Endobronchial Ultrasound-guided Transbronchial Needle Aspiration for the Diagnosis of Intrathoracic Lesions : Experience of a Single Academic Medical Center

Article信州医学雑誌 60(5): 249-255(2012)journal articl

Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice

Background IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33(-/-) mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33(-/-) mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33(-/-) and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33(-/-) mice than WT mice. IL-33(-/-) mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD

IgG4-Related Airway Involvement Which Developed in a Patient Receiving Corticosteroid Therapy for Autoimmune Pancreatitis

A 66-year-old man was diagnosed with autoimmune pancreatitis in February 2009 and started 40 mg of oral prednisolone followed by a maintenance dose of 5 mg daily. The patient developed a cough in October 2010 and visited our division. He had a high serum concentration of immunoglobulin (Ig) G4 and his chest computed tomography showed airway stenosis without bilateral hilar lymphadenopathy (BHL). The bronchial biopsy specimens revealed lymphoplasmacytic infiltrations with IgG4-positive/IgG-positive plasma cells of more than 50%. Thus, we diagnosed the airway lesion with IgG4-related airway involvement. This is the first report of a patient with IgG4-related airway involvement without BHL.ArticleINTERNAL MEDICINE. 50(24):3023-3026 (2011)journal articl

Respiratory lesions in IgG4-related disease: classification using 2019 American College of Rheumatology/European League Against Rheumatism criteria

In this study, ILDs involving IgG4-positive plasma cell infiltration were classified using the 2019 ACR/EULAR criteria. Most IgG4-positive interstitial pneumonia cases were excluded, suggesting the need for a unique treatment strategy. https://bit.ly/38GiUJ