Early host interactions that drive the dysregulated response in sepsis.
journal contributionposted on 29.03.2021, 13:25 by Steven Kerrigan, Tatyana Devine, Glenn Fitzpatrick, Jecko Thachil, Dermot Cox
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. While many individual cells and systems in the body are involved in driving the excessive and sometimes sustained host response, pathogen engagement with endothelial cells and platelets early in sepsis progression, are believed to be key. Significant progress has been made in establishing key molecular interactions between platelets and pathogens and endothelial cells and pathogens. This review will explore the growing number of compensatory connections between bacteria and viruses with platelets and endothelial cells and how a better understanding of these interactions are informing the field of potential novel ways to treat the dysregulated host response during sepsis.
Higher Education Authority Project grant [grant number (11/BioAT/1377E)
Science Foundation Ireland (SFI) Career Development Award (grant number 13/CDA/2119)
Health Research Board (grant number 06/RP/211)
CommentsThe original article is available at https://www.frontiersin.org
Published CitationKerrigan SW, Devine T, Fitzpatrick G, Thachil J, Cox D. Early host interactions that drive the dysregulated response in sepsis. Frontiers in Immunology. 2019;10:1748.
Publication Date6 August 2019
- Irish Centre for Vascular Biology
- School of Pharmacy and Biomolecular Sciences
- Vascular Biology
- Biomaterials and Regenerative Medicine
- Immunity, Infection and Inflammation
- Published Version (Version of Record)