Neighborhood violence is associated with a range of health consequences but little is known about the biological processes involved. Research in disease pathogenesis has identified low-grade inflammation as a process that, beginning in the first decades of life, is both induced by chronic stress and a contributor to multiple cardiometabolic diseases that present throughout the lifecourse. Previous research has examined whether neighborhood violence is associated with inflammatory biomarkers, but has been limited to cytokine indicators of inflammation. In a sample of adolescents (n = 203) residing in Chicago, we tested cross-sectional associations between neighborhood violence and cellular and cytokine indicators of inflammation. Neighborhood-level violence was measured in multiple ways (as murder rates of Census block groups and as the sum of homicides within 1 and ½ mile zones) in the areas surrounding where youth lived and attended school. At the individual level, violence exposure was measured by self-report (direct victimization, witnessing violence, and/or victimization of family or friends in the past year). Adolescents residing in high-violence neighborhoods evidenced higher numbers of pro-inflammatory classical (CD14++CD16-) monocytes relative to those in less violent neighborhoods. In contrast, neighborhood-level violence was not consistently associated with cytokine levels across different model specifications. Self-reported violence exposure was also not consistently associated with inflammatory biomarkers. Neighborhood-level violence and self-reported violence exposure interacted, such that the positive association between neighborhood-level violence and classical monocytes was observed only among adolescents who reported being exposed to violence. Associations were largely specific to the neighborhoods in which youth lived as opposed to those in which they attended school. Findings provide the first evidence that youth residing in high-violence neighborhoods show mobilization of classical monocytes, suggesting a pro-inflammatory mechanism through which contextual stressors such as neighborhood violence may compromise health.

中文翻译：

---

社区暴力以及青少年炎症的细胞和细胞因子指标

邻里暴力与一系列健康后果有关，但对所涉及的生物过程知之甚少。疾病发病机制研究已确定低度炎症是一个从生命最初几十年开始的过程，它既是由慢性压力诱发的，也是导致整个生命过程中存在的多种心脏代谢疾病的因素。先前的研究已经检查了邻里暴力是否与炎症生物标志物有关，但仅限于炎症的细胞因子指标。在居住在芝加哥的青少年 (n = 203) 样本中，我们测试了邻里暴力与炎症的细胞和细胞因子指标之间的横断面关联。在青年居住和上学的周围地区，社区层面的暴力行为以多种方式衡量（如人口普查街区群体的谋杀率以及 1 英里和 1/2 英里区域内的凶杀案总和）。在个人层面，暴力暴露是通过自我报告（在过去一年中直接受害、目睹暴力和/或家人或朋友受害）来衡量的。与生活在暴力程度较低的社区的青少年相比，居住在高暴力社区的青少年的促炎经典 (CD14++CD16-) 单核细胞数量更多。相比之下，社区级别的暴力与不同模型规范中的细胞因子水平不一致。自我报告的暴力暴露也并非始终与炎症生物标志物相关。邻里暴力和自我报告的暴力暴露相互作用，因此只有在报告暴露于暴力的青少年中观察到邻里暴力和经典单核细胞之间的正相关。协会主要针对青年居住的社区，而不是他们上学的社区。研究结果提供了第一个证据，表明居住在高暴力社区的青年表现出经典单核细胞的动员，这表明一种促炎机制，通过这种机制，诸如社区暴力之类的环境压力因素可能会损害健康。协会主要针对青年居住的社区而不是他们上学的社区。研究结果提供了第一个证据，表明居住在高暴力社区的青年表现出经典单核细胞的动员，这表明一种促炎机制，通过这种机制，诸如社区暴力之类的环境压力因素可能会损害健康。协会主要针对青年居住的社区而不是他们上学的社区。研究结果提供了第一个证据，表明居住在高暴力社区的青年表现出经典单核细胞的动员，这表明一种促炎机制，通过这种机制，诸如社区暴力之类的环境压力因素可能会损害健康。