The bronchial circulation—worth a closer look: A review of the relationship between the bronchial vasculature and airway inflammation

Abstract

Until recently, the bronchial circulation has been relatively ignored in the research and clinical arenas, perhaps because of its small volume and seeming dispensability relative to the pulmonary circulation. Although the bronchial circulation only receives around 1% of the cardiac output in health, it serves functions that are critical to maintaining airway and lung function. The bronchial circulation also plays an important role in many lung and airway diseases; through its ability to increase in size, the bronchial circulation is able to provide lung parenchymal perfusion when the pulmonary circulation is compromised, and more recently the role of the bronchial circulation in the pathogenesis of inflammatory airway disease has been explored. Due to the anatomic variability and small volume of the bronchial circulation, much of the research to date has necessitated the use of animal models and invasive procedures. More recently, non-invasive techniques for measuring bronchial blood flow in the mucosal microvascular network have been developed and offer a new avenue for the study of this circulation in humans. In conjunction with molecular research, measurement of airway blood flow (Q(aw)) may help elucidate the role of the bronchial circulation in inflammatory airway disease and become a useful tool for monitoring therapy.

Pulmonary vascular changes in asthma and COPD

“…These older asthmatic patients also showed increased angiogenin levels compared to younger asthmatics (26±5yr), and age matched healthy controls [90], demonstrating that airway vascularity may further alter with age. In the same study, angiogenin expression was significantly elevated in severe asthmatic subjects compared to mild asthmatic subjects and negatively related to [91].…”

CFTR dysfunction induces vascular endothelial growth factor synthesis in airway epithelium

“…The bronchial circulation has the ability to proliferate and peribronchial angiogenesis (the proliferation of new blood vessels from existing vessels) is increasingly recognised as an important component in chronic airway diseases [7,8]. Abnormalities in peribronchial blood vessels may contribute to immune responses via microvascular leakage and recruitment of inflammatory cells [9,10].…”

Bead-size directed distribution of Pseudomonas aeruginosa results in distinct inflammatory response in a mouse model of chronic lung infection

“…The mechanism involves the mobilization of inflammatory cells from the bone marrow, up-regulation of blood cell integrins and selectins and endothelium adhesion molecules, as well as dilatation and leaking of capillaries to allow humoral and cellular components to pass into the pulmonary lumen and the invading microbes. In contrast, the blood to the upper conductive zone is limited to the arterial blood supply, comprising only 1% of the total cardiac output [5]. Despite the presence of a submucosal plexus, recruitment of inflammation to the conductive zone is relatively limited, probably because of the thicker tissue wall, the mucus produced by the goblet cells and the submucosal glands and the non-phlogistic s-immunoglobulin (IgA) in contrast to the phlogistic IgG response in the respiratory zone [6,7].…”

“…The PRRs include the Toll-like receptors (TLRs) and nucleotide-binding oligomerization domaine (NOD)-like receptors (NLRs) and activation of the PRRs initiates the host response, resulting in release of cytokines [3,4]. Furthermore, the respiratory zones of the lung are in close contact with blood supply, as the total blood volume pumped from the right cardiac ventricle passes through the capillaries of the respiratory zone and back to the left cardiac ventricle as oxygenated blood [5]. Due to close contact between the alveolar space and the vascular lumen, this is also the major focus for recruitment of inflammatory cells through the endothelium, basal membrane and alveolar epithelium into the alveolar lumen [3,4].…”