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Environmental Pollutants in COPD and Lung Cancer

RECRUITINGSponsored by University of Campania Luigi Vanvitelli
Actively Recruiting
SponsorUniversity of Campania Luigi Vanvitelli
Started2023-05-01
Est. completion2026-05-01
Eligibility
Age18 Years+
Healthy vol.Accepted

Summary

Epidemiological studies describe a statistically significant correlation between hospitalization rate and exposure to environmental pollutants such as atmospheric particulates (PM10 and PM2.5) and polycyclic aromatic hydrocarbons (PAH). Indeed, they induced the release of inflammation mediators and oxidative stress, involved in remodeling and destruction of the alveolar parenchyma, in turn associated with the respiratory disease onset and progression such as asthma, COPD, pulmonary fibrosis and lung cancer. Interestingly, oxidative stress associated with environmental pollutants could also induce DNA damage by affecting the stability of G-quadruplex (G4) sequences. Given the role of G4 in physiological and pathological processes and their presence in mitochondrial DNA, telomeres and proto-oncogene promoters, it is interesting to investigate the potential involvement in cellular mechanisms of response to oxidative stress associated with pollutants. Moreover, it is known that pollutant-induced oxidative stress has the ability to alter mitochondrial integrity, leading to mitochondrial dysfunction. The mitochondria involvement in the innate and adaptive immune response regulation corroborates the role of pollutants in respiratory diseases pathogenesis. Indeed, mitochondrial function and integrity are critical for both the effector and memory stages of differentiation of T cells which play a primary role in respiratory diseases. In this context, the PD-1/PD-L1 immune check-points are essential in promoting the immune system homeostasis. Currently, although the role of environmental pollutants, mitochondrial dysfunction and the PD-1/PD-L1 axis in the pathogenesis of many respiratory diseases is recognized, it is useful to further clarify the underlying molecular interconnections and the mechanisms by which pollutants could affect mitochondrial integrity and immune checkpoints.

Eligibility

Age: 18 Years+Healthy volunteers accepted
Inclusion Criteria:

* All patients of both sexes and over the age of 18 years
* Clinical diagnosis of suspected lung cancer

Exclusion Criteria:

* Patients with infectious diseases,
* Patients with interstitiopathy
* Patients with autoimmune diseases
* Patients with cancers not covered by the inclusion criteria
* subjects on glucocorticoid therapy
* subjects who cannot undergo bronchial biopsy
* subjects who will not sign informed consent.

Conditions4

COPDCOPD and Lung CancerCancerLung Cancer

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