Airway inflammation and hypersensitivity induced by chronic smoking.
Summary of "Airway inflammation and hypersensitivity induced by chronic smoking."
Airway hypersensitivity, characterized by enhanced excitability of airway sensory nerves, is a prominent pathophysiological feature in patients with airway inflammatory diseases. Although the underlying pathogenic mechanism is not fully understood, chronic airway inflammation is believed to be primarily responsible. Cigarette smoking is known to cause chronic airway inflammation, accompanied by airway hyperresponsiveness. Experimental evidence indicates that enhanced excitability of vagal bronchopulmonary sensory nerves and increased tachykinin synthesis in these nerves resulting from chronic inflammation are important contributing factors to the airway hyperresponsiveness. Multiple inflammatory mediators released from various types of structural and inflammatory cells are involved in the smoking-induced airway inflammation, which is mainly regulated by redox-sensitive signaling pathways and transcription factors. Furthermore, recent studies have reported potent sensitizing and stimulatory effects of these inflammatory mediators such as prostanoids and reactive oxygen species on these sensory nerves. In summary, these studies using cigarette smoking as an experimental approach have identified certain potentially important cell signaling pathways and underlying mechanisms of the airway hypersensitivity induced by chronic airway inflammation.
Institute of Physiology, School of Medicine, National Yang-Ming University, Taipei 11221, Taiwan, ROC.
This article was published in the following journal.
Name: Respiratory physiology & neurobiology
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21397052
- DOI: http://dx.doi.org/10.1016/j.resp.2011.03.004
Airway inflammation persists after smoking cessation in established chronic obstructive pulmonary disease (COPD), suggesting that other factors drive the airway inflammatory response.
The influence of occupation and ex/passive smoking on inflammatory phenotype is not well understood. The aim of this study was to examine the relationship between occupation, past smoking and current ...
Asthma is a chronic airway inflammatory disease with functional and structural changes, leading to bronchial hyperresponsiveness and airflow obstruction. Airway structural changes or airway remodellin...
Environmental fungi have been linked to TH2 cell-related airway inflammation and the TH2-associated chronic airway diseases asthma, chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP), and allergi...
To investigate the characteristics of gastroesophageal reflux induced cough (GERC) with airway hyperresponsiveness (AHR). Compared to patients with GERC alone and healthy subjects, cough sensitivity, ...
The term exercise-induced bronchospasm (EIB) describes acute, transient airway narrowing that occurs during, and most often after, exercise. Manifestations of EIB can range from mild impai...
We wish to investigate the effects of 3 weeks of orally administered fish oil supplements on the airway sensitivity (provoking dose to cause a 15% fall in FEV1, PD15) to inhaled mannitol (...
Studies have shown that the prevalence of respiratory symptoms, airway hyperresponsiveness (AHR) and asthma is high and increasing in elite athletes. The inflammation seen in the airways o...
COPD is a progressive pulmonary disease that is characterized by an inflammatory process in the airways and the lungs which leads to progressive airway obstruction. The inflammation is ass...
- The inflammatory process that leads to the development of asthma may be present before the onset of asthma symptoms and cause a certain degree of airway hyperresponsiveness. W...
Medical and Biotech [MESH] Definitions
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).
Asthma attacks following a period of exercise. Usually the induced attack is short-lived and regresses spontaneously. The magnitude of postexertional airway obstruction is strongly influenced by the environment in which exercise is performed (i.e. inhalation of cold air during physical exertion markedly augments the severity of the airway obstruction; conversely, warm humid air blunts or abolishes it).
A subtype of bradykinin receptor that is induced in response to INFLAMMATION. It may play a role in chronic inflammation and has a high specificity for KININS lacking the C-terminal ARGININE such as des-Arg(10)-kallidin and des-Arg(9)-bradykinin. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke.
The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.