Additionally, viral and bacterial coinfection is common, and has been shown to correlate with an increased severity of exacerbations and longer duration of hospitalisation (Papi 2006; Singanayagam 2012). It is widely known that respiratory exacerbations in COPD are associated with increased mortality, accelerated decline in lung function, increased hospitalisation and readmission rates, and decreased quality of life (Kanner 2001; Soler\Catalu?a 2005). indirect costs placing significant financial strain on individuals, their families, wider society and healthcare systems worldwide (ATS Foundation 2014; Jinjuvadia 2017). The symptoms of COPD include dyspnoea (breathlessness), chronic cough and sputum production. COPD encompasses a range of clinical phenotypes, including emphysema and chronic bronchitis, with the latter condition classically being defined as chronic cough and sputum production for at least three months per year for two consecutive years (Ferris 1978). Alternate definitions of chronic bronchitis exist, including cough and phlegm almost every day or several times a week (Kim 2015). Whilst chronic bronchitis is not technically defined by airflow limitation, it may precede the development of this, and is still thought to be associated with airway disease and inflammation, an increased risk in the total number and severity of respiratory exacerbations, and functional limitation (Kim 2011; Woodruff 2016). A COPD exacerbation is usually defined as an acute worsening of respiratory symptoms that results in additional treatment (Wedzicha 2007). Exacerbations are often associated with increased airway inflammation, gas trapping, and mucus production (Platinum 2019); these changes typically lead to symptoms of increased dyspnoea, alteration in sputum colour or volume, increased cough and wheeze, or a combination of these. Most COPD exacerbations are brought on by viral or bacterial respiratory infections (or both); however, environmental changes and air pollution may also play a role in either causing or worsening exacerbations (Platinum 2019; Woodhead 2011). Studies have suggested that viruses are the causative pathogen in 34% to Chitinase-IN-2 56% of COPD exacerbations (Mohan 2010; Papi 2006; Rohde 2003), with bacterial infections reportedly associated with up to 50% of exacerbations (Papi 2006). Additionally, viral and bacterial coinfection is usually common, and has been shown to correlate with an increased severity of exacerbations and longer period of hospitalisation (Papi 2006; Singanayagam 2012). It is widely known that respiratory exacerbations in COPD are associated with increased mortality, accelerated decline in lung function, increased hospitalisation and readmission rates, and decreased quality of life (Kanner 2001; Soler\Catalu?a 2005). In addition, a history of previous exacerbations is usually said to be the single biggest risk factor for future exacerbations (Hurst 2010). Some patients with COPD are more prone to having frequent exacerbations (defined as two or more exacerbations per year) Chitinase-IN-2 and this group has been shown to have worse outcomes and morbidity than those who experience less frequent exacerbations (Seemungal Chitinase-IN-2 1998). Aside Chitinase-IN-2 from impacting the health status and prognosis of individual patients, exacerbations also impose a significant socioeconomic burden on society, particularly those that necessitate hospital admission. A number of evidence\based therapies exist to reduce symptoms and exacerbations, and improve lung function, exercise tolerance and quality of life, in patients with COPD. Key aspects of COPD management include smoking cessation, exercise, pulmonary rehabilitation, and regular vaccinations for both influenza and pneumococcal infections (GOLD 2019). Other non\pharmacological options for select patients include treatment of hypoxaemia with long\term oxygen therapy (Cranston 2005), treatment of hypercapnia with long\term non\invasive ventilation (Kohnlein 2014), and surgical or bronchoscopic lung volume reduction procedures (Marruchella 2018). Pharmacologically, the mainstay of treatment Chitinase-IN-2 in Pik3r2 stable COPD involves inhaled bronchodilators, including beta\agonists and anti\muscarinic agents (GOLD 2019; Kew 2010; Tashkin 2008). If patients still have a high symptom or exacerbation burden, the addition of inhaled corticosteroids (ICS) to a long\acting beta\agonist (LABA) is recommended (Nannini 2012). A number of oral anti\inflammatory agents have also been found to reduce.