Adiponectin-deficient mice are protected against tobacco-induced inflammation and increased emphysema

Miller, Marina; Pham, Alex D.; Cho, Jae Youn; Rosenthal, Peter; Broide, David H.

doi:10.1152/ajplung.00326.2009

Cited by 42 publications

(33 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…35) Although several methods 14,[36][37][38][39] have been used to cause COPD or emphysema in animals, the complications seen in human COPD are frequently not found in these experimental COPD animal models or their long term consistency over time has not been determined. Therefore, these animal models are only used in short-term observation and are not suitable for long term research and for clarifying the mechanisms of COPD.…”

Section: Discussionmentioning

confidence: 99%

“…35,40) In addition to smoking 36,37,41,42) and bacterial infection 43,44) exposure to particulate air pollution, 38,45) occupational dust, smoke 27,46) and bio-fuels for cooking 47) are also risk factors for COPD. Previous experimental COPD or emphysema models have been developed in guinea pigs.…”

Section: Discussionmentioning

confidence: 99%

“…Previous experimental COPD or emphysema models have been developed in guinea pigs. 14) mice, 36,37) rats, 38) and dogs 39) by exposing the animals to sulfur dioxide (SO 2 ), 17) smoke from solid fuel, 19) cigarette smoke, 14,24,42) lipopolysaccharide, 39) proteases and their secretagogues, such as PAE, PPE, NE, proteinase 3, MMP, 44,48,49) and the factors used can enhance the effect of each other. 50,51) However, the rat model seems to be more economical and more feasible, and smoke and bacterial infections appear to be the most frequently used initiators.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

et al. 2012

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

To develop a stable chronic obstructive pulmonary disease (COPD) model in rats. Sprague-Dawley rats were treated with cigarette-smoke inhalation (CSI) for 12 weeks, repetitive bacterial infection (RBI) for 8 weeks, or the combination of the two (CCR) for 12 weeks and followed up for the additional 20 weeks. Tidal volume (V T ), peak expiratory flow (PEF) and 50% V T expiratory flow (EF 50 ), histological changes in the lungs, and levels of the cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-8, and IL-10 in serum and bronchial alveolar lavage fluid (BALF) were examined at intervals during the 32 week study period. The right ventricular hypertrophy index (RVHI) was also determined at the same times. V T , PEF, and EF 50 were decreased in rats with COPD compared to the control. The expression of TNF-α, IL-8 and IL-10 increased in both serum and BALF with a similar trend. Bronchiole and arteriole wall thickness and the degree of bronchiole stenosis and alveolar size increased in COPD rats. RVHI was reduced gradually following the treatment. All of these changes were more pronounced in the CCR-treatment group than in the other groups. Our results have shown that CSI or RBI alone can induce COPD in rats, but that the combination of CSI with RBI induces a stable COPD that has more similarity to complications seen in patients with COPD. This combination may therefore provide a more appropriate model for study of human COPD.Key words pulmonary disease; chronic obstructive; animal model; pulmonary function; histological change; right ventricular hypertrophy index Chronic obstructive pulmonary disease (COPD) has been defined as a preventable and treatable pathologic condition characterized by partially reversible airflow limitation, 1) and is a major cause of morbidity and mortality throughout the world.2) Its prevalence among the Chinese population aged 40 or older is 8.2%.3) Development of COPD is slow and progressive in humans, with occasional exacerbations caused by an inflammatory response to triggering substances such as noxious gases, 1) bacteria 4-6) or viruses. [7][8][9][10][11] Four abnormalities are present in chronic, stable COPD: emphysema, small airway remodeling, pulmonary hypertension, and chronic bronchitis.Tobacco smoking and bacterial infection are the most common and important risk factors for COPD, 1,12,13) and they have each been used to establish animal COPD models. [14][15][16] Animal models have also used other noxious gases [17][18][19] and Pneumocystis carinii infection 20) in COPD induction. Short term induction protocols (days) 17,21) have resulted in a pulmonary inflammatory infiltrate, increased mucus production, and pulmonary edema. Long term induction protocols (weeks or months) 15,[17][18][19] have produced, in addition to the inflammatory infiltrate, emphysema and pulmonary remodeling characterized by fibrosis, and thickened bronchiole and arterial walls. Problems with animal models are that most of them are of short duration and the COPD produced does not correspond to the late...

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

et al. 2012

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…Effects of adiponectin on expression of M2 genes in lung macrophages has not previously been examined, although there is evidence that adiponectin deficiency increases M1 type activation of lung macrophages, as indicated by increased MHC class 2 expression and augmented TNF production [26,27]. However, adiponectin can also have proinflammatory effects on lung macrophages, since macrophages from adiponectin deficient mice produce less TNF in response to cigarette smoke extract than wildtype mice [54].…”

Section: Discussionmentioning

confidence: 99%

Impact Of Adiponectin Overexpression On Allergic Airways Responses In Mice

Verbout¹,

Hug²,

Si³

et al. 2010

C103. Dietary Influences for Asthma and Chronic Obstructive Pulmonary Disease: It's All About What You Eat

View full text Add to dashboard Cite

Obesity is an important risk factor for asthma. Obese individuals have decreased circulating adiponectin, an adipose-derived hormone with anti-inflammatory properties. We hypothesized that transgenic overexpression of adiponectin would attenuate allergic airways inflammation and mucous hyperplasia in mice. To test this hypothesis, we used mice overexpressing adiponectin (Adipo Tg). Adipo Tg mice had marked increases in both serum adiponectin and bronchoalveolar lavage (BAL) fluid adiponectin. Both acute and chronic ovalbumin (OVA) sensitization and challenge protocols were used. In both protocols, OVA-induced increases in total BAL cells were attenuated in Adipo Tg versus WT mice. In the acute protocol, OVA-induced increases in several IL-13 dependent genes were attenuated in Adipo Tg versus WT mice, even though IL-13 per se was not affected. With chronic exposure, though OVA-induced increases in goblet cells numbers per millimeter of basement membrane were greater in Adipo Tg versus WT mice, mRNA abundance of mucous genes in lungs was not different. Also, adiponectin overexpression did not induce M2 polarization in alveolar macrophages. Our results indicate that adiponectin protects against allergen-induced inflammatory cell recruitment to the airspaces, but not development of goblet cell hyperplasia.

show abstract

“…Chan et al (11) studied the association between adiponectin, interleukin (IL)-6, IL-8 and C-reactive protein with COPD, and found that adiponectin, IL-6 and C-reactive protein were significantly elevated in patients with COPD. Miller et al (12) used an adiponectin null mouse model to study the association between adiponectin and emphysema and observed an increase in diseased animals. Daniele et al (13) used ELISA technique and demonstrated that in patients with COPD, adiponectin levels were significantly upregulated, (14) indicated that in patients with COPD, the anti-inflammatory effect of adiponectin was primarily achieved through inhibiting the activity of macrophages and the release of pro-inflammatory cytokines, such as IL-6 and tumor necrosis factor (TNF)-α, from macrophages.…”

Section: Introductionmentioning

confidence: 99%

Different forms of adiponectin reduce the apoptotic and damaging effect of cigarette smoke extract on human bronchial epithelial cells

Cheng

Liu

Zhang

et al. 2016

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Chronic obstructive pulmonary disease (COPD) is a common respiratory disease, in which adiponectin may serve an important role. The present study investigated the role of adiponectin in the apoptotic and damaging effect of cigarette smoke extract (CSE) on human bronchial epithelial cells (16HBECs). An MTT assay showed that CSE significantly inhibited the proliferation of 16HBECs (F=1808.88, P<0.01). The 16HBECs were treated with different concentrations of high molecular weight (HMW) adiponectin and globular domain (gAd) adiponectin and it was observed that HMW and gAd dose-dependently inhibited the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-8, and the generation of 4-hydroxy-nonenal and reactive oxygen species (ROS) in 16HBECs, thereby blocking the upregulating effect of CSE on these factors. However, the inhibitory effect of gAd on TNF-α and IL-8 expression was stronger compared with that of HMW, but the suppressing effect of HMW on ROS production was superior compared with that of gAd. Further testing of apoptosis indicated that CSE and HMW promoted the apoptosis of 16HBECs. However, such effects of HMW declined with an increase in concentration. In contrast, gAd showed an inhibitory effect on apoptosis and inhibited the occurrence of CSE-induced apoptosis in a dose-dependent manner. Therefore, the present study demonstrated that different forms of adiponectin may have different mechanisms of action, suggesting that further exploration of their effects may open a new avenue for the treatment of COPD. IntroductionCOPD is a chronic inflammatory disease characterized by airflow limitation, with a high morbidity and mortality. According to previously reported statistics, COPD ranks fourth in the cause of mortality worldwide, and its rank is expected to move up to third in 2030 (1). The prevalence rate of COPD among people over age 40 is 8.2% in China (2). COPD has already become an important global public health problem. Therefore, further study and understanding of COPD are of great significance.Epidemiological studies have shown that smoking is the most important pathogenic factor of human COPD (3). Long-term exposure to tobacco smoke can cause the infiltration and recruitment of lung inflammatory cells, which can then release various cytokines and finally cause the formation of COPD through a variety of mechanisms (4). Among COPD patients, 80-90% are smokers or ex-smokers (5,6). Studies showed that ~15-20% of smokers eventually develop COPD (7), and a survey in China indicated that the prevalence of COPD among smokers was 2-4 times of that among non-smokers, and was directly associated with the duration and quantity of smoking, i.e., a longer duration and a greater amount of smoking results in a higher prevalence of COPD (8).Adiponectin is an adipokine secreted by adipocytes. Previously, a study identified that airway epithelial cells also secrete adiponectin, which through autocrine and paracrine mechanisms regulates chronic inflammation in COPD (9). Tomoda et al (10) used ELIS...

show abstract

Adiponectin-deficient mice are protected against tobacco-induced inflammation and increased emphysema

Abstract: Miller M, Pham A, Cho JY, Rosenthal P, Broide DH. Adiponectindeficient mice are protected against tobacco-induced inflammation and increased emphysema.

Cited by 42 publications

References 20 publications

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

Impact Of Adiponectin Overexpression On Allergic Airways Responses In Mice

Different forms of adiponectin reduce the apoptotic and damaging effect of cigarette smoke extract on human bronchial epithelial cells

Contact Info

Product

Resources

About