Eosinophil-Associated Lung Diseases. A Cry for Surfactant Proteins A and D Help?

Abstract

Surfactant proteins (SP)-A and SP-D (SP-A/-D) play important roles in numerous eosinophil-dominated diseases, including asthma, allergic bronchopulmonary aspergillosis, and allergic rhinitis. In these settings, SP-A/-D have been shown to modulate eosinophil chemotaxis, inhibit eosinophil mediator release, and mediate macrophage clearance of apoptotic eosinophils. Dysregulation of SP-A/-D function in eosinophil-dominated diseases is also not uncommon. Alterations in serum SP-A/-D levels are associated with disease severity in allergic rhinitis and chronic obstructive pulmonary disease. Furthermore, oligimerization of SP-A/-D, necessary for their proper function, can be perturbed by reactive nitrogen species, which are increased in eosinophilic disease. In this review, we highlight the associations of eosinophilic lung diseases with SP-A and SP-D levels and functions.

Limonene and its ozone-initiated reaction products attenuate allergic lung inflammation in mice

“…Thus, the significantly lower content of SP-D in BALF of the allergic LIM and MIX mice may reflect lower requirement for protection against oxidative stress. Also, a feedback regulation between eosinophils and SP-D occurs in allergic inflammation (Ledford et al 2014); this was reflected in particular in the MIX group in the present data set. Overall, this study supports SP-D as being a marker of oxidative stress and/or of immunomodulation.…”

“…Post-translational modifications of SP-D occur due to reactive oxygen species (ROS) exposure, which enhances the pro-inflammatory signaling of SP-D (Ledford et al 2014). Thus, the significantly lower content of SP-D in BALF of the allergic LIM and MIX mice may reflect lower requirement for protection against oxidative stress.…”

Asthmatics with high levels of serum surfactant protein D have more severe disease

“…The number of recruited subjects is relatively small since the study was intended as explorative, and therefore, conclusions should be drawn with caution. Indeed, SP-D promotes the clearance of pathogens, enhances the phagocytosis of apoptotic cells and inhibits pro-inflammatory cytokine release by effector cells [11][12][13]. We favour the hypothesis that altered surfactant would be the underlying cause of the impairment in the bronchodilatory effect of deep inspirations that has been observed in asthma [14].…”

Effect of controlled human exposure to diesel exhaust and allergen on airway surfactant protein D, myeloperoxidase and club (Clara) cell secretory protein 16

“…Surfactant protein D is primarily produced by Type II pneumocytes in the distal airways, and has both direct and indirect effects on the innate immunity of the lung, including the regulation of eosinophils . Bronchial SPD is reduced in healthy smokers compared to controls and increased in asthmatic patients when compared to healthy controls .…”