Insuficiencia respiratoria progresiva secundaria a fibrosis pulmonar en una escolar: Caso clínico

D, Ignacio Sánchez; M, Paula Pérez-Canto; M, Gonzalo Urcelay; B, Cristián García; Vega-Briceño, Luis Enrique; B, Sergio González

doi:10.4067/s0034-98872005000100011

Cited by 2 publications

(2 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is further demonstrated by the alleviation of respiratory symptoms and improvement in pulmonary function after the use of macrolides to treat MP infection . The symptoms of pneumonia caused by MP are correlated with the upregulated expression of proinflammatory cytokines and induction of pulmonary fibrosis . In this study, the expression levels of the inflammation factors IL‐6, IL‐1β, TNF‐α, and MCP‐1 were increased in mouse serum after MP infection, while PD treatment suppressed these trends, suggesting that PD has conveyed anti‐inflammation effects, as reported in previous studies .…”

Section: Discussionsupporting

confidence: 83%

“…25 The symptoms of pneumonia caused by MP are correlated with the upregulated expression of proinflammatory cytokines 26 and induction of pulmonary fibrosis. 10,27 In this study, the expression levels of the inflammation factors IL-6, IL-1β, TNF-α, and MCP-1 were increased in mouse serum after MP infection, while PD treatment suppressed these trends, suggesting that PD has conveyed anti-inflammation effects, as reported in previous studies. 28,29 Meanwhile, PD treatment also suppressed pulmonary injury by suppressing MPP-induced apoptosis and pulmonary fibrosis.…”

Section: Discussionsupporting

confidence: 82%

See 1 more Smart Citation

Polydatin suppresses the development of lung inflammation and fibrosis by inhibiting activation of the NACHT domain‐, leucine‐rich repeat‐, and pyd‐containing protein 3 inflammasome and the nuclear factor‐κB pathway after Mycoplasma pneumoniae infection

Tang

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Mycoplasma pneumoniae (MP) can infect both the upper and lower respiratory tracts. Polydatin (PD), a traditional Chinese medicine, is known to have anti-inflammation and antifibrosis properties. However, the protective effects of PD against MP pneumonia (MPP) remain unclear. So, the aim of this study was to describe the therapeutic effects and underlying mechanisms of PD against MPP. BALB/c mice were assigned to three groups: a normal control group, MP infection group, or PD-treated MP infection group. BEAS-2B cells transfected with or without NACHT domain-, leucine-rich repeat-, and pyd-containing protein 3 (NLRP3) were used to confirm the protective mechanisms of PD. Immunohistochemical analysis, Western blot analysis, enzyme-linked immunosorbent assay, and flow cytometry were used in this study. The results showed that PD treatment suppressed MP-induced lung injury in mice by suppressing the expression of inflammatory factors and inhibiting the development of pulmonary fibrosis. Meanwhile, PD treatment inhibited activation of the NLRP3 inflammasome and nuclear factor κB (NF-κB) pathway. Overexpression of NLRP3 reversed the protective effect of PD against MPinduced injury of BEAS-2B cells. Taken together, these results indicate that PD treatment suppressed the inflammatory response and the development of pulmonary fibrosis by inhibiting the NLRP3 inflammasome and NF-κB pathway after MP infection. K E Y W O R D S fibrosis, inflammation, Mycoplasma pneumoniae, NACHT domain-, leucine-rich repeat-, and pyd-containing protein 3, polydatin

show abstract

Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 82%

Polydatin suppresses the development of lung inflammation and fibrosis by inhibiting activation of the NACHT domain‐, leucine‐rich repeat‐, and pyd‐containing protein 3 inflammasome and the nuclear factor‐κB pathway after Mycoplasma pneumoniae infection

Tang

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

The Protective Effect of Naringenin on Airway Remodeling afterMycoplasma PneumoniaeInfection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis

Tan

Kan

Xiao

et al. 2018

Mediators of Inflammation

View full text Add to dashboard Cite

Our previous study has shown that Chinese medicine, Qingfei Tongluo formula (QTF), has a significantly therapeutic effect to Mycoplasma pneumoniae (MP) pneumonia (MPP). The aim of this study was to investigate the therapeutic effect and mechanism of naringenin (NRG) on MPP which was an important component of QTF. Here, we studied 124 children with or without MPP and compared inflammatory cytokines and fibrinogen-related protein expression with enzyme-linked immunosorbent assay. We also employed a BALB/c mouse model of MPP and divided the mice into three groups: ctrl (normal control mice), MPP (MP-infected mice), and MPP + NRG (MP-infected mice treated with NRG). BEAS-2B cells were used to confirm the relationship between autophagy, inflammation, and fibrosis. The results show proinflammatory cytokines (interleukin- [IL-] 6, IL-1β, and tumor necrosis factor-α), and transforming growth factor beta (TGF-β) expression was significantly increased after MP infection from both clinical and animal experiment. In vivo experimental confirmation showed that NRG treatment decreased MPP-induced lung injury in mice by inhibiting autophagy-mediated inflammatory cytokine expression and pulmonary fibrosis. In vitro experiments confirmed it. These results indicate that NRG treatment suppressed the inflammatory response and pulmonary fibrosis by inhibition of autophagy after MP infection.

show abstract

Insuficiencia respiratoria progresiva secundaria a fibrosis pulmonar en una escolar: Caso clínico

Cited by 2 publications

References 15 publications

Polydatin suppresses the development of lung inflammation and fibrosis by inhibiting activation of the NACHT domain‐, leucine‐rich repeat‐, and pyd‐containing protein 3 inflammasome and the nuclear factor‐κB pathway after Mycoplasma pneumoniae infection

Polydatin suppresses the development of lung inflammation and fibrosis by inhibiting activation of the NACHT domain‐, leucine‐rich repeat‐, and pyd‐containing protein 3 inflammasome and the nuclear factor‐κB pathway after Mycoplasma pneumoniae infection

The Protective Effect of Naringenin on Airway Remodeling afterMycoplasma PneumoniaeInfection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis

Contact Info

Product

Resources

About