Immunity & Inflammation 是由中国免疫学会主办，与施普林格自然出版集团 （Springer Nature） 合作出版的完全开放获取 （OA） 英文期刊，期刊 聚焦免疫 与炎症领域重大科学问题和前沿进展。 该期刊由 曹雪涛 院士和 Jules A. Hoffmann 教授 （因发现 Toll 通路在先天免疫激活中的作用，荣获 2011 年诺贝尔生理 或医学奖） 担任主编，由国内外一流免疫学家 Luke O'Neill 、 Frederick Alt 、 陈志坚 、 Tadatsugu Taniguchi 、 邵峰 院士担任副主编， 程根宏 教授任执行 主编。 2025 年 9 月 4 日， Immunity & Inflammation 上线了首批 4 篇文章，包括 曹雪涛 / Jules A. Hoffmann 撰写的社论；诺贝尔奖得主 David Baltimore 等人的 NF-κB 综述论文；中国医学科学院北京协和医学院/华中科技大学同济医学院 黄波 教授团队的逆转肺纤维化研究论文；以及 曹雪涛 院士的亮点评述。 编辑丨王多鱼 排版丨水成文 从 梅契尼科夫 （1908 年诺贝尔奖得 ...

Core Viewpoint - The article discusses the increasing consumption of fructose and its potential health risks, particularly its role in aggravating inflammation and its association with various diseases, including cancer and metabolic disorders [2][3][4]. Group 1: Fructose Consumption and Health Risks - Fructose is a monosaccharide that has been widely used as a sweetener in beverages and processed foods, leading to a significant increase in its consumption over the past 50 years [2]. - Excessive intake of fructose is linked to various health issues, including high blood sugar, obesity, type 2 diabetes, fatty liver, cardiovascular diseases, and an increased risk of certain cancers such as colorectal, pancreatic, ovarian, and liver cancer [2][3]. - Recent studies indicate that high fructose consumption may also be associated with anxiety disorders, particularly among adolescents [2]. Group 2: Immune System Impact - The impact of fructose on the immune system, particularly its role in regulating acquired immunity and T cell immunity, has not been sufficiently studied [3][6]. - A recent study found that high fructose intake promotes the generation of effector T cells (Th1 and Th17), exacerbating inflammation and potentially worsening inflammatory bowel disease (IBD) [4][7]. - The study suggests that the common antidiabetic drug metformin can reverse the effects of high fructose intake by inhibiting mTORC1 activation and reducing reactive oxygen species (ROS) mediated TGF-β activation, thus alleviating T cell inflammation and colitis [4][9]. Group 3: Mechanisms of Fructose-Induced Inflammation - High fructose intake enhances the differentiation of Th1 and Th17 cells through a glutamine metabolism-dependent pathway that activates mTORC1, contributing to the progression of IBD [7]. - The study highlights that fructose can directly mediate immune responses and disrupt immune homeostasis, leading to increased inflammation [9]. Group 4: Fructose and Cancer Growth - Additional research indicates that fructose may indirectly promote tumor growth by enhancing lipid transfer between organs, providing cancer cells with the necessary lipids for rapid proliferation [13]. - Another study reveals that fructose inhibits the polarization of M1-like tumor-associated macrophages, promoting the development of colorectal cancer through mechanisms that do not rely on its downstream metabolites [15].

Core Insights - The article discusses a significant research study published in Nature Microbiology, which reveals the mechanisms behind lung damage in patients with a history of Mycobacterium tuberculosis infection [2][7]. Group 1: Research Findings - The research team constructed the first high-precision cellular molecular network of lung tissue post-tuberculosis infection, identifying cellular senescence and inflammation as key pathological features of lung damage [2][6]. - A total of 19 post-tuberculosis lung tissue samples and 13 matched normal lung samples were analyzed using single-cell transcriptomics, focusing on the lesions and surrounding areas [5]. - The study identified molecular characteristics associated with tuberculosis, including gene expression patterns related to senescence, inflammation, fibrosis, and apoptosis [6]. Group 2: Mechanisms and Implications - The research highlighted that exacerbated vascular inflammation is a critical feature of lung tissue following tuberculosis [6]. - The team discovered that silencing FOXO3 and treating with thrombin exacerbated endothelial cell senescence and inflammation, confirming the role of FOXO3 signaling and NF-κB-dependent thrombo-inflammatory processes [6]. - These findings provide new insights into the mechanisms of tuberculosis-related lung damage and suggest potential therapeutic targets to alleviate lung injury in affected patients [7].

Investment Rating - The report does not provide a specific investment rating for the industry. Core Insights - The report emphasizes the significant negative health impacts of air pollution, detailing how pollutants enter the human body and affect various organs, leading to both short-term and long-term health consequences [5][6][29]. - It highlights the importance of understanding the epidemiological and toxicological evidence surrounding air pollution and its health effects, which is crucial for developing effective public health strategies [11][88][98]. Summary by Sections Section 1: Adverse Health Effects of Air Pollution - Air pollution has been linked to various health issues, including acute and chronic diseases, with epidemiological studies providing strong evidence of its impact on mortality rates [15][16][25]. - The definition of adverse health effects has evolved to include not only respiratory outcomes but also cardiovascular diseases and other systemic impacts [22][25][26]. Section 2: From Exposure to Disease - The report discusses the continuum between exposure to air pollution and the onset of health issues, emphasizing that there is no threshold below which no negative effects are observed [41][46]. - It outlines the pathways through which pollutants enter the body, primarily through inhalation, and the factors influencing the dose received [50][54]. Section 3: Building Scientific Evidence - Epidemiological studies are categorized into cohort studies for long-term exposure and time-series analyses for short-term exposure, both of which have been instrumental in linking air pollution to health outcomes [87][89]. - Toxicological studies are highlighted as essential for understanding the physiological effects of pollutants, allowing for the assessment of individual and combined effects of various air contaminants [98][100].