scholarly journals Pendekatan Diagnosis Terbaru Vaping Associated Pulmonary Injury (VAPI)

2020 ◽  
Vol 2 (1) ◽  
pp. 74-80
Author(s):  
Anisa Ramadhanti

Rokok elektronik atau vape diklaim lebih aman dan lebih tidak berbahaya karena lebih sedikit mengandung bahan kimia toksik dibandingkan rokok konvensional. Walaupun demikian, masih banyak pihak yang mempertanyakan keamanan rokok elektronik. Liquid dalam rokok elektronik dan aerosol yang dihasilkan terbukti mengandung sejumlah komponen kimia yang kemungkinan memiliki efek yang berbahaya terhadap kesehatan, terutama paru yang dapat menyebabkan vaping-associated pulmonary injury (VAPI). Berdasarkan laporan kasus sebelumnya, VAPI terbagi menjadi beberapa spektrum penyakit, diantaranya adalah pneumonia eosinofilik akut, organizing pneumonia, lipoid pneumonia, kerusakan alveolus difus, dan acute respiratory distress syndrome (ARDS), perdarahan alveolar difus, pneumonitis hipersensitif, dan yang paling jarang yaitu giant-cell interstitial pneumonitis. Terdapat definisi kasus yang terbaru dalam menegakkan diagnosis VAPI, serta tatalaksana

2020 ◽  
Author(s):  
Xianyu Mu ◽  
Hongrong Wang ◽  
Haiyong Li

Abstract Background: This study aimed to explore the function of long noncoding RNA H19 (H19) on pulmonary injury, inflammation and fibrosis in lipoproteins (LPS)-induced acute respiratory distress syndrome (ARDS) rats. Methods: The LPS-induced ARDS rat model was established by intratracheal instillation with 2 mg/kg LPS. QRT-PCR was performed to detect the expression of H19, miR-423-5p, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6,, monocyte chemoattractant protein (MCP)-1 and vascular endothelial growth factor (VEGF). Histology score was detected by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines and the concentration of VEGF in bronchoalveolar lavage fluid (BALF). The protein expression of fiber factors was measured by western blot. The degree of fibrosis was observed by masson-trichrome staining. Dual-luciferase reporter assay was used to determine the binding site between miR-423-5p and H19.Results: The expression of H19 was significantly increased, while miR-423-5p was decreased in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1β, IL-6, MCP-1 and VEGF in LPS-induced ARDS rats, and decreased the levels of TNF-α, IL-1β, IL-6and the concentration of VEGF in BALF, histology score of LPS-induced ARDS rats. H19 inhibition also decreased the fibrosis score and the proteins expression of fiber factors of LPS-induced ARDS rats. Furthermore, miR-423-5p eliminated the effect of H19 on LPS-induced MH-S cells.Conclusions: Silencing of H19 ameliorated the pulmonary injury, inflammation and fibrosis of LPS-induced ARDS through regulating miR-423-5p, which may be a promising therapeutic strategy to treat ARDS.


2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Yufeng Liang ◽  
Junjie Xie ◽  
Di Che ◽  
Chunmin Zhang ◽  
Yongmin Lin ◽  
...  

Abstract Background: Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury that has a high mortality rate and leads to substantial healthcare costs. MicroRNA-124-3p (miR-124-3p) helps to suppress inflammation during a pulmonary injury. However, its mechanism of action is largely unknown, and its role in ARDS remains to be determined. Methods: Mice and NR8383 cells were exposed to lipopolysaccharides (LPS) to induce ARDS, and their miR-124-3p levels were determined. After a miRNA agomir was administrated to the mice, their pulmonary injuries were evaluated by H&E staining and assays for peripheral inflammatory cytokine levels. The direct interaction between miR-124-3p and p65 was predicted, and then confirmed by a luciferase activity assay. The role played by miRNA-124-3p in regulating p65 expression was further examined by transfection with its agomir, and its role in cell apoptosis was investigated by observing the effects of miRNA overexpression in vitro and in vivo. Results: After exposure to LPS, there was a consistent decrease in miR-124-3p expression in the lungs of mice and in NR8383 cells. After treatment with the miR-124-3p agomir, the degrees of pulmonary injury (e.g. alveolar hemorrhage and interstitial edema), and the increases in IL-1β, IL-6, and TNF-α levels induced by LPS were significantly attenuated. Overexpression of miR-124-3p in NC8383 cells and lung tissues significantly suppressed LPS-induced p65 expression and cell apoptosis. Conclusions: These results suggest that miR-124-3p directly targeted p65, and thereby decreased the levels of inflammation and pulmonary injury in a mouse model of ARDS.


2011 ◽  
Vol 9 (3) ◽  
pp. 386-388
Author(s):  
João Fernando Lourenço de Almeida ◽  
Adalberto Stape ◽  
Eduardo Juan Troster

ABSTRACT Mycoplasma pneumoniae is recognized as an important agent of pneumonia in pediatric population. In rare situations, severe pulmonary injury can develop. The use of corticoids in these cases remains controversial. A case of a girl with acute respiratory distress syndrome and bilateral pleural effusion secondary to pneumonia due to Mycoplasma pneumoniae is described, with good recovery after appropriate use of methylprednisolone and clarythromicyn.


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