Tu1732 Colon Pathology in a Mouse Model of Cigarette Smoke Induced Chronic Obstructive Pulmonary Disease (COPD) -A Model for Induction of Crohn's Disease?

Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). Methods Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. Results Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-β (TGF-β) expression and collagen deposition that were inhibited in PJH-treated mice. Conclusions This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.

Download Full-text

Treating Viral Exacerbations of Chronic Obstructive Pulmonary Disease: Insights from a Mouse Model of Cigarette Smoke and H1N1 Influenza Infection

PLoS ONE ◽

10.1371/journal.pone.0013251 ◽

2010 ◽

Vol 5 (10) ◽

pp. e13251 ◽

Cited By ~ 64

Author(s):

Carla M. T. Bauer ◽

Caleb C. J. Zavitz ◽

Fernando M. Botelho ◽

Kristen N. Lambert ◽

Earl G. Brown ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Mouse Model ◽

Pulmonary Disease ◽

Cigarette Smoke ◽

Influenza Infection ◽

H1n1 Influenza ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease

Download Full-text

Anomalous asthma and chronic obstructive pulmonary disease Google Trends patterns during the COVID-19 pandemic

Clinical and Translational Allergy ◽

10.1186/s13601-020-00352-9 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Bernardo Sousa-Pinto ◽

Enrico Heffler ◽

Aram Antó ◽

Wienczyslawa Czarlewski ◽

Anna Bedbrook ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Crohn’S Disease ◽

Crohn's Disease ◽

Pulmonary Disease ◽

Media Coverage ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

The Past ◽

Search Patterns ◽

Online Searches

Abstract Background An increase in online searches on health topics may either mirror epidemiological changes or reflect media coverage. In the context of COVID-19, this is particularly relevant, as COVID-19 symptoms may be mistaken for those of respiratory disease exacerbations. Therefore, we aimed to assess Internet search patterns on asthma and chronic obstructive pulmonary disease (COPD) in the context of COVID-19, as compared to searches on other chronic diseases. Methods We retrieved Google Trends (GTs) data on two respiratory (asthma and COPD) and three non-respiratory (diabetes, hypertension, and Crohn’s disease) chronic diseases over the past 5 years (up to May 31, 2020). For 54 countries, and for each disease, we built autoregressive integrated moving average (ARIMA) models to predict GTs for 2020 based on 2015–2019 search patterns. In addition, we estimated the proportion of searches in which COVID-19-related terms were used. To assess the potential impact of media coverage on online searches, we assessed whether weekly “asthma” GTs correlated with the number of Google News items on asthma. Results Over the past 5 years, worldwide search volumes for asthma and COPD reached their maximum values in March 2020. Such was not observed for diabetes, hypertension and Crohn’s disease. In 38 (70%) countries, GTs on asthma were higher in March 2020 than the respective maximum predicted values. This compares to 19 countries for COPD, 23 for hypertension, 11 for Crohn’s disease, and 9 for diabetes. Queries with COVID-19-related terms represented up to 47.8% of the monthly searches on asthma, and up to 21.3% of COPD searches. In most of the assessed countries, moderate-strong correlations were observed between “asthma” GTs and the number of news items on asthma. Conclusions During March 2020, there was a peak in searches on asthma and COPD, which was probably mostly driven by media coverage, as suggested by their simultaneity in several countries with different epidemiological situations.

Download Full-text

Protective Effect of Jianpiyifei II Granule against Chronic Obstructive Pulmonary Disease via NF-κB Signaling Pathway

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2018/4265790 ◽

2018 ◽

Vol 2018 ◽

pp. 1-13 ◽

Cited By ~ 2

Author(s):

Long Fan ◽

Ruifeng Chen ◽

Leng Li ◽

Ziyao Liang ◽

Xuhua Yu ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Mouse Model ◽

Pulmonary Disease ◽

Cigarette Smoke ◽

Inflammatory Cell ◽

Raw264.7 Cells ◽

Chronic Obstructive ◽

Mrna Levels ◽

Obstructive Pulmonary Disease ◽

Anti Inflammatory

Jianpiyifei II granule (JPYF II) is an oriental herbal formula used clinically in China to treat chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the anti-inflammatory and antioxidative activities of JPYF II in a mouse model of COPD induced by lipopolysaccharide (LPS) and cigarette smoke (CS) and in RAW264.7 cells stimulated with cigarette smoke extract (CSE). Mice were given LPS via intratracheal instillation on days 1 and 15 and exposed to CS generated from 4 cigarettes/day for 28 days. The mice were treated with 0.75, 1.5, or 3 g/kg/d JPYF II by intragastric administration in low, middle, and high dose groups, respectively, for two weeks. RAW264.7 cells were stimulated by CSE and treated with JPYF II at doses of 12.5, 25, or 50 μg/mL. In the mouse model of LPS and CS-induced COPD, JPYF II decreased inflammatory cell counts in broncho alveolar lavage fluid (BALF), in addition to mRNA expression of proinflammatory cytokines and metalloproteinases (MMPs) in lung tissues. In addition, JPYF II elevated catalase (CAT) and glutathione peroxidase (GSH-Px) activities and reduced the levels of malondialdehyde (MDA) and IκBα and p65 phosphorylation and inflammatory cell infiltration in the lung tissues. In RAW264.7 cells stimulated with CSE, JPYF II inhibited the mRNA levels of inflammatory mediators and the phosphorylation of IκBα and p65. Our results suggest that JPYF II enhanced anti-inflammatory and antioxidative activities in a mouse model of COPD induced by LPS and CS and in RAW264.7 cells stimulated with CSE via inhibition of the NF-κB pathway.

Download Full-text