Ccr2-dependent monocytes exacerbate intestinal inflammation and modulate gut serotonergic signaling following traumatic brain injury.
Mahmoud G El BaassiriZachariah RaoufHee-Seong JangDaniel ScheeseJohannes W DuessWilliam B FultonChhinder P SodhiDavid J HackamIsam W NasrPublished in: The journal of trauma and acute care surgery (2024)
Our study reveals a critical role for Ccr2 + monocytes in modulating intestinal homeostasis after TBI. Ccr2 + monocytes aggravate intestinal inflammation and alter gut-derived serotonergic signaling. Therefore, targeting Ccr2 + monocyte-dependent responses could provide a better understanding of TBI-induced gut inflammation. Further studies are required to elucidate the impact of these changes on brain neuroinflammation and cognitive outcomes.
Keyphrases
- dendritic cells
- traumatic brain injury
- oxidative stress
- regulatory t cells
- peripheral blood
- immune response
- severe traumatic brain injury
- signaling pathway
- endothelial cells
- white matter
- resting state
- drug induced
- type diabetes
- weight loss
- cancer therapy
- brain injury
- functional connectivity
- cognitive impairment
- glycemic control