Background Surfactant protein D (SP-D) is a collection that plays important roles in modulating host defense functions and maintaining phospholipid homeostasis in the lung. The aim of current study was to characterize comparatively the SP-D response in bronchoalveolar lavage (BAL) and serum in three murine models of lung injury, using a validated ELISA technology for estimation of SP-D levels. Methods Mice were exposed to lipopolysaccharide, bleomycin, or Pneumocystis carinii (Pc) and sacrificed at different time points. Results In lipopolysaccharide-challenged mice, the level of SP-D in BAL increased within 6 h, peaked at 51 h (4,518 ng/ml), and returned to base level at 99 h (612 ng/ml). Serum levels of SP-D increased immediately (8.6 ng/ml), peaked at 51 h (16 ng/ml), and returned to base levels at 99 h (3.8 ng/ml). In a subacute bleomycin inflammation model, SP-D levels were 4,625 and 367 ng/ml in BAL and serum, respectively, 8 days after exposure. In a chronic Pc inflammation model, the highest level of SP-D was observed 6 weeks after inoculation, with BAL and serum levels of 1,868 and 335 ng/ml, respectively. Conclusions We conclude that serum levels of SP-D increase during lung injury, with a sustained increment during chronic inflammation compared with acute inflammation. A quick upregulation of SP-D in serum in response to acute airway inflammation supports the notion that SP-D translocates from the airways into the vascular system, in favor of being synthesized systemically. The study also confirms the concept of using increased SP-D serum levels as a biomarker of especially chronic airway inflammation.
The complement system is an important part of our immune system, and complement defects lead generally to increased susceptibility to infections and autoimmune diseases. We have studied the role of complement activity in relation with chronic rhinosinusitis (CRS), and more specifically studied whether complement defects collectively predispose individuals for CRS or affect CRS severity. The participants comprised 87 CRS patients randomly selected from the general population, and a control group of 150 healthy blood donors. The CRS patients were diagnosed according to the European Position Paper on Rhinosinusitis and nasal Polyps criteria, and severity was evaluated by the Sino-nasal Outcome Test-22. Serum samples were analysed by ELISA for activity of the respective pathways of complement, and subsequently for serum levels of relevant components. We found that the frequency of complement defects was significantly higher among CRS patients than among healthy control subjects. A majority of Mannan-binding lectin deficient CRS patients was observed. The presence of complement defects had no influence on the severity of subjective symptoms. Our studies show that defects in the complement system collectively may play an immunological role related to the development of CRS. However, an association between severity of symptoms and presence of complement defects could not be demonstrated.
Aims: To investigate the presence of surfactant protein (SP) A, B, C and D in nasal airways and to determine whether the proteins exert their main functions in nasal secretions or in the deeper layers of the nasal mucosa. Methods: Volunteers were recruited from the Department of ENT Head and Neck Surgery, Odense University Hospital, Denmark. The study included 39 subjects. Nasal mucosal biopsies were analyzed by immunohistochemistry, and bronchoalveolar and nasal lavages, nasal brush biopsies and nasal mucus were analyzed for SP-A, -B, -C and -D by SDS-PAGE and Western blotting. The presence of SP-A and SP-D in the first three samplings were also analyzed by enzyme-linked immunosorbent assay. Results: In nasal mucosal biopsies, SP-A, -B, -C and -D were all demonstrated in the serous acini of the submucosal glands and in the surface epithelium. SP-D was detected in nasal brush biopsies, whereas the other SPs were absent. Moreover, SP-A, -B, -C and -D were absent in nasal lavage and mucus. Conclusion: SP-A, -B, -C and -D exert their protective effect in the ductal epithelium of the submucosal glands rather than in nasal secretions and mucus. Further studies are required to clarify the functions of these proteins in nasal secretory pathways for understanding upper airway diseases. i 2014 S. Karger AG, Basel
Objective Vocal cord paralysis (VCP) may be caused by a primary malignancy and associated immune cross‐reactivity. We aimed to illuminate underlying causes of VCP and to assess if onconeural antibodies occur in association to VCP as an early predictor of cancer. Methods A prospective study was performed in patients with newly diagnosed VCP from 2014 to 2016. All patients underwent fiberoptic laryngoscopy, ultrasound of the neck and computed tomography (CT) of the neck and thorax. Patients with idiopathic VCP underwent neurological examination, positron emission tomography/CT, and serum analysis for onconeural antibodies. All patients were offered a one‐year clinical follow‐up. Results In total 53 patients fulfilled the inclusion criteria. Left VCP occurred in 37 (70%), right in 15 (28%), and bilateral in one patient (2%). The cause of VCP was cancer in 27 (51%) patients, of those 15 (56%) had VCP as the primary symptom, including all cases with laryngeal and esophageal cancer. Median time interval between VCP and cancer was 7 days (range 1–30). In 12 (23%) VCP was a secondary symptom. Lung cancer was the most common etiology, 14 of 27 (52%), 12 patients (86%) with non‐small cell lung cancer. Idiopathic VCP was diagnosed in 18 (34%) patients, of those nine patients had a neurological examination and were screened for well‐known onconeural antibodies, which were not detected. Reactions against Purkinje cell nuclei were seen in three patients, none showed symptoms or signs of cancer at follow‐up. Conclusions The causes of VCP were described. VCP was frequently the primary symptom, and also occurred as a secondary symptom of cancer. Exclusion of malignancy is important in patients with VCP. Level of Evidence 1b
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.