Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two male patients ages 54 and 58 years had persisting pneumonia with dry cough, dyspnea, weight loss, and fever up to 39 degrees C that did not respond to erythromycin treatment. There was extensive restrictive impairment of ventilation and loss of diffusing capacity for carbon monoxide. Histologic examination of the basal pulmonary infiltrates showed fibrosing alveolitis. Serologic titers indicated that the patients had suffered from Legionella pneumophila infection. We believe that Legionella had caused the fibrosing alveolitis since there was absence of any other causative agents or factors. Both patients responded to corticosteroid treatment with rapid clinical improvement but delayed radiologic regression.
 ...
PMID:Fibrosing alveolitis responsive to corticosteroids following Legionnaires' disease pneumonia. 812 53

Pneumonia was diagnosed radiologically in three patients (43, 54 and 58 years old, respectively), presenting with temperatures between 39 degrees and 40 degrees C, cough and weight loss. These signs persisted for 6, 7 and 13 weeks, respectively, but the pathogens could not be cultivated. Lung function analysis showed partial respiratory insufficiency with extensive restrictive impairment of ventilation. Samples of lung tissue were obtained in all three cases and histology revealed fibrosing alveolitis. In two patients serology yielded antibody titres of 1:512 and in one patient of 1:128, against Legionella pneumophila. Treatment with 1 g erythromycin three times daily was unsuccessful. Therefore, the patients were given prednisone at an initial dosage of 50-100 mg which was subsequently reduced. Lung function normalised during this treatment course, radiological findings and antibody titres receded. Hence, treatment with corticosteroids should be attempted if there is an urgent suspicion of fibrosing alveolitis caused by Legionella pneumophila, after having excluded a florid infectious pneumonia and after failure of erythromycin treatment.
 ...
PMID:[Persisting alveolitis after Legionella pneumonia]. 237 67

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.
 ...
PMID:Intraluminal fibrosis in interstitial lung disorders. 395 68

We reported a case of fibrosing alveolitis following Legionella pneumonia. A 62-year-old man was admitted to our hospital with fever after a visit to a hot spring. Chest X-ray films on admission demonstrated air-space consolidation in the right lower lung. Legionella pneumonia was diagnosed because the patient had elevated serum antibody to Legionella pneumophila serogroup Ia and tested positive for urinary antigen. Although he was initially treated with rifampicin and erythromycin, he experienced drug-induced eruptions. Antibiotic therapy was accordingly changed to clarithromycin, levofloxacin, and minocycline, which together alleviated the patient's clinical symptoms but delayed radiologic regression. Chest X-ray films 2 months after the onset of illness revealed diffuse ground-glass opacities and progressive reduction of volume in the right lung. Long-term corticosteroid treatment was required. Three and half months after disease onset, fever recurred with the appearance of interstitial shadows in the left lung and positive tests for urinary antigen. Increasing the corticosteroid dose resolved the patient's symptoms.
 ...
PMID:[Fibrosing alveolitis following Legionella pneumonia]. 1087 37

Toll-interacting protein (TOLLIP) is an intracellular adaptor protein with diverse actions throughout the body. In a context- and cell type-specific manner, TOLLIP can function as an inhibitor of inflammation and endoplasmic reticulum stress, an activator of autophagy, or a critical regulator of intracellular vacuole trafficking. The distinct functions of this protein have been linked to innate immune responses and lung epithelial cell apoptosis. TOLLIP genetic variants have been associated with a variety of chronic lung diseases including idiopathic pulmonary fibrosis, asthma, primary graft dysfunction following lung transplantation, and with infections such as tuberculosis, Legionella pneumonia, and respiratory viruses. TOLLIP exists in a delicate homeostatic balance, with both positive and negative effects on the trajectory of pulmonary diseases. This translational review summarizes the genetic and molecular associations that link TOLLIP to the development and progression of non-infectious and infectious pulmonary diseases. We highlight current limitations of in vitro and in vivo models in assessing the role of TOLLIP in these conditions, and we describe future approaches that will enable a more nuanced exploration of the role of TOLLIP in pulmonary conditions. There has been a surge in recent research evaluating the role of of this protein in human diseases, but critical mechanistic pathways require further exploration. By understanding its biologic functions in disease-specific contexts, we will be able to determine whether TOLLIP can be therapeutically modulated to treat pulmonary diseases.
 ...
PMID:TOLL-interacting Protein in Pulmonary Diseases: Abiding by the Goldilocks Principle. 3323 20