Primary diffuse Rosai-Dorfman disease in central airway: a case report and literature review.

BACKGROUND: Rosai-Dorfman disease (RDD) is a rare benign non-langerhans cell histiocytosis, mainly involving lymph nodes and skin. It is even rarer occurring only in central airway of lung and in diffuse form. Central airway RDD is similar to malignant tumor in imaging by radiological method and in bronchoscopy features. It is difficult to differentiate it from primary airway malignant tumor and to diagnose correctively in time. CASE PRESENTATION: Here we present a rare case of 18-year-old male diagnosed with primary diffuse RDD in central airway. Although the features examined by enhanced chest computed tomography, positron emission tomography/computed tomography, diffusion-weighted imaging of enhanced chest MRI and bronchoscopy indicate to be malignant tumor, the patient was definitely confirmed by multiple transbronchial biopsies and immunohistochemistry. After two transbronchial resections, the patient's symptoms of paroxysmal cough, whistle sound and shortness of breath were significantly reduced, as well as the airway stenosis was significantly improved. After 5 months of follow-up, the patient had no symptoms and the central airway were unobstructed. CONCLUSIONS: Primary diffuse RDD in central airway is characterized by intratracheal neoplasm, which is usually suspected as malignant tumor according to radiological image and bronchoscopy. Pathology and immunohistochemistry are necessary for definite diagnosis. Transbronchial resection is effective and safe for patients with primary diffuse RDD in central airway.

Down-regulation of SNHG16 alleviates the acute lung injury in sepsis rats through miR-128-3p/HMGB3 axis.

BACKGROUND: Long noncoding RNAs contribute to various inflammatory diseases, including sepsis. We explore the role of small nucleolar RNA host gene 16 (SNHG16) in sepsis-mediated acute lung injury (ALI) and inflammation. METHODS: A sepsis-induced ALI rat model was constructed by the cecal ligation and perforation method. The profiles of SNHG16, miR-128-3p, and high-mobility group box 3 (HMGB3) were monitored by quantitative reverse transcription PCR and Western blot. The pathologic changes of lung tissues were evaluated by Hematoxylin-Eosin staining, immunohistochemistry, and dry and wet method. Meanwhile, the pro-inflammatory factors and proteins were determined by ELISA and Western blot. In contrast, a sepsis model in BEAS-2B was induced with lipopolysaccharide (LPS) to verify the effects of SNHG16/miR-128-3p/HMGB3 on lung epithelial cell viability and apoptosis. RESULTS: As a result, SNHG16 and HMGB3 were up-regulated, while miR-128-3p was down-regulated in sepsis-induced ALI both in vivo and in vitro. Inhibiting SNHG16 reduced the apoptosis and inflammation in the sepsis-induced ALI model. Overexpressing SNHG16 promoted LPS-mediated lung epithelial apoptosis and inhibited cell viability and inflammation, while miR-128-3p had the opposite effects. Mechanistically, SNHG16 targeted miR-128-3p and attenuated its expression, while miR-128-3p targeted the 3' untranslated region of HMGB3. CONCLUSIONS: Overall, down-regulating SNHG16 alleviated the sepsis-mediated ALI by regulating miR-128-3p/HMGB3.

High expression of miR-483-5p aggravates sepsis-induced acute lung injury.

Sepsis-induced acute lung injury (ALI) has high morbidity and mortality rates, and there remains a need for therapeutic methods to improve the outcome of ALI patients. miR-483-5p is an important regulator for the development of various diseases such as sepsis. Nevertheless, it is not known whether miR-483-5p has an effect on sepsis-induced ALI. To explore this issue, this study used cecal ligation and puncture (CLP)-treated mice and lipopolysaccharide (LPS)-treated pulmonary microvascular endothelial cells (PMVECs) cells to simulate the models of sepsis-induced ALI in vivo and in vitro. Pathological and histological changes of lungs from sepsis-induced ALI mice were detected by Hematoxylin-eosin staining. The detection levels of caspase-3, interleukin (IL)-6 and IL-1ß were used to reflect the effect of miR-483-5p on apoptosis and inflammation of sepsis-induced ALI. The detection level of lactate dehydrogenase (LDH) in PMVECs cells was used to reflect the severe extent of sepsis-induced injury. The expression of miR-483-5p in lung tissues of sepsis-induced ALI mice was determined by qRT-PCR. In addition, the interaction of miR-483-5p with PIAS1 was identified and validated by Targetscan website and luciferase reporter assay, respectively. The results showed that miR-483-5p was up-regulated in the lung tissues of sepsis-induced ALI mice. Knockdown of miR-483-5p effectively ameliorated lung injury in mice with sepsis-induced ALI and inhibited inflammation and apoptosis of LPS-treated PMVECs cells. Furthermore, in vitro experiment revealed that PIAS1 was a potential target of miR-483-5p. Moreover, miR-483-5p could suppress PIAS1 expression to aggravate inflammation and apoptosis of LPS-treated PMVECs cells. These findings suggest miR-483-5p is a potential therapeutic and diagnostic biomarker for sepsis-induced ALI and provide a new insight for understanding the molecular mechanism of sepsis-induced ALI.