Abstract
Chronic obstructive airway diseases are characterized by airflow obstruction and airflow limitation as well as chronic airway inflammation. Especially bronchial asthma and chronic obstructive pulmonary disease (COPD) cause considerable morbidity and mortality worldwide, can be difficult to treat, and ultimately lack cures. While there are substantial knowledge gaps with respect to disease pathophysiology, our awareness of the role of neurological and neuro-immunological processes in the development of symptoms, the progression, and the outcome of these chronic obstructive respiratory diseases, is growing. Likewise, the role of pathogenic and colonizing microorganisms of the respiratory tract in the development and manifestation of asthma and COPD is increasingly appreciated. However, their role remains poorly understood with respect to the underlying mechanisms. Common bacteria and viruses causing respiratory infections and exacerbations of chronic obstructive respiratory diseases have also been implicated to affect the local neuro-immune crosstalk. In this review, we provide an overview of previously described neuro-immune interactions in asthma, COPD, and respiratory infections that support the hypothesis of a neuro-immunological component in the interplay between chronic obstructive respiratory diseases, respiratory infections, and respiratory microbial colonization.
Highlights
Chronic obstructive airway diseases such as chronic obstructive pulmonary disease (COPD) and bronchial asthma are generally characterized by airway inflammation leading to symptoms such as coughing, wheezing, and shortness of breath, and greatly affect the patient’s quality of life [1,2]
We provide an overview of previously described neuro-immune interactions in the two main chronic respiratory diseases, asthma and chronic obstructive pulmonary disease (COPD)
It has long been recognized that respiratory viral infections trigger exacerbations of asthma in both children and adults, whereas for many years bacterial infection was thought to be the main trigger of exacerbations in COPD [93]
Summary
Chronic obstructive airway diseases such as chronic obstructive pulmonary disease (COPD) and bronchial asthma are generally characterized by airway inflammation leading to symptoms such as coughing, wheezing, and shortness of breath, and greatly affect the patient’s quality of life [1,2]. Acute exacerbations occur due to the presence of allergens; pollutants; smoke; cold or dry air; and pathogenic bacteria, viruses or both [3,4]. Among these agents, viral infection is one of the major drivers of asthma exacerbations [5,6], and viral involvement in COPD exacerbations is high [7]. While our knowledge regarding neuro-inflammation in chronic respiratory diseases is increasing, here there still are substantial gaps These include the contribution to the initiation of disease as well as to the manifestation with respect to inflammatory phenotypes and the risk for exacerbations. We discuss interactions along the neuro-immune axis as a potential mechanism of respiratory infections to contribute to the pathophysiology of chronic respiratory diseases
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