Endothelial Dysfunction and Pentraxin-3 in Clinically Stable Adult Asthma Patients

Asthma is associated with low-grade systemic inflammation, prothrombotic state, and premature atherosclerosis. Objective: To evaluate the relationships between asthma, inflammatory biomarkers, and parameters of endothelial dysfunction.

We analyzed flow-mediated dilatation (FMD) of the brachial artery and intima-media thickness (IMT) of the common carotid artery using ultrasound in 92 clinically stable adult asthmatics and 62 well-matched controls. We also measured blood levels of selected inflammatory and asthma-specific biomarkers, including interleukin (IL) 4, IL-5, IL-6, IL-10, IL-12 (p70), IL-17A, IL-23, and interferon γ, as well as a disintegrin and metalloproteinase domain-containing protein 33 (ADAM-33). In addition, we assessed endothelial damage using 2 laboratory biomarkers: circulating von Willebrand factor (vWF) and pentraxin-3. We analyzed relationships between the study variables and asthma severity, lung function abnormalities, airway remodeling indices on computed tomography, and transthoracic echocardiography parameters.

Asthmatics had higher IL-6, IL-10, and ADAM-33 levels. They were also characterized by 23% lower FMD% and 15% thicker IMT, as compared with controls (P<.001, both). In asthma, vWF was related to age (ß=0.28 [95%CI, 0.15-0.41]) and remained inversely associated with FEV1 (ß=-0.2 [95%CI, -0.05 to -0.35]). Surprisingly, a negative correlation was revealed between vWF and pentraxin-3 (ß=-0.17 [95%CI, -0.3 to -0.04]). Pentraxin-3 remained positively associated with airway remodeling indices.

Asthma is characterized by endothelial dysfunction associated with airway obstruction. The biological role of pentraxin-3 is unknown, although our data suggest a protective role against endothelial damage and atherosclerosis.