Community Health Worker Activities in Public Health Programs to Prevent Violence: Coding Roles and Scope.

In multiple and related forms, violence is a serious public health issue with lasting impacts on health and wellness in the United States. Community health workers (CHWs) are frontline public health workers and trusted members of communities. We aimed to analyze recent examples of CHW activities in violence prevention public health programs with a goal of informing future programs and research. We collected more than 300 documents published between 2010 and 2020 to identify public health programs to prevent violence including CHW activities. We used an iterative process to develop and apply a coding scheme to the CHW activities. We identified 20 public health programs to prevent violence which included CHW activities. CHWs most often addressed community violence, youth violence, and family violence and played an average of 8 of 10 core roles per program. Fewer than a third (i.e., 6 programs) reported community-focused CHW activities to address upstream and structural determinants of health inequities. This first examination, to our knowledge, of the intersection of the CHW and violence prevention literature shows that CHWs have played many of their core roles in public health programs to address multiple forms of violence. (Am J Public Health. 2022;112(8):1191-1201. https://doi.org/10.2105/AJPH.2022.306865).

TCA cycle remodeling drives proinflammatory signaling in humans with pulmonary tuberculosis.

The metabolic signaling pathways that drive pathologic tissue inflammation and damage in humans with pulmonary tuberculosis (TB) are not well understood. Using combined methods in plasma high-resolution metabolomics, lipidomics and cytokine profiling from a multicohort study of humans with pulmonary TB disease, we discovered that IL-1ß-mediated inflammatory signaling was closely associated with TCA cycle remodeling, characterized by accumulation of the proinflammatory metabolite succinate and decreased concentrations of the anti-inflammatory metabolite itaconate. This inflammatory metabolic response was particularly active in persons with multidrug-resistant (MDR)-TB that received at least 2 months of ineffective treatment and was only reversed after 1 year of appropriate anti-TB chemotherapy. Both succinate and IL-1ß were significantly associated with proinflammatory lipid signaling, including increases in the products of phospholipase A2, increased arachidonic acid formation, and metabolism of arachidonic acid to proinflammatory eicosanoids. Together, these results indicate that decreased itaconate and accumulation of succinate and other TCA cycle intermediates is associated with IL-1ß-mediated proinflammatory eicosanoid signaling in pulmonary TB disease. These findings support host metabolic remodeling as a key driver of pathologic inflammation in human TB disease.