Abstract
Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory disease and one of the leading causes of morbidity and mortality worldwide. It is characterized by persistent respiratory symptoms and airflow limitation due to abnormalities in the lower airway following consistent exposure to noxious particles or gases. Acute exacerbations of COPD (AECOPD) are characterized by increased cough, purulent sputum production, and dyspnea. The AECOPD is mostly associated with infection caused by common cold viruses or bacteria, or co-infections. Chronic and persistent infection by non-typeable Haemophilus influenzae (NTHi), a Gram-negative coccobacillus, contributes to almost half of the infective exacerbations caused by bacteria. This is supported by reports that NTHi is commonly isolated in the sputum from COPD patients during exacerbations. Persistent colonization of NTHi in the lower airway requires a plethora of phenotypic adaptation and virulent mechanisms that are developed over time to cope with changing environmental pressures in the airway such as host immuno-inflammatory response. Chronic inhalation of noxious irritants in COPD causes a changed balance in the lung microbiome, abnormal inflammatory response, and an impaired airway immune system. These conditions significantly provide an opportunistic platform for NTHi colonization and infection resulting in a “vicious circle.” Episodes of large inflammation as the consequences of multiple interactions between airway immune cells and NTHi, accumulatively contribute to COPD exacerbations and may result in worsening of the clinical status. In this review, we discuss in detail the interplay and crosstalk between airway immune residents and NTHi, and their effect in AECOPD for better understanding of NTHi pathogenesis in COPD patients.
Highlights
The lungs are vital organs involved in gas exchange between the vascular system and the external environment, they are greatly exposed to the environment-derived microorganisms, including fungi, viruses, and bacteria
This review describes the disease progression of chronic obstructive pulmonary disease (COPD) in the context of host immuneinteractions linked to Non-typeable Haemophilus influenzae (NTHi), and the overall impact in disease exacerbation
NTHi recovered in 7% of intubated patients with respiratory exacerbation Isolation of a new strain of NTHi significantly associated with exacerbation Patients with a new NTHi-strain twice as likely to have Acute exacerbations of COPD (AECOPD) Potentially pathogenic bacteria found in 70% of exacerbations
Summary
The lungs are vital organs involved in gas exchange between the vascular system and the external environment, they are greatly exposed to the environment-derived microorganisms, including fungi, viruses, and bacteria. COPD is a severe inflammatory lung disease characterized by airflow limitation with a range of pathological changes Both genetics and environmental factors trigger the onset of COPD, microbes including NTHi play an important role in the acute exacerbations. By elastolytic destruction and enlargement of the alveolar wall distal to the terminal bronchioles This results in the loss of alveolar attachments to the small airways and limitation of airflow and gaseous exchanges. Chronic bronchitis is characterized by consecutive and chronic cough with expectorations that last for more than 3 months within 2 years It is associated with inflammation of the bronchial walls with increased inflammatory infiltrates, hyperplasia of goblet cells, hypertrophy of tracheobronchial submucosa, increased mucous secretion and, dilatation of the airway ducts (airways of about 2–4 mm in internal diameter). The comorbidities are commonly seen in COPD patients despite the actual mechanism responsible for the systemic inflammation remains to be elucidated
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