Links between fecal microplastics and parameters related to metabolic dysfunction-associated steatotic liver disease (MASLD) in humans: An exploratory study

Abstract

Microplastics (MPs) can persist in the environment and human body. Murine studies showed that exposure to MPs could cause metabolic dysregulation, contributing metabolic dysfunction-associated steatotic liver disease (MASLD) or steatohepatitis (MASH). However, research on the role of MPs in humans is limited. Thus, we aimed to assess links between human fecal MPs and liver histology, gene expression, immune cells and intestinal microbiota (IM). We included 6 lean healthy liver donors and 6 normal liver (obese) and 11 MASH patients. Overall, pre-BSx, we observed no significant differences in fecal MPs between groups. However, fecal MP fibers and total MPs positively correlated with portal and total macrophages and total killer T cells while total fecal MPs were positively correlated with natural killer cells. Additionally, 19 genes related to immune system and apoptosis correlated with fecal MPs at baseline. Fecal MP fibers correlated positively with fecal Bifidobacterium and negatively with Lachnospiraceae. Patients with MASH (n = 11) were re-assessed 12-months post-bariatric surgery (BSx) and we found that those with persistent disease (n = 4) had higher fecal MP fragments than those with normalized liver histology (n = 7). At 12-month post-BSx, MP fragments positively correlated with helper T cells and total MPs positively correlated with natural killer T cells and B cells. Our study is the first to look at 1) the role of MPs in MASH and its association with IM, immune cells and hepatic gene expression and 2) look at the role of MPs longitudinally in MASH persistence following BSx. Future research should further explore this relationship.

Keywords: Hepatic gene expression; Immune cells; Metabolic dysfunction-associated steatotic liver disease; Microplastics; Steatohepatitis.