Objective To analyze the data from patients with pathologically proved granulomatous lung disease, including etiology, clinical, radiological features and laboratory results. Methods 36 patients with granulomatous lung disease confirmed by lung biopsy in Shanghai First People’s Hospital of Shanghai Jiao Tong University from January 2008 to June 2012 were retrospectively reviewed. The clinical presentation, radiological features and laboratory results were collected and statistically analyzed.Results After haematoxylin and eosin stain combined with special stain, the diagnoses were comfirmed, ie.13 cases of mycobacterial infection, 5 cases of aspergillar infection, 4 cases of cryptococcal infection, 6 cases of sarcoidosis, 4 cases of Wegener’s granulomatosis, 4 cases of unknown causes. Cough was the most common clinical symptom, followed by expectoration. Some patients also developed fever, chest tightness and weight loss. The lesions were widely distributed, of which the right upper lung was the common lesion of mycobacterial infection, inferior lobe of right lung was the common lesion of aspergillar infection. The common lesion of cryptococcal infection was uncertain. The common lesions of sarcoidosis and Wegener ’s granulomatosis were in left upper lung. Small nodule was the most common shapes of lesion, while mass and consolidation were present sometimes. Cavity, air bronchogram, pleural effusion, hilar and mediastinal lymph node enlargement could be found in the chest CT. Interferon gamma release assay, galactomannan antigen assay and latex agglutination test were helpful in the diagnosis of mycobacterial infection, aspergillar infection and cryptococcal infection induced granuloma. Conclusions The clinical presentations and radiological features of granulomatous lung disease are nonspecific. Histopathology obtained through biopsy is the key for the diagnosis. Immunological examination, test of new antigens to microorganism and clinical microorganism detection are valuble in the diagnosis and differential diagnosis of granulomatous lung disease.
ObjectiveTo investigate the effects of interleukin (IL)-26 on the late phase of lipopolysaccharides (LPS)-induced lung inflammation in mouse model.MethodsThirty-two mice were equally and randomly divided into four groups: blank control group, IL-26 control group, LPS model group, and IL-26 intervention group. The blank control group was given intranasal administration of phosphate buffered solution (PBS, 40 μl) and PBS (40 μl) 10 minutes apart. The IL-26 control group was given recombinant human interleukin-26 (rhIL-26; 50 μg/kg, dissolved in 40 μg PBS) and PBS successively. The LPS model group was given intranasal administration of PBS (40 μl) and LPS (10 mg/kg, dissolved in 40 μl PBS) at 10 minutes interval. The IL-26 intervention group was given intranasal administration of rhIL-26 and LPS at 10 minutes interval. Seventy-two hours later after treatment, bronchoalveolar lavage fluid (BALF) cell count, cytokine assay and pathological staining of lung tissue were performed in each group. The gene expression of inflammatory pathway in lung tissue was detected by RT-PCR. One-way ANOVA was used for comparison between groups. ResultsCompared with the blank control group, the expression of tumor necrosis factor-α and activating transcription factor 3 in IL-26 control group increased significantly (all P < 0.05). The number of peripheral blood mononuclear cells, total BALF cells, lymphocytes and neutrophils, and the content of macrophage inflammatory protein-1a in BALF were significantly increased in IL-26 intervention group comparing with LPS model group (all P < 0.05). IL-26 intervention group had more inflammatory subsidence in interstitial, perivascular, peribronchial and mean values than LPS model group (all P < 0.05). The expressions of Toll-like receptor 4, Toll-like receptor 2 and interferon γ induced protein 10 in IL-26 intervention group were significantly higher than those in LPS model group (all P < 0.05).ConclusionIL-26 can significantly alleviate the late inflammatory reaction of lung tissue in LPS-induced mouse inflammation model.