J Pediatr Intensive Care 2019; 08(01): 042-050
DOI: 10.1055/s-0038-1676607
Review Article
Georg Thieme Verlag KG Stuttgart · New York

Immune Modulation in Pediatric Sepsis

Mark W. Hall
1  Division of Critical Care Medicine, Nationwide Children's Hospital, Columbus, Ohio, United States
2  The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, United States
› Author Affiliations
Further Information

Publication History

30 October 2018

02 November 2018

Publication Date:
02 January 2019 (online)


The initial host immune response to sepsis in children is characterized by a proinflammatory surge that can be associated with fever, capillary leak, and organ dysfunction. There is, however, a concurrent anti-inflammatory response that results in hyporesponsiveness of innate and adaptive immune cells. When severe, this response is termed immunoparalysis and is known to be associated with prolonged organ dysfunction, increased risk for nosocomial infection, and death in septic adults and children. Sepsis-induced immune suppression can be defined in the laboratory by reduced whole blood ex vivo-stimulated cytokine production capacities, reduced expression of human leukocyte antigen (HLA)-DR on circulating monocytes, and reduced absolute cell counts. While anti-inflammatory therapies have largely been unsuccessful at improving outcomes from adult and pediatric sepsis, the use of immunostimulatory therapies such as granulocyte macrophage colony-stimulating factor (GM-CSF) in patients with sepsis-induced immunoparalysis shows promise. A greater understanding of the risk factors for immunoparalysis along with the development and execution of immunophenotype-specific clinical trials of strategies to optimize innate and adaptive immune function are needed to further improve outcomes in septic children.