Sepsis pp 47-69 | Cite as

Overview of the Molecular Pathways and Mediators of Sepsis

  • Tristen T. Chun
  • Brittany A. Potz
  • Whitney A. Young
  • Alfred AyalaEmail author
Part of the Respiratory Medicine book series (RM)


Sepsis is a common clinical problem among the critically ill, and it is associated with high morbidity and mortality due to lack of effective therapeutic options. Sepsis results from dysregulation of immune responses to infection, characterized by mixed antagonistic response syndrome (MARS) in which both aspects of the pro-inflammatory and anti-inflammatory responses are believed to be present concomitantly. These immune responses are mediated by a number of immune cells, including monocytes, macrophages, dendritic cells, neutrophils, natural killer cells, γδ T cells, natural killer T cells, and T and B lymphocyte cells that comprise innate and adaptive immune system. In addition, a variety of molecules and pathways exist to help maintain a delicate balance between protection against invading pathogens and bystander host damage. This chapter will present a general overview of the molecular pathways and mediators involved in sepsis in an attempt to provide a framework for understanding potential targets for sepsis treatment.


Sepsis Innate and adaptive immunity Systemic Inflammatory Response Syndrome (SIRS) Compensatory Anti-Inflammatory Response Syndrome (CARS) Mixed Antagonistic Response Syndrome (MARS) Pathogen-Associated Molecular Patterns (PAMPs) Danger-Associated Molecular Patterns (DAMPs) Pattern Recognition Receptors (PRRs) Toll-like Receptors (TLRs) Intracellular Patterns Recognition Systems (iPRSs) Cytokines and chemokines Immune resolution 



Antigen presenting cell


Adenosine triphosphate


Compensatory anti-inflammatory response syndrome


Catheter-associated urinary tract infections


Central line-associated blood stream infections


Danger-associated molecular patterns


Dendritic cell


Disseminated intravascular coagulation


Deoxyribonucleic acid




High density lipoprotein


High mobility group box-1


Heat shock protein


Intensive care units




Invariant natural killer T cell


Intracellular patterns recognition systems


Lipopolysaccharide biding protein


Low density lipoprotein




Lipoteichoic acid


Membrane attack complex


Mitogen-activated protein kinase


Mixed antagonistic response syndrome


Monocyte chemotactic protein


Major histocompatibility complex


Migration inhibitory factor


Matrix metalloproteinase


Multiple organ failure


Multisystem organ failure


Nicotinamide adenine dinucleotide phosphate


Natural killer cell


Natural killer T cell


Nitric oxide


Pathogen-associated molecular patterns


Protease-activated receptor




Pattern recognition receptors


Receptor antagonist


Retinoic-acid-inducible gene I


Ribonucleic acid


Reactive nitrogen species


Reactive oxygen species


Sphingosine-1 phosphate


Soluble interleukin receptor


Systemic inflammatory response syndrome


T cell receptor


Transforming growth factor


Toll-like receptors


Tumor necrosis factor


Ventilator-associated pneumonia


Very low density lipoprotein


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Copyright information

© Springer International Publishing AG 2017

Authors and Affiliations

  • Tristen T. Chun
    • 1
  • Brittany A. Potz
    • 2
  • Whitney A. Young
    • 3
  • Alfred Ayala
    • 4
    Email author
  1. 1.Division of Surgical Research, Department of SurgeryRhode Island HospitalProvidenceUSA
  2. 2.Division of Surgical Research, Department of SurgeryRhode Island HospitalProvidenceUSA
  3. 3.Division of Surgical Research, Department of SurgeryRhode Island HospitalProvidenceUSA
  4. 4.Division of Surgical Research, Department of SurgeryRhode Island HospitalProvidenceUSA

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