Perinatal liver inflammation is associated with persistent elevation of CXCL10 and its canonical receptor CXCR3 on common myeloid progenitors.

Biliary atresia (BA) is a leading cause of liver failure in infants. Despite effective surgical drainage, patients with BA exhibit attenuated immune responses to childhood vaccines, suggesting there are long-lasting alterations to immune function. The perinatal liver is home to hematopoietic stem and progenitor cells (HSPCs) and serves as the epicenter for rapidly progressive and significantly morbid inflammatory diseases like BA.

Neonatal Hepatic Myeloid Progenitors Expand and Propagate Liver Injury in Mice.

Background: Biliary atresia (BA) is a progressive pediatric inflammatory disease of the liver that leads to cirrhosis and necessitates liver transplantation. The rapid progression from liver injury to liver failure in children with BA suggests that factors specific to the perinatal hepatic environment are important for disease propagation. Hematopoietic stem and progenitor cells (HSPCs) reside in the fetal liver and are known to serve as central hubs of inflammation.

Hepatic Ly6C Non-Classical Monocytes Have Increased Nr4a1 (Nur77) in Murine Biliary Atresia.

Biliary atresia (BA) is a rapidly progressive perinatal inflammatory disease, resulting in liver failure. Hepatic Ly6CLo non-classical monocytes promote the resolution of perinatal liver inflammation during rhesus rotavirus-mediated (RRV) BA in mice. In this study, we aim to investigate the effects of inflammation on the transcription factor Nr4a1, a known regulator of non-classical monocytes.

The Role of Myeloid Populations during Perinatal Liver Injury and Repair.

Perinatal liver inflammation can have life-threatening consequences, particularly in infants and young children. An example of a hepatic inflammatory disease during infancy is biliary atresia (BA), an obliterative cholangiopathy that rapidly progresses to hepatic fibrosis and liver failure. The aggressive nature of BA in neonates compared to the pathogenesis of inflammatory liver diseases in adults, suggests that the mechanisms responsible for restoring tissue homeostasis following inflammation are impaired in affected infants.

Ly6c non-classical monocytes promote resolution of rhesus rotavirus-mediated perinatal hepatic inflammation.

Perinatal hepatic inflammation can have devastating consequences. Monocytes play an important role in the initiation and resolution of inflammation, and their diverse functions can be attributed to specific cellular subsets: pro-inflammatory or classical monocytes (Ly6c) and pro-reparative or non-classical monocytes (Ly6c). We hypothesized that inherent differences in Ly6c classical monocytes and Ly6c non-classical monocytes determine susceptibility to perinatal hepatic inflammation in late gestation fetuses and neonates.

The relative abundance of monocyte subsets determines susceptibility to perinatal hepatic inflammation.

The devastating consequences of perinatal liver inflammation contribute to a pressing need to develop therapeutics for the diseases that underly this condition. Biliary atresia (BA) is a perinatal inflammatory disease of the liver that results in obliterative cholangiopathy and rapidly progresses to liver failure, requiring transplantation. The ability to develop targeted therapies requires an understanding of the immune mechanisms that mitigate perinatal liver inflammation.

An international basic science and clinical research summer program for medical students.

An important part of training the next generation of physicians is ensuring that they are exposed to the integral role that research plays in improving medical treatment. However, medical students often do not have sufficient time to be trained to carry out any projects in biomedical and clinical research. Many medical students also fail to understand and grasp translational research as an important concept today.