BE is a chronic lung disease characterized by irreversible dilation of one or more bronchi. It is associated by a chronic cough, sputum production, chronic airway inflammation, and airway obstruction (Boyton, 2008, Baydarian and Walter, 2008, Chalmers and Hill, 2013). Although the prevalence of bronchiectasis declined in the later decades of last century, more recently databases have indicated increasing rate of BE prevalence in adults (Kapur and Karadag, 2011). Sex and age may have impacts on the pathogenesis of BE. It is more prevalent in women and occurs more in older people (Baydarian and Walter, 2008, King, 2011). In addition to its being a costly disorder to treat (Baydarian and Walter, 2008), BE is responsible for reduced life quality and high morbidity (Keistinen et al., 1997). It remains an important cause of childhood impairment in developing countries (Boyton et al., 2013).
The vicious cycle hypothesis which was proposed by Cole (1986) attempted to define the underlying pathogenesis of BE by connecting three main components: infection, abnormal immunity, and tissue damage (Boyton, 2008, Tsang and Bilton, 2009, Chalmers and Hill, 2013). It is difficult to determine the starting point of the “vicious cycle” but the disease process involves two main stages in. The initial insult: it is proposed there are essential abnormalities of the innate and adaptive immune response that could predispose to BE by impairing respiratory pathogen clearance and exaggerating immune response. This situation leads to the second stage: recurrent infection and cumulative airway damage (Boyton, 2008, Chalmers and Hill, 2013).
Increasing levels of some interleukins and chemokines in BE such as TNF-α, IL-6, IL-8, and C5a during airway inflammation result in intense neutrophil infiltration (Boyton, 2008, Boyton, 2009). It is also possible that IL-17, which is released from lung T cells and NK cells as a consequence to local bacterial infection, promotes neutrophil recruitment and leads to excessive inflammation as a result (Boyton and Altmann, 2012). The variety of mediators such as metalloproteinases, elastase, and reactive oxygen species produced by these neutrophils cause bronchial dilation by digesting airway elastin and basement membrane collagen (King, 2011). Damaging elastic and muscle tissue in bronchial airways, and forming abnormal dilatation as a result, facilitates accumulation of mucus and encourages bacterial infection (Boyton et al., 2013). The results of analysis of sputum or bronchoalveolar lavage (BAL) by microbiological cultures have revealed a large number of pathogens which are present in the infected airways. Non-typeable Haemophilus influenzae, Streptococcus pneumonia, Moraxella catarrhalis and Pseudomonas aeruginosa are the main pathogens that have been described in BE subjects (Grimwood, 2011, King, 2011, Boyton and Altmann, 2012, Kadowaki et al., 2015) . Bacterial adaptations have an important role in persistence of these bacteria, for example biofilm formation (bacteria having mucoid phenotype) (Starner et al., 2006) or survival within macrophages (Murphy et al., 2009), are successful strategies that make bacteria more resistant to mechanisms of host clearance (Grimwood, 2011, King, 2011, Chalmers and Hill, 2013). In addition, one of the causes of bacteria persisting in alveolae is recurrent viral infections. Viruses cause distortion of airway surface and disrupt cilial function (Wong et al., 2005) and that leads to triggering of inflammation (Stafler and Carr, 2010), and viral infection prevents the effective removal of mucus and bacteria (Boyton et al., 2013).
Dr.Sajidah F. Hasan
Branch of Clinical Laboratory Sciences
