{"title":"免疫开关和巨噬细胞操作:创伤、排卵和抑郁是潜在的结核病再激活风险。","authors":"Stacie Burke","doi":"10.1002/ajhb.70146","DOIUrl":null,"url":null,"abstract":"<p>Inflammation is the immune system's natural response to initial tuberculosis infection. Tuberculosis bacteria have gained adaptations to manipulate the inflammatory process, sometimes settling into latency and containment in granulomas, ensuring their survival. Grounded in an evolutionary framework, this hypothesis-driven narrative synthesis centers upon immune-related switches, macrophage manipulations, and the critical roles of vascular endothelial growth factor A (VEGFA) in the body, exploring how this pro-inflammatory mitogen expressed by M1 macrophages frames risks for latent tuberculosis reactivation. The review focuses on trauma, ovulation, and depression, three case studies of pro-inflammatory switches creating risks for reactivation because of M1 macrophage polarization, the up-regulation of VEGFA expression, and angiogenesis (the sprouting of new blood vessels). A biological rationale is extended for why skeletal tuberculosis is so often connected with onsets in childhood, why adolescent and reproductive age females may experience heightened risks for latent tuberculosis reactivation relative to males, and why there is a potential for latent tuberculosis reactivation following onsets of depression. The immunity switches and reactivation risks of trauma, ovulation, and depression are problematic, particularly in contexts of endemic tuberculosis if large numbers of people are routinely latently infected, and among individuals with natural “high producer” VEGFA phenotypes, or those with strong type 1/M1/T<sub>H</sub>1 or type 3/M1/T<sub>H</sub>17 pro-inflammatory switch tendencies, and in infections with tuberculosis bacteria possessing macrophage- and granuloma-manipulating adaptations (virulence factors). Arguably, any disease or physiological state engaging pro-inflammatory switches (common and sometimes chronic in the modern population) and M1 macrophage polarizations, and any drug treatments or therapeutics intending to alter VEGFA expression should be considered for latent tuberculosis reactivation risk.</p>","PeriodicalId":50809,"journal":{"name":"American Journal of Human Biology","volume":"37 9","pages":""},"PeriodicalIF":1.7000,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ajhb.70146","citationCount":"0","resultStr":"{\"title\":\"Immunity Switches and Macrophage Manipulations: Trauma, Ovulation, and Depression as Latent Tuberculosis Reactivation Risks\",\"authors\":\"Stacie Burke\",\"doi\":\"10.1002/ajhb.70146\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Inflammation is the immune system's natural response to initial tuberculosis infection. Tuberculosis bacteria have gained adaptations to manipulate the inflammatory process, sometimes settling into latency and containment in granulomas, ensuring their survival. Grounded in an evolutionary framework, this hypothesis-driven narrative synthesis centers upon immune-related switches, macrophage manipulations, and the critical roles of vascular endothelial growth factor A (VEGFA) in the body, exploring how this pro-inflammatory mitogen expressed by M1 macrophages frames risks for latent tuberculosis reactivation. The review focuses on trauma, ovulation, and depression, three case studies of pro-inflammatory switches creating risks for reactivation because of M1 macrophage polarization, the up-regulation of VEGFA expression, and angiogenesis (the sprouting of new blood vessels). A biological rationale is extended for why skeletal tuberculosis is so often connected with onsets in childhood, why adolescent and reproductive age females may experience heightened risks for latent tuberculosis reactivation relative to males, and why there is a potential for latent tuberculosis reactivation following onsets of depression. The immunity switches and reactivation risks of trauma, ovulation, and depression are problematic, particularly in contexts of endemic tuberculosis if large numbers of people are routinely latently infected, and among individuals with natural “high producer” VEGFA phenotypes, or those with strong type 1/M1/T<sub>H</sub>1 or type 3/M1/T<sub>H</sub>17 pro-inflammatory switch tendencies, and in infections with tuberculosis bacteria possessing macrophage- and granuloma-manipulating adaptations (virulence factors). Arguably, any disease or physiological state engaging pro-inflammatory switches (common and sometimes chronic in the modern population) and M1 macrophage polarizations, and any drug treatments or therapeutics intending to alter VEGFA expression should be considered for latent tuberculosis reactivation risk.</p>\",\"PeriodicalId\":50809,\"journal\":{\"name\":\"American Journal of Human Biology\",\"volume\":\"37 9\",\"pages\":\"\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2025-09-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ajhb.70146\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of Human Biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/ajhb.70146\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ANTHROPOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Human Biology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/ajhb.70146","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ANTHROPOLOGY","Score":null,"Total":0}
Immunity Switches and Macrophage Manipulations: Trauma, Ovulation, and Depression as Latent Tuberculosis Reactivation Risks
Inflammation is the immune system's natural response to initial tuberculosis infection. Tuberculosis bacteria have gained adaptations to manipulate the inflammatory process, sometimes settling into latency and containment in granulomas, ensuring their survival. Grounded in an evolutionary framework, this hypothesis-driven narrative synthesis centers upon immune-related switches, macrophage manipulations, and the critical roles of vascular endothelial growth factor A (VEGFA) in the body, exploring how this pro-inflammatory mitogen expressed by M1 macrophages frames risks for latent tuberculosis reactivation. The review focuses on trauma, ovulation, and depression, three case studies of pro-inflammatory switches creating risks for reactivation because of M1 macrophage polarization, the up-regulation of VEGFA expression, and angiogenesis (the sprouting of new blood vessels). A biological rationale is extended for why skeletal tuberculosis is so often connected with onsets in childhood, why adolescent and reproductive age females may experience heightened risks for latent tuberculosis reactivation relative to males, and why there is a potential for latent tuberculosis reactivation following onsets of depression. The immunity switches and reactivation risks of trauma, ovulation, and depression are problematic, particularly in contexts of endemic tuberculosis if large numbers of people are routinely latently infected, and among individuals with natural “high producer” VEGFA phenotypes, or those with strong type 1/M1/TH1 or type 3/M1/TH17 pro-inflammatory switch tendencies, and in infections with tuberculosis bacteria possessing macrophage- and granuloma-manipulating adaptations (virulence factors). Arguably, any disease or physiological state engaging pro-inflammatory switches (common and sometimes chronic in the modern population) and M1 macrophage polarizations, and any drug treatments or therapeutics intending to alter VEGFA expression should be considered for latent tuberculosis reactivation risk.
期刊介绍:
The American Journal of Human Biology is the Official Journal of the Human Biology Association.
The American Journal of Human Biology is a bimonthly, peer-reviewed, internationally circulated journal that publishes reports of original research, theoretical articles and timely reviews, and brief communications in the interdisciplinary field of human biology. As the official journal of the Human Biology Association, the Journal also publishes abstracts of research presented at its annual scientific meeting and book reviews relevant to the field.
The Journal seeks scholarly manuscripts that address all aspects of human biology, health, and disease, particularly those that stress comparative, developmental, ecological, or evolutionary perspectives. The transdisciplinary areas covered in the Journal include, but are not limited to, epidemiology, genetic variation, population biology and demography, physiology, anatomy, nutrition, growth and aging, physical performance, physical activity and fitness, ecology, and evolution, along with their interactions. The Journal publishes basic, applied, and methodologically oriented research from all areas, including measurement, analytical techniques and strategies, and computer applications in human biology.
Like many other biologically oriented disciplines, the field of human biology has undergone considerable growth and diversification in recent years, and the expansion of the aims and scope of the Journal is a reflection of this growth and membership diversification.
The Journal is committed to prompt review, and priority publication is given to manuscripts with novel or timely findings, and to manuscripts of unusual interest.