A review of inflammatory mechanism in airway diseases

Aghasafari, Parya; George, Uduak Z.; Pidaparti, Ramana M.

doi:10.1007/s00011-018-1191-2

Cited by 199 publications

(145 citation statements)

References 179 publications

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“…We also demonstrated that, compared with COT, HFNC effectively elevated PO 2 in patients with severe bronchial asthma complicated with respiratory failure. Although related studies on HFNC in treating adult patients with asthma are rare, these findings corroborated previous studies evaluating type I respiratory failure [23,24]. Many studies on severe pneumonia, ARDS, status-post surgery, and weaning of mechanical ventilation showed that HFNC elevates PO 2 in patients with type I respiratory failure and mild type 2 respiratory failure [8][9][10][11]25].…”

Section: Discussionsupporting

confidence: 75%

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High-Flow Nasal Cannula: A Promising Oxygen Therapy for Patients with Severe Bronchial Asthma Complicated with Respiratory Failure

Geng

Batu

You

et al. 2020

Canadian Respiratory Journal

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Severe bronchial asthma complicated with respiratory failure, a common critical illness in respiratory medicine, may be lifethreatening. High-flow nasal cannula (HFNC) is a novel oxygen therapy technique developed in recent years. HFNC was applied in this study for treating adult patients with severe bronchial asthma complicated with respiratory failure. Its efficacy was analyzed comparatively to conventional oxygen therapy (COT). HFNC and COT were randomly performed based on conventional treatment. e HFNC group was similar to COT-treated patients in terms of response rate, with no significant difference in efficacy between the two groups. In patients with bronchial asthma, effectively increased PO 2 and reduced PCO 2 were observed after treatment in both groups. However, HFNC was more efficient than COT in elevating PO 2 in patients with severe bronchial asthma complicated with respiratory failure, while no statistically significant difference in PCO 2 reduction was found between the two groups. Heart rate (HR) and respiratory rate (RR) between the two groups on admission (0 h) and at 2, 8, 24, and 48 h after admission were compared. Both indicators significantly decreased with time. No significant differences in HR and RR were found between the groups at 0, 2, and 8 h after admission. However, these indicators were significantly lower in the HFNC group compared with the COT group at 24 and 48 h after admission. HFNC could significantly elevate PO 2 and reduce HR and RR. us, it is a promising option for patients with severe bronchial asthma complicated with respiratory failure.

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Section: Discussionsupporting

confidence: 75%

“…(2) hyperventilation and excessive sweating leading to water loss cause difficulty in expectorating and further result in ventilatory dysfunction and its exacerbation; and (3) infection causes bronchial mucosal edema, increases secretions, aggravates obstruction, and ultimately leads to respiratory failure [1,23].…”

Section: Discussionmentioning

confidence: 99%

High-Flow Nasal Cannula: A Promising Oxygen Therapy for Patients with Severe Bronchial Asthma Complicated with Respiratory Failure

Geng

Batu

You

et al. 2020

Canadian Respiratory Journal

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“…Epithelial cells recognized microorganisms through toll-like receptors (TLRs), activated NF-κΒ signaling pathways and increased airway epithelial in ammatory cytokines such as IL-8, IL-1α and tumor necrosis factor-α (TNF-α) [3].…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade

Chen

Zhang

Xiao

et al. 2020

Preprint

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Objective: To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under treatment of Dexamethasone (Dex).Methods: IL-1β (10 ng/mL) and LPS (1 μg/mL) was used to induce an inflammatory cell model with A549 cells, and the results showed that IL-1β performed better against LPS. Dex with different concentration was used to attenuate inflammation by IL-1β, and its effect was assessed by RT-PCR to detect the inflammatory related mRNA, including IKβ-α, IKKβ, IL-6, IL-8, and TNF-α. And ELISA to detect the inflammatory cytokines TNF-α, IL-6 and IL-8. RT-PCR was used to quantify levels of lncRNAs, including lncMALAT1, lncHotair, lncH19, and lncNeat1. LncH19 was most closely correlated with the inflammatory response, which was induced by IL-1β and attenuated by Dex. Among the lncRNAs, the level of lncH19 exhibited the highest increase following treatment with 1 μM and 10 μM Dex. Therefore, lncH19 was selected for further function study. LncH19 expression was inhibited by shRNA transduced by lentivirus. Cell assays for cell proliferation and apoptosis as well as RT-PCR, western blot, and ELISA for inflammatory related genes were conducted to confirm the functions of lncH19. Predicted target miRNAs of lncH19 included the following: hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p and hsa-miR-19a-3p. Following estimation by RT-PCR, hsa-miR-346, hsa-miR-18a-3p and hsa-miR-324-3p showed consistent patterns in A549 NC and A549 shlncH19. miRNA inhibitor was transfected into A549 NC and A549 shlncH19cells, and expression levels were determined by RT-PCR. Hsa-miR-324-3p was inhibited the most relative to hsa-miR-346 and hsa-miR-18a-3p and was subjected to further function study. RT-PCR, ELISA and western blotting for inflammatory related genes detection were conducted to validate the functions of the target hsa-miR-324-3p.Results: Dex with 1 μM and 10 μM were shown to be effective in attenuating the inflammatory response. During this process, lncH19 significantly increased in expression (P < 0.05). Dex with 1 μM was for further study. Under IL-1β treatment with or without Dex, the inhibition of lncH19 lead to an increase cell proliferation, a decrease in cell apoptosis, an increase in the protein level of inflammatory-related genes, the phosphorylation of P65, ICAM-1 and VCAM-1, and inflammatory cytokines. Following prediction of the targets of lncH19 and validation by RT-PCR, miR-346, miR-18a-3p and miR-324-3p were found to be negatively correlated to lncH19. Additionally, Dex increased the expression of lncH19, but the expression of the miRNAs was reduced. Among miRNAs, miR-324-3p was the most markedly down-regulated following treatment of miRNA inhibitors. The MTS assay and cell apoptosis assay showed that the miR-324-3p inhibitor inhibited cell proliferation and induced cell apoptosis, thereby significantly attenuating the inflammatory response, which reversed the effect of lncH19 in regulating cell proliferation and the secretion of inflammatory cytokines (P < 0.05). Therefore, lncH19 might regulate miR-324-3p during Dex treatment in pulmonary inflammatory response.Conclusion: Dex can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade.

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“…It has been demonstrated that the mechanism of COPD is complex and involves a number of pathways. Most importantly, the in ammatory signaling exhibit the vital effects on pulmonary in ammation, which may provide major therapeutic targets in COPD [24,25]. TLR4 is a pattern recognition receptor that is typically known to play a major role in generating an in ammatory response by way of activating various essential downstream components [26].…”

Section: Discussionmentioning

confidence: 99%

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

Zhang¹,

Wang²,

Liu³

et al. 2020

Preprint

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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A review of inflammatory mechanism in airway diseases

Cited by 199 publications

References 179 publications

High-Flow Nasal Cannula: A Promising Oxygen Therapy for Patients with Severe Bronchial Asthma Complicated with Respiratory Failure

High-Flow Nasal Cannula: A Promising Oxygen Therapy for Patients with Severe Bronchial Asthma Complicated with Respiratory Failure

Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

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