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Particulate matter 2.5 triggers airway inflammation and bronchial hyperresponsiveness in mice by activating

《医学前沿（英文）》 2021年 第15卷 第5期   页码 750-766 doi: 10.1007/s11684-021-0839-4

摘要： Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation by activating nuclear factor-κB (NF-κB). Sirtuin 2 (SIRT2) is a key modulator in inflammation. However, the function and specific mechanisms of SIRT2 in PM2.5-induced airway inflammation are largely understudied. Therefore, this work investigated the mechanisms of SIRT2 in regulating the phosphorylation and acetylation of p65 influenced by PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Results revealed that PM2.5 exposure lowered the expression and activity of SIRT2 in bronchial tissues. Subsequently, SIRT2 impairment promoted the phosphorylation and acetylation of p65 and activated the NF-κB signaling pathway. The activation of p65 triggered airway inflammation, increment of mucus secretion by goblet cells, and acceleration of tracheal stenosis. Meanwhile, p65 phosphorylation and acetylation, airway inflammation, and bronchial hyperresponsiveness were deteriorated in SIRT2 knockout mice exposed to PM2.5. Triptolide (a specific p65 inhibitor) reversed p65 activation and ameliorated PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Our findings provide novel insights into the molecular mechanisms underlying the toxicity of PM2.5 exposure. Triptolide inhibition of p65 phosphorylation and acetylation could be an effective therapeutic approach in averting PM2.5-induced airway inflammation and bronchial hyperresponsiveness.

关键词： particulate matter 2.5     sirtuin 2     p65     airway inflammation     bronchial hyperresponsiveness     triptolide    

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Tim-3 mRNA expression in peripheral blood lymphocytes from asthmatic patients

Xiaoxia LU, Weikun HU, Shengdao XIONG, Guopeng XU, Fen LAN

《医学前沿（英文）》 2009年 第3卷 第2期   页码 187-190 doi: 10.1007/s11684-009-0033-6

摘要： The study aimed to detect the expression of the Th1-specific cell surface protein T cell Ig and mucin domain-containing molecule-3 (Tim-3) mRNA in peripheral blood lymphocytes isolated from asthmatic patients and to examine the correlation among Tim-3 mRNA, interleukin-4 (IL-4), interferon-γ (IFN-γ) level, and FEV1/FVC (force expiratory volume in one second/forced vital capacity) to explore the role of Tim-3 in the development and progression of asthmatic inflammation. Tim-3 mRNA expression was detected by reverse transcription polymerase chain reaction (RT-PCR). The IL-4 and IFN-γ levels were determined by using enzyme-linked immunosorbent assay (ELISA). The correlation among Tim-3 mRNA, IL-4, IFN-γ level, and pulmonary ventilatory capacity was analyzed. The expression of Tim-3 mRNA in patients with acute asthma exacerbation was 0.39±0.06, significantly higher than that in patients at the remission stage and controls (0.18±0.05 and 0.07±0.03, <0.05). The level of IL-4 in patients with acute asthma exacerbation was 68.42±10.54, significantly higher than that in the patients at the remission stage and controls (41.83±9.37 and 32.75±8.16, <0.05). The level of IL-4 in patients in remission was significantly higher than that in controls ( <0.05). The level of IFN-γ in patients with acute asthma exacerbation was 65.74±7.85, significantly lower than that in patients in remission and the control group (120.84±11.62 and 139.65±13.47, <0.05). The level of IFN-γ in patients in asthma remission was significantly lower than that in controls ( <0.05). Tim-3 mRNA expression was positively correlated with the level of IL-4 ( =0.68, <0.05) and negatively with the level of IFN-γ and pulmonary ventilatory capacity ( =-0.85, =-0.76, both <0.01). The increased expression of Tim-3 mRNA in peripheral blood lymphocytes might be involved in the development and progression of asthmatic inflammation.

关键词： asthma     airway inflammation     peripheral blood lymphocyte     Tim-3    

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Insult of gastroesophageal reflux on airway: clinical significance of pharyngeal nozzle

null

《医学前沿（英文）》 2015年 第9卷 第1期   页码 117-122 doi: 10.1007/s11684-014-0343-1

摘要：

At the very time of global paying the highest attention to the worst insults of smoking as well as haze on the airway, everybody knows both are exogenous and noticeable. However, people mostly, including many medical personnel, do not know how badly the gastroesophageal reflux (GER) insults on our own airway. Symptoms of GER are commonly seen as heartburn and regurgitation, which can be mostly tolerated. However, when the up going gastric content reversely passes the esophagus and then the distal pharynx, where it appears a beak like stricture, serving as a nozzle, so as to produce numerous micro-particles and reach the oro-nasal cavity and also the airway causing allergic rhinitis and asthmatic attacks, even pulmonary parenchyma lesions. It will reduce life quality or even jeopardize life. The point that the endogenous insult appears in the respiratory system, but originates from the digestive tract is not well known and often undiagnosed and not correctly treated. The GER induced airway challenge is a treatable and preventive entity, as soon as a diagnosis is made, a good relief could be expected by means of life style adjustment, medicine, or fixation of the patulous cardia through radiofrequency or fundoplication. The author Dr. Zhonggao Wang had suffered it for long and symptoms disappeared for 8 years after anti-reflux surgery. Here is a presentation of Dr. Zhonggao Wang and his team’s work and would call attention to the public so as to recognize this relatively unknown entity — a treatable condition occurring from human itself, but not from outside surroundings as smoking or haze does.

关键词： gastroesophageal reflux     airway     pharyngeal nozzle     micro-aspiration     asthma    

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Cytokines and inflammation in adipogenesis: an updated review

Ning Jiang, Yao Li, Ting Shu, Jing Wang

《医学前沿（英文）》 2019年 第13卷 第3期   页码 314-329 doi: 10.1007/s11684-018-0625-0

摘要： The biological relevance of cytokines is known for more than 20 years. Evidence suggests that adipogenesis is one of the biological events involved in the regulation of cytokines, and pro-inflammatory cytokines (e.g., TNF and IL-1 ) inhibit adipogenesis through various pathways. This inhibitory effect can constrain the hyperplastic expandability of adipose tissues. Meanwhile, chronic low-grade inflammation is commonly observed in obese populations. In some individuals, the impaired ability of adipose tissues to recruit new adipocytes to adipose depots during overnutrition results in adipocyte hypertrophy, ectopic lipid accumulation, and insulin resistance. Intervention studies showed that pro-inflammatory cytokine antagonists improve metabolism in patients with metabolic syndrome. This review focuses on the cytokines currently known to regulate adipogenesis under physiological and pathophysiological circumstances. Recent studies on how inhibited adipogenesis leads to metabolic disorders were summarized. Although the interplay of cytokines and lipid metabolism is yet incompletely understood, cytokines represent a class of potential therapeutic targets in the treatment of metabolic disorders.

关键词： cytokines     inflammation     adipogenesis     type 2 diabetes mellitus     metabolic disorder    

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Appendiceal inflammation affects the length of stay following appendicectomy amongst children: a myth

null

《医学前沿（英文）》 2013年 第7卷 第2期   页码 264-269 doi: 10.1007/s11684-013-0259-1

摘要：

The effect of the severity of appendiceal inflammation on post-operative stay in children following appendicectomy has shown conflicting results. This study was conducted to determine the association between the severity of appendiceal inflammation and post-operative stay amongst children undergoing open appendicectomy. A retrospective cohort study was conducted at a District General Hospital for two years. A total of 204 patients were included in the study with an age range between 3 and 16 years. Females were 54.9% while the rest were male. Mean age was 12.5±3 years. The association of the severity of appendiceal inflammation and post-operative stay was assessed by multivariable Cox Proportional hazards model. Mean post-operative stay was 2.32 days (95% CI 2.14–2.51). Macroscopically perforated appendix, histological inflammation and post-operative complications were significantly associated with post-operative stay on univariable analysis (P<0.05). Whereas, the multivariable analysis showed that the post-operative stay was significantly prolonged only in case of either perforated appendix or post-operative complications while it remained unaffected by the histological inflammation.

关键词： appendiceal inflammation     post-operative stay     paediatrics    

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for preventing peritoneal fibrosis in peritoneal dialysis patients: new insights based on peritoneal inflammation

null

《医学前沿（英文）》 2017年 第11卷 第3期   页码 349-358 doi: 10.1007/s11684-017-0571-2

摘要：

Peritoneal dialysis (PD) is an established form of renal replacement therapy. Long-term PD leads to morphologic and functional changes to the peritoneal membrane (PM), which is defined as peritoneal fibrosis, a known cause of loss of peritoneal ultrafiltration capacity. Inflammation and angiogenesis are key events during the pathogenesis of peritoneal fibrosis. This review discusses the pathophysiology of peritoneal fibrosis and recent research progress on key fibrogenic molecular mechanisms in peritoneal inflammation and angiogenesis, including Toll-like receptor ligand-mediated, NOD-like receptor protein 3/interleukin-1β, vascular endothelial growth factor, and angiopoietin-2/Tie2 signaling pathways. Furthermore, novel strategies targeting peritoneal inflammation and angiogenesis to preserve the PM are discussed in depth.

关键词： peritoneal dialysis     peritoneal fibrosis     inflammation     angiogenesis    

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Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium in inflammation

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

《医学前沿（英文）》 2021年 第15卷 第4期   页码 638-643 doi: 10.1007/s11684-021-0831-z

摘要： The COVID-19 pandemic has caused numerous deaths around the world. A growing body of evidence points to the important role of overwhelming inflammatory responses in the pathogenesis of COVID-19 and the effectiveness of anti-inflammation therapy against COVID-19 is emerging. In addition to affecting the lungs, COVID-19 can be a severe systemic inflammatory disease that is related to endothelial dysfunction. We are calling for closer attention to endothelial dysfunction in COVID-19 not only for fully revealing the pathogenic mechanism of COVID-19 but also for properly adjusting the strategy of clinical intervention.

关键词： COVID-19     endothelial dysfunction     inflammation reaction     cytokine storm    

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Expression of renal cubilin and its potential role in tubulointerstitial inflammation induced by albumin

YANG Jurong, HE Yani, SHEN Haiying, DING Hanlu, LI Kailong, WANG Huiming

《医学前沿（英文）》 2008年 第2卷 第1期   页码 25-34 doi: 10.1007/s11684-008-0006-1

摘要： Sustained proteinuria is an independent risk factor leading to kidney fibrosis and end-stage renal failure. Over-reabsorption of filtered proteins, notably albumin, has been proved to trigger interstitial inflammation and fibrosis in proteinuric renal disease. Cubilin, an endocytic receptor expressed on the renal tubular brush border, is responsible for albumin reabsorption in physiologic condition. However, little is known about whether it is required for activation of tubular cells induced by albumin overload. In this work, we investigated the change of cubilin expression and its potential role in albumin-induced up-regulation of chemokines synthesis and . Twenty-six patients with nephrotic syndrome were enrolled in this study. Proximal tubule uptake of albumin, expression of apical membrane cubilin and infiltrating cells in kidney interstitium were determined by immunocytochemistry. , the transcription of cubilin in HK2 cells after exposure to albumin was analyzed by real-time PCR. Endocytosis of albumin in HK2 cells was examined by fluorescent microscope. The influence of inhibition of cubilin on albumin-induced expressions of monocyte chemoattractant protein 1 (MCP-1) and regulated upon activation normal T-cell expressed and secreted (RANTES) was investigated by Western blot. The intensity of luminal cubilin and tubular accumulation of albumin were significantly increased in nephrotic kidneys. The expression of MCP-1 and RANTES was up-regulated, and there were spatial relationships in localization between these chemokines and cubilin as well as intracellular albumin in kidney tissues. Infiltration of CD-3 and ED-1-positive cells was predominant in tubulointerstitial areas displaying signs of increases of cubilin expression and albumin accumulation. , the transcription of cubilin mRNA in HK2 cells was enhanced after 24 h exposure to albumin in a dose-dependent manner. Inhibition of endocytosis of albumin by antisense cubilin nucleotide markedly reduced expression of MCP-1 and RANTES. Cubilin was required for handling a greater amount of protein in nephrotic status and albumin-induced production of MCP-1 and RANTES by renal tubular cells, which further initiated tubulointerstitial inflammation in proteinuric disease.
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Inflammation and liver tumorigenesis

null

《医学前沿（英文）》 2013年 第7卷 第2期   页码 242-254 doi: 10.1007/s11684-013-0256-4

摘要：

Inflammation has been considered as one of the hallmarks of cancer, and chronic hepatitis is a major cause of liver cancer. This review will focus on the pathogenic role of inflammation in hepatocarcinogenesis and will discuss recent advances in understanding the chronic hepatitis-liver cancer link based on hot spots in liver cancer research, including cellular interaction, cytokines, microRNA and stem cells. All of these mechanisms should be taken into consideration because they are crucial for the development of more efficacious therapeutic strategies for preventing and treating human chronic hepatitis and hepatocellular carcinoma.

关键词： hepatocellular carcinoma     hepatitis     cytokine     stem cell     miRNA    

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Discovery and repurposing of artemisinin

《医学前沿（英文）》 2022年 第16卷 第1期   页码 1-9 doi: 10.1007/s11684-021-0898-6

摘要： Malaria is an ancient infectious disease that threatens millions of lives globally even today. The discovery of artemisinin, inspired by traditional Chinese medicine (TCM), has brought in a paradigm shift and been recognized as the “best hope for the treatment of malaria” by World Health Organization. With its high potency and low toxicity, the wide use of artemisinin effectively treats the otherwise drug-resistant parasites and helps many countries, including China, to eventually eradicate malaria. Here, we will first review the initial discovery of artemisinin, an extraordinary journey that was in stark contrast with many drugs in western medicine. We will then discuss how artemisinin and its derivatives could be repurposed to treat cancer, inflammation, immunoregulation-related diseases, and COVID-19. Finally, we will discuss the implications of the “artemisinin story” and how that can better guide the development of TCM today. We believe that artemisinin is just a starting point and TCM will play an even bigger role in healthcare in the 21st century.

关键词： artemisinin     drug repurposing     cancer     inflammation     COVID-19     traditional Chinese medicine    

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Plasma transthyretin is a nutritional biomarker in human morbidities

《医学前沿（英文）》 2022年 第16卷 第4期   页码 540-550 doi: 10.1007/s11684-022-0940-3

摘要： Transthyretin (TTR) is a small liver-secreted plasma protein that shows close correlations with changes in lean body mass (LBM) during the entire human lifespan and agglomerates the bulk of nitrogen (N)-containing substrates, hence constituting the cornerstone of body building. Amino acids (AAs) dietary restriction causes inhibition of TTR production and impairs the accretion of LBM reserves. Inflammatory disorders result in cytokine-induced abrogation of TTR synthesis and urinary leakage of nitrogenous catabolites. Taken together, the data indicate that malnutrition and inflammation may similarly suppress the production of TTR through distinct and unrelated pathophysiological mechanisms while operating in concert to downsize LBM stores. The hepatic synthesis of TTR integrates both machineries, acting as a marker of reduced LBM resources still available for defense and repair processes. TTR operates as a universal surrogate analyte that allows for the grading of residual LBM capacity to reflect disease burden. Measurement of TTR is a simple, rapid, and inexpensive micro-method that may be reproduced on a daily basis, hence ideally suited for the follow-up of the most intricated clinical situations and as a reliable predictor of any morbidity outcome.

关键词： lean body mass     nutritional status     transthyretin     malnutrition     inflammation     amyloidosis    

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Mechanisms of insulin resistance in obesity

null

《医学前沿（英文）》 2013年 第7卷 第1期   页码 14-24 doi: 10.1007/s11684-013-0262-6

摘要：

Obesity increases the risk for type 2 diabetes through induction of insulin resistance. Treatment of type 2 diabetes has been limited by little translational knowledge of insulin resistance although there have been several well-documented hypotheses for insulin resistance. In those hypotheses, inflammation, mitochondrial dysfunction, hyperinsulinemia and lipotoxicity have been the major concepts and have received a lot of attention. Oxidative stress, endoplasmic reticulum (ER) stress, genetic background, aging, fatty liver, hypoxia and lipodystrophy are active subjects in the study of these concepts. However, none of those concepts or views has led to an effective therapy for type 2 diabetes. The reason is that, there has been no consensus for a unifying mechanism of insulin resistance. In this review article, literature is critically analyzed and reinterpreted for a new energy-based concept of insulin resistance, in which insulin resistance is a result of energy surplus in cells. The energy surplus signal is mediated by ATP and sensed by adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Decreasing ATP level by suppression of production or stimulation of utilization is a promising approach in the treatment of insulin resistance. In support, many of existing insulin sensitizing medicines inhibit ATP production in mitochondria. The effective therapies such as weight loss, exercise, and caloric restriction all reduce ATP in insulin sensitive cells. This new concept provides a unifying cellular and molecular mechanism of insulin resistance in obesity, which may apply to insulin resistance in aging and lipodystrophy.

关键词： type 2 diabetes     energy expenditure     inflammation     lipotoxicity     mitochondria     hyperinsulinemia     adenosine monophosphate-activated protein kinase (AMPK)    

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Role of Akkermansia muciniphila in the development of nonalcoholic fatty liver disease: current knowledge and perspectives

《医学前沿（英文）》 2022年 第16卷 第5期   页码 667-685 doi: 10.1007/s11684-022-0960-z

摘要： Nonalcoholic fatty liver disease (NAFLD) is a hepatic manifestation of metabolic syndrome and a common cause of liver cirrhosis and cancer. Akkermansia muciniphila (A. muciniphila) is a next-generation probiotic that has been reported to improve metabolic disorders. Emerging evidence indicates the therapeutic potential of A. muciniphila for NAFLD, especially in the inflammatory stage, nonalcoholic steatohepatitis. Here, the current knowledge on the role of A. muciniphila in the progression of NAFLD was summarized. A. muciniphila abundancy is decreased in animals and humans with NAFLD. The recovery of A. muciniphila presented benefits in preventing hepatic fat accumulation and inflammation in NAFLD. The details of how microbes regulate hepatic immunity and lipid accumulation in NAFLD were further discussed. The modulation mechanisms by which A. muciniphila acts to improve hepatic inflammation are mainly attributed to the alleviation of inflammatory cytokines and LPS signals and the downregulation of microbiota-related innate immune cells (such as macrophages). This review provides insights into the roles of A. muciniphila in NAFLD, thereby providing a blueprint to facilitate clinical therapeutic applications.

关键词： Akkermansia muciniphila     NAFLD     NASH     steatosis     inflammation    

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Beneficial metabolic activities of inflammatory cytokine interleukin 15 in obesity and type 2 diabetes

null

《医学前沿（英文）》 2015年 第9卷 第2期   页码 139-145 doi: 10.1007/s11684-015-0377-z

摘要：

In obesity, chronic inflammation is believed to induce insulin resistance and impairs adipose tissue function. Although this view is supported by a large body of literature, it has been challenged by growing evidence that pro-inflammatory cytokines may favor insulin sensitivity through induction of energy expenditure. In this review article, interleukin 15 (IL-15) is used as a new example to explain the beneficial effects of the pro-inflammatory cytokines. IL-15 is secreted by multiple types of cells including macrophages, neutrophils and skeletal muscle cells. IL-15 expression is induced in immune cells by endotoxin and in muscle cells by physical exercise. Its transcription is induced by transcription factor NF-κB. IL-15 binds to its receptor that contains three different subunits (α, β and γ) to activate JAK/STAT, PI3K/Akt, IKK/NF-κB and JNK/AP1 pathways in cells. In the regulation of metabolism, IL-15 reduces weight gain without inhibiting food intake in rodents. IL-15 suppresses lipogenesis, stimulates brown fat function, improves insulin sensitivity through weight loss and energy expenditure. In human, circulating IL-15 is negatively associated with body weight. In the immune system, IL-15 stimulates proliferation and differentiation of T cells, NK cells, monocytes and neutrophils. In the anti-obesity effects of IL-15, T cells and NK cells are not required, but leptin receptor is required. In summary, evidence from human and rodents supports that the pro-inflammatory cytokine IL-15 may enhance energy expenditure to protect the body from obesity and type 2 diabetes. The mechanism of IL-15 action remains to be fully uncovered in the regulation of energy expenditure.

关键词： inflammation     obesity     cytokine     energy expenditure     insulin resistance    

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Hyperosmolarity promotes macrophage pyroptosis by driving the glycolytic reprogramming of corneal epithelial cells in dry eye disease

《医学前沿（英文）》 2023年 第17卷 第4期   页码 781-795 doi: 10.1007/s11684-023-0986-x

摘要： Tear film hyperosmolarity plays a core role in the development of dry eye disease (DED) by mediating the disruption of ocular surface homeostasis and triggering inflammation in ocular surface epithelium. In this study, the mechanisms involving the hyperosmolar microenvironment, glycolysis mediating metabolic reprogramming, and pyroptosis were explored clinically, in vitro, and in vivo. Data from DED clinical samples indicated that the expression of glycolysis and pyroptosis-related genes, including PKM2 and GSDMD, was significantly upregulated and that the secretion of IL-1β significantly increased. In vitro, the indirect coculture of macrophages derived from THP-1 and human corneal epithelial cells (HCECs) was used to discuss the interaction among cells. The hyperosmolar environment was found to greatly induce HCECs’ metabolic reprogramming, which may be the primary cause of the subsequent inflammation in macrophages upon the activation of the related gene and protein expression. 2-Deoxy-d-glucose (2-DG) could inhibit the glycolysis of HCECs and subsequently suppress the pyroptosis of macrophages. In vivo, 2-DG showed potential efficacy in relieving DED activity and could significantly reduce the overexpression of genes and proteins related to glycolysis and pyroptosis. In summary, our findings suggested that hyperosmolar-induced glycolytic reprogramming played an active role in promoting DED inflammation by mediating pyroptosis.

关键词： dry eye disease     glycolytic reprogramming     pyroptosis     inflammation     2-DG    

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标题 作者 时间 类型 操作

Particulate matter 2.5 triggers airway inflammation and bronchial hyperresponsiveness in mice by activating

期刊论文

Tim-3 mRNA expression in peripheral blood lymphocytes from asthmatic patients

Xiaoxia LU, Weikun HU, Shengdao XIONG, Guopeng XU, Fen LAN

期刊论文

Insult of gastroesophageal reflux on airway: clinical significance of pharyngeal nozzle

null

期刊论文

Cytokines and inflammation in adipogenesis: an updated review

Ning Jiang, Yao Li, Ting Shu, Jing Wang

期刊论文

Appendiceal inflammation affects the length of stay following appendicectomy amongst children: a myth

null

期刊论文

for preventing peritoneal fibrosis in peritoneal dialysis patients: new insights based on peritoneal inflammation

null

期刊论文

Endothelial dysfunction in COVID-19 calls for immediate attention: the emerging roles of the endothelium in inflammation

Weijian Hang, Chen Chen, Xin A. Zhang, Dao Wen Wang

期刊论文

Expression of renal cubilin and its potential role in tubulointerstitial inflammation induced by albumin

YANG Jurong, HE Yani, SHEN Haiying, DING Hanlu, LI Kailong, WANG Huiming

期刊论文

Inflammation and liver tumorigenesis

null

期刊论文

Discovery and repurposing of artemisinin

期刊论文

Plasma transthyretin is a nutritional biomarker in human morbidities

期刊论文

Mechanisms of insulin resistance in obesity

null

期刊论文

Role of Akkermansia muciniphila in the development of nonalcoholic fatty liver disease: current knowledge and perspectives

期刊论文

Beneficial metabolic activities of inflammatory cytokine interleukin 15 in obesity and type 2 diabetes

null

期刊论文

Hyperosmolarity promotes macrophage pyroptosis by driving the glycolytic reprogramming of corneal epithelial cells in dry eye disease

期刊论文