’ blood cells.

Researchers observed that ACOS patients exhibited an increase in mtDNA/nDNA ratio, with patients evaluated according to the Spanish guidelines showing a higher value of mtDNA/nDNA, when compared to ACOS patients from GINA/GOLD guidelines (specifically, a ratio of 92.69 versus 80.68, respectively). Continuing the differential analysis of ACOS according to the two sets of guidelines, the team noted that ACOS patients were similar to the asthma group but different from COPD. Those diagnosed by the Spanish guidelines had the reverse association, being significantly different from asthma and closer to COPD.

In conclusion, researchers reported for the first time that ACOS patients are also characterized by mitochondria dysfunction, as they exhibit an increased mtDNA/nDNA ratio. Moreover, the team suggested that ACOS is a phenotype of COPD, since the increased mtDNA/nDNA ratio in these patients is close to COPD (according to ACOS Spanish guidelines) in detriment of ACOS as a new different entity among asthma and COPD. Future studies are required to further characterize ACOS.