Chronic obstructive pulmonary disease (COPD): Evaluation from clinical, immunological and bacterial pathogenesis perspectives

Abstract

Chronic obstructive pulmonary disease (COPD), a disease manifested by significantly impaired airflow, afflicts ∼14.2 million cases in the United States alone with an estimated 63 million people world-wide. Although there are a number of causes, the predominant cause is excessive tobacco smoke. In fact, in China, there have been estimates of 315,000,000 people that smoke. Other less frequent causes are associated with indirect cigarette smoke, air pollutants, biomass fuels, and genetic mutations. COPD is often associated with heart disease, lung cancer, osteoporosis and conditions can worsen in patients with sudden falls. COPD also affects both innate and adaptive immune processes. Cigarette smoke increases the expression of matrix metalloproteases and proinflammatory chemokines and increases lung titers of natural killer cells and neutrophils. Yet, neutrophil reactive oxygen species (ROS) mediated by the phagocytic respiratory burst and phagocytosis is impaired by nicotine. In contrast to innate immunity in COPD, dendritic cells represent leukocytes recruited to the lung that link the innate immune responses to adaptive immune responses by activating naïve T cells through antigen presentation. The autoimmune process that is also a significant part of inflammation associated with COPD. Moreover, coupled with restricted FEV1 values, are the prevalence of patients with single or multiple infections by bacteria, viruses and fungi. Finally, we focus on one of the more problematic infectious agents, the Gram-negative opportunistic pathogenic bacterium, Pseudomonas aeruginosa. Specifically, we delve into the development of highly problematic biofilm infections that are highly refractory to conventional antibiotic therapies in COPD. We offer a non-conventional, biocidal treatment that may be effective for COPD airway infections as well as with combinations of current antibiotic regimens for more effective treatment outcomes and relief for patients with COPD.

Population pharmacokinetics of fluticasone propionate/salmeterol using two different dry powder inhalers

“…COPD is characterized by a progressive airflow limitation, which in some cases is not fully reversible (Csikesz and Gartman, 2014;Goldcopd, 2014;Hassett et al, 2014). The management of COPD focuses primarily on reducing exposure to risk factors, alleviating respiratory symptoms, preventing exacerbations, and treating COPD-related co-morbidities.…”

Novel Therapies to Inhibit Mucus Synthesis and Secretion in Airway Hypersecretory Diseases

“…Chronic bronchitis defines the long-term airway inflammation causing mucus hypersecretion (since the airway epithelium is irritated). The main clinical symptoms of many COPD patients are those pertaining to chronic bronchitis: persistent cough with sputum production and breathlessness, causing lack of energy [19,20]. The Medical Research Council has proposed that these symptoms should appear ‘for at least 3 months of the year on 2 consecutive years' in order to diagnose chronic bronchitis [21].…”

Molecular microbiology in antibacterial research

“…In a broader sense, this pulmonary dysfunction can be considered as another cause of microbial imbalance in the upper and possibly lower respiratory tracts, and thus should also be viewed from a microbiological standpoint. All these aspects are summarized in the review by Hassett et al (2014), with an emphasis on the microbiological perspective featuring Pseudomonas aeruginosa, the most common bacterial species isolated from COPD patients, which can prosper in the limited oxygen supply via anaerobiosis within its complex biofilm community. The second review by Walling and Lau (2014) describes new in vitro and in vivo studies to understand pulmonary dysfunction upon exposure to air pollutants that provoke similar responses observed in COPD.…”