Alveolar NF-κB signaling regulates endotoxin-induced lung inflammation

López, Benjamín; Maisonet, Tiffany M.; Londhe, Vedang A.

doi:10.3109/01902148.2014.977461

Cited by 20 publications

(15 citation statements)

References 43 publications

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“…Clinical research has reported that the degree of NF-jB activation was increased in patients with sepsis or acute lung injury (Schwartz et al 1996). Additionally, animal studies showed that inactivation of NF-jB pathway by pharmacological inhibition or gene modification decreased the expression of pro-inflammatory mediators and diminished the severity of endotoxemia-induced acute lung injury Lopez et al 2015). In the present study, the nuclear proteins from lung tissues were extracted.…”

Section: Discussionmentioning

confidence: 83%

Standardized myrtol attenuates lipopolysaccharide induced acute lung injury in mice

Wan

et al. 2016

Pharmaceutical Biology

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Context: Standardized myrtol, an essential oil containing primarily cineole, limonene and a-pinene, has been used for treating nasosinusitis, bronchitis and chronic obstructive pulmonary disease (COPD). Objective: To investigate the effects of standardized myrtol in a model of acute lung injury (ALI) induced by lipopolysaccharides (LPS). Materials and methods: Male BALB/c mice were treated with standardized myrtol for 1.5 h prior to exposure of atomized LPS. Six hours after LPS challenge, lung injury was determined by the neutrophil recruitment, cytokine levels and total protein concentration in the bronchoalveolar lavage fluid (BALF) and myeloperoxidase (MPO) activity in the lung tissue. Additionally, pathological changes and NF-jB activation in the lung were examined by haematoxylin and eosin staining and western blot, respectively. Results: In LPS-challenged mice, standardized myrtol at a dose of 1200 mg/kg significantly inhibited the neutrophile counts (from 820.97 ± 142.44 to 280.42 ± 65.45, 10 3 /mL), protein concentration (from 0.331 ± 0.02 to 0.183 ± 0.01, mg/mL) and inflammatory cytokines level (TNF-a: from 6072.70 ± 748.40 to 2317.70 ± 500.14, ng/mL; IL-6: from 1184.85 ± 143.58 to 509.57 ± 133.03, ng/mL) in BALF. Standardized myrtol also attenuated LPS-induced MPO activity (from 0.82 ± 0.04 to 0.48 ± 0.06, U/g) and pathological changes (lung injury score: from 11.67 ± 0.33 to 7.83 ± 0.79) in the lung. Further study demonstrated that standardized myrtol prevented LPS-induced NF-jB activation in lung tissues. Discussion and conclusion: Together, these data suggest that standardized myrtol has the potential to protect against LPS-induced airway inflammation in a model of ALI. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 83%

Standardized myrtol attenuates lipopolysaccharide induced acute lung injury in mice

Wan

et al. 2016

Pharmaceutical Biology

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“…AECII can decrease surface tension to prevent atelectasis and absorb fluid to prevent pulmonary edema. AECII help maintain normal air exchange function of the lung, and possess stem cell function in lung development and damage repair [5,6]. Because the biological characters of AECII are highly dependent on lung microenvironment, AECII would lose specific characteristics and differentiate into AECI after in vitro culture [22].…”

Section: Discussionmentioning

confidence: 99%

“…Abnormal inflammatory response to cigarette smoke in the lung promotes COPD development [4]. Alveolar type II epithelial cells (AECII) play important role in the maintenance of normal lung structure and help the repair and recovery of the lung after biological and physical lung damages [5,6]. Cigarette smoking has been shown to cause the apoptosis of AECII [7].…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic Reticulum Stress Induces HRD1 to Protect Alveolar Type II Epithelial Cells from Apoptosis Induced by Cigarette Smoke Extract

Tan

Jiang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cigarette smoking is a major risk factor of chronic obstructive pulmonary disease. This study aimed to examine the effects of cigarette smoke extract (CSE) on alveolar type II epithelial cells (AECII) and investigate the underlying mechanism. Methods: Primary AECII were isolated from rat lung tissues and exposed to CSE. Apoptosis was detected by flow cytometry. Protein expression was detected by Western blot analysis. Results: Primary rat AECII maintained morphological and physiological characteristic after 3 passages. CSE increased the expression of ER specific pro-apoptosis factors CHOP and caspase 12, and the phosphorylation of JNK in AECII. CSE activated ER stress signaling and increased the phosphorylation of PERK, eIF2α and IRE1. Furthermore, CSE induced the expression of Hrd1, a key factor of ER-associated degradation, in AECII. Knockdown of Hrd1 led to more than 2 fold increase of apoptosis, while overexpression of Hrd1 attenuated CSE induced apoptosis of AECII. Conclusions: Our results suggest that ER stress induces HRD1 to protect alveolar type II epithelial cells from apoptosis induced by CSE.

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“…Inadequate re-epithelialization following injury triggers a cascade of events leading to pathological fibrosis. Increased type II alveolar epithelial cell (AECII) apoptosis and senescence are considered to have important roles in the development of pathological fibrosis in IPF and ARDS (Matute-Bello et al, 1999 ; Plataki et al, 2005 ; Hecker et al, 2014 ; Lopez et al, 2015 ). Following injury, the stages of fibrosis in cardiac and respiratory disease are similar, as are the cellular and molecular mechanisms that lead to scar formation.…”

Section: Molecular and Cellular Fibrotic Mechanismsmentioning

confidence: 99%

The Processes and Mechanisms of Cardiac and Pulmonary Fibrosis

et al. 2017

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Fibrosis is the formation of fibrous connective tissue in response to injury. It is characterized by the accumulation of extracellular matrix components, particularly collagen, at the site of injury. Fibrosis is an adaptive response that is a vital component of wound healing and tissue repair. However, its continued activation is highly detrimental and a common final pathway of numerous disease states including cardiovascular and respiratory disease. Worldwide, fibrotic diseases cause over 800,000 deaths per year, accounting for ~45% of total deaths. With an aging population, the incidence of fibrotic disease and subsequently the number of fibrosis-related deaths will rise further. Although, fibrosis is a well-recognized cause of morbidity and mortality in a range of disease states, there are currently no viable therapies to reverse the effects of chronic fibrosis. Numerous predisposing factors contribute to the development of fibrosis. Biological aging in particular, interferes with repair of damaged tissue, accelerating the transition to pathological remodeling, rather than a process of resolution and regeneration. When fibrosis progresses in an uncontrolled manner, it results in the irreversible stiffening of the affected tissue, which can lead to organ malfunction and death. Further investigation into the mechanisms of fibrosis is necessary to elucidate novel, much needed, therapeutic targets. Fibrosis of the heart and lung make up a significant proportion of fibrosis-related deaths. It has long been established that the heart and lung are functionally and geographically linked when it comes to health and disease, and thus exploring the processes and mechanisms that contribute to fibrosis of each organ, the focus of this review, may help to highlight potential avenues of therapeutic investigation.

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Alveolar NF-κB signaling regulates endotoxin-induced lung inflammation

Abstract: Overexpression of NF-κB targeted to the lung epithelium worsened lung inflammation and injury in response to LPS exposure while conditional deletion of NF-κB signaling reduced lung inflammation. Lung inflammation and injury were associated with increased cell apoptosis.

Cited by 20 publications

References 43 publications

Standardized myrtol attenuates lipopolysaccharide induced acute lung injury in mice

Standardized myrtol attenuates lipopolysaccharide induced acute lung injury in mice

Endoplasmic Reticulum Stress Induces HRD1 to Protect Alveolar Type II Epithelial Cells from Apoptosis Induced by Cigarette Smoke Extract

The Processes and Mechanisms of Cardiac and Pulmonary Fibrosis

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