Ongoing Lung Inflammation and Disease Progression in Mice after Smoking Cessation: Beneficial Effects of Formyl-Peptide Receptor Blockade

The American Journal of Pathology
Giovanna De CuntoMonica Lucattelli

Abstract

The most important risk factor for chronic obstructive pulmonary disease (COPD) is cigarette smoking. Until now, smoking cessation (SC) is the only treatment effective in slowing down the progression of the disease. However, in many cases SC may only relieve the airflow obstruction and inflammatory response. Consequently, a persistent lung inflammation in ex-smokers is associated with progressive deterioration of respiratory functions. This is an increasingly important clinical problem whose mechanistic basis remains poorly understood. Available therapies do not adequately suppress inflammation and are not able to stop the vicious cycle that is at the basis of persistent inflammation. In addition, in mice after SC an ongoing inflammation and progressive lung deterioration is observed. After 4 months of smoke exposure mice show mild emphysematous changes. Lung inflammation is still present after SC, and emphysema progresses during the next 6-month period of observation. Destruction of alveolar walls is associated with airways remodeling (goblet cell metaplasia and peribronchiolar fibrosis). Modulation of formyl-peptide receptor signaling with antagonists mitigates inflammation and prevents deterioration of lung structures. This ...Continue Reading

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Citations

Sep 10, 2019·British Journal of Pharmacology·Giovanna De CuntoFiorentina Roviezzo
Aug 21, 2020·COPD·Jader Joel Machado JunqueiraFernanda Degobbi Tenorio Quirino Dos Santos Lopes
Jun 18, 2020·International Journal of Chronic Obstructive Pulmonary Disease·Giovanna De CuntoGiuseppe Lungarella
Oct 21, 2020·Respirology : Official Journal of the Asian Pacific Society of Respirology·Simon D PouwelsAlen Faiz
Oct 22, 2020·Experimental & Molecular Medicine·Yu Sun Jeong, Yoe-Sik Bae
Apr 7, 2021·Revue des maladies respiratoires·G PeifferG Fond
Mar 16, 2021·American Journal of Physiology. Lung Cellular and Molecular Physiology·Abderrahim NemmarBadreldin H Ali

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