Does Perinatal Infection Affect the Capacity of Umbilical Vein Endothelial Cells to Produce Adenosine Triphosphate?

Efficient energy production forms the very core of human health, and the key of this process lies within the cell's mitochondria. By way of oxidative phosphorylation, cells produce the high amount of adenosine triphosphate (ATP) that they need to sustain themselves, and to grow and divide. Disruption of this energy production system is implicated in diverse human diseases, which range from primary mitochondrial disease[1] to cancer.[2]

Perinatal infection, caused by bacteria or viruses that are passed on from the mother to her offspring during pregnancy or delivery, is a commonly observed complication in neonatology. The mechanisms underlying this complication, however, remain partly unknown. As human umbilical vein endothelial cells (HUVEC) play an important role as regulators of fetal blood flow, dysfunction of HUVEC metabolism may result in compromised fetal development. In view of the established complex interactions between mitochondrial function and the immune system,[3] it is assumed that mitochondrial activity of HUVEC could be relevant to perinatal infection outcome, but the precise mechanism has not been elucidated as yet. The tight relationship between energy metabolism and the immune system is further illustrated by the fact that a significant fraction of patients with primary mitochondrial disorders experience serious or recurrent (mostly bacterial) infections.[4]

In this issue of the Journal of Pediatric Biochemistry, Thomas Neisse and coworkers present their data in a model that describes lipopolysaccharide (LPS)-induced changes observed in HUVEC cells from mature and premature neonates. They report no differences between naïve and LPS-incubated cells. Cytochrome c oxidase-activity, however, was found to differ whether HUVEC were derived from term or premature newborns, indicating a form of timed regulation in these cells.

The current work represents a necessary step to increase our understanding of the mechanisms that arise from early life inflammatory events. Further study is needed to develop this growing knowhow into strategies to combat infection-associated complications.

• References

• 1 Katsetos CD, Koutzaki S, Melvin JJ. Mitochondrial dysfunction in neuromuscular disorders. Semin Pediatr Neurol 2013; 20 (3) 202-215
• 2 De Paepe B. Mitochondrial markers for cancer: Relevance to diagnosis, therapy, and prognosis and general understanding of malignant disease mechanisms. ISRN Pathology 2012; ; article ID 217162
• 3 Weinberg SE, Sena LA, Chandel NS. Mitochondria in the regulation of innate and adaptive immunity. Immunity 2015; 42 (3) 406-417
• 4 Cloonan SM, Choi AM. Mitochondria: commanders of innate immunity and disease?. Curr Opin Immunol 2012; 24 (1) 32-40