Search

Here we report a rare case of immunoglobulin G4 (IgG4)–related pleural disease diagnosed using a thoracoscopic pleural biopsy. A 66‐year‐old man was admitted to our hospital with right‐dominant bilateral pleural effusions and gradually worsening dyspnoea. Chest radiographs revealed right‐dominant pleural effusions, while chest computed tomography showed bilateral pleural effusions without parenchymal lesions. Although the bilateral pleural effusions were exudative with an increased number of lymphocytes, the definitive diagnosis was initially elusive. High IgG4 levels in the serum and pleural effusions were observed. A pathological evaluation of a right pleural biopsy specimen collected via video‐assisted thoracoscopic surgery showed fibrosis‐associated lymphoplasmacytic infiltration, 45–60 IgG4‐positive plasma cells per high‐power field, and an IgG4/immunoglobulin G ratio of 40%. Consequently, the patient was diagnosed with IgG4‐related pleural disease. The bilateral pleural effusions improved after corticosteroid therapy. [ABSTRACT FROM AUTHOR]

Introduction: Eosinophilic pneumonia (EP) is characterized by a marked accumulation of eosinophils in the lungs and blood. Eosinophils and mast cells play an important role in the pathogenesis of EP via release of biomarkers such as tryptase and interleukin (IL)-33. However, the potential role of these biomarkers is not fully understood. Objectives: We aimed to evaluate the differences among the levels of tryptase and IL-33 in bronchoalveolar lavage fluid (BALF) from several types of EP. We evaluated the differences between the levels of these biomarkers in the recurrent and nonrecurrent cases. Method: We prospectively collected the clinical data of patients with EP, diagnosed between 2006 and 2015 in our institution. Bronchoscopy was performed before steroid treatment; BALF was collected. The clinical characteristics of EP patients and the levels of tryptase and IL-33 in BALF were evaluated. Results: We enrolled 15 patients with chronic EP (CEP), 5 with acute EP (AEP), 10 with drug-induced EP, and 6 with angiitis-related EP. Tryptase levels in the CEP group were significantly higher than that in the drug-induced EP group (p = 0.048), while the AEP group had the highest IL-33 levels. Recurrence of EP was noted in 67% of patients with CEP. The levels of tryptase and IL-33 were notably higher in the recurrent cases than that in the nonrecurrent CEP group (p = 0.004, p = 0.04, respectively). Furthermore, there was a positive correlation between the levels of tryptase and IL-33 in the BALF of patients with CEP (ρ = 0.69, p = 0.004). Conclusions: Tryptase and IL-33 in BALF are useful biomarkers for the assessment of EP types. These biomarkers could be used to predict disease recurrence. [ABSTRACT FROM AUTHOR]

To examine the effect of adenosine [A.sub.3] receptor stimulation on airway mucociliary clearance, we measured transport of Evans blue dye in rabbit trachea in vivo and ciliary motility of epithelium by the photoelectric method in vitro. Mucociliary transport was enhanced dose dependently by the selective [A.sub.3] agonist [N.sup.6]-(3-iodobenzyl)-5'-N-methylcarbamoyladenosine (IB-MECA) and to a lesser extent by the less-selective [N.sup.6]-2-(4-amino-3-iodophenyl)ethyladenosine, whereas the [A.sub.1] agonist N-cyclopentyladenosine (CPA) and the [A.sub.2] agonist CGS-21680 had no effect. The effect of IB-MECA was abolished by pretreatment with the selective [A.sub.3] antagonist MRS-1220 but not by the [A.sub.1] antagonist 1,3-dipropyly-8-cyclopentylxanthine or the [A.sub.2] antagonist 3,7-dimethyl-L-propargylxanthine. Epithelial ciliary beat frequency was increased by IB-MECA in a concentration-dependent manner, the maximal increase being 33%, and this effect was inhibited by MRS-1220. The IB-MECA-induced ciliary stimulation was not altered by the Rp diastereomer of cAMP but was greatly inhibited by [Ca.sup.2+]-free medium containing BAPTAAM. Incubation with IB-MECA increased intracellular [Ca.sup.2+] contents. Therefore, [A.sub.3] agonist enhances airway mucociliary clearance probably through [Ca.sup.2+]-mediated stimulation of ciliary motility of airway epithelium. airway epithelium; adenine nucleotide; ciliary beat frequency; calcium

A study was conducted to demonstrate Ca2+ oscillations induced by exogenous adenosine triphosphate and its inhibition by FK506 in fura 2-loaded cow tracheal epithelial cells. Previous studies have reported that airway epithelial cells exhibit Ca2+ oscillations when responding to mechanical stimulation. Cow tracheal epithelial cells were used and later subjected to a Ca2+ image analysis. Findings reveal that FK506 has an inhibitory action on the Ca2+ response via intracellular FK-binding proteins, but not via calcineurin.

Experimental evidence shows that the antiallergic agent azelastine inhibits platelet-activating factor-induced microvascular leakage in airways in pathogen-free rats. This observation was confirmed in an experiment that assessed the amount of vascular leakage in rat airways by measuring the percent area occupied by Monastral blue-labeled blood vessels in the mucosae of the rat trachea and bronchus with a stereological point-counting technique. Findings showed that azelastine suppresses platelet-activating factor-induced airway inflammation, probably by attenuating the release of neutrophil elastase from activated neutrophils.