TY - JOUR
T1 - Auf Wiedersehen SIRS? Angeborene, trainierte und adaptive Immunität und Pathogenese von Organfunktionsstörungen
AU - Ghnewa, Y. G.
AU - Fish, M.
AU - Jennings, A.
AU - Carter, M. J.
AU - Shankar-Hari, M.
N1 - Funding Information:
Y.G. Ghnewa and A. Jennings declare that they have no competing interests. M. Shankar-Hari is supported by the National Institute for Health Research Clinician Scientist Award (CS-2016-16-011). M. Shankar-Hari is on the Editorial Board for Intensive Care Medicine and declares no competing interests. M.J. Carter is supported by the National Institute for Health Research Academic Clinical Lectureship. M. Fish is supported by the National Institute of Academic Anaesthesia BJA-RCOA PhD Fellowship. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the National Institute for Health Research or the Department of Health and Social Care.
Publisher Copyright:
© 2020, Springer Medizin Verlag GmbH, ein Teil von Springer Nature.
PY - 2020/5/1
Y1 - 2020/5/1
N2 - The novel concepts within Sepsis‑3 criteria include a focus on dysregulated host responses, removal of the systemic inflammation response syndrome (SIRS) criteria from sepsis diagnosis, the use of Sepsis-related (Sequential) Organ Failure Assessment (SOFA) scores to define organ dysfunction, and the explicit recognition of the septic shock as a subset of sepsis. Protection against infection requires a surveillance system, an effector response against “perceived” pathogens, a method for regaining immune homeostasis following an immune response, and generation of immunological memory. In comparison to normally regulated responses to infection, the innate immune system shows profoundly abnormal neutrophil and macrophage function. Similarly, the adaptive immune system is typically depleted numerically of lymphocytes and functionally with T and B cell exhaustion. Although there are numerous proposed mechanisms by which these dysregulated immune responses may be associated with organ failure, it is unclear what the unifying organ failure mechanisms in sepsis are. Furthermore, in sepsis survivors, the epigenetic changes on immune cells and widespread changes to lymphocyte populations may increase the risk of adverse events such as rehospitalisation and mortality. Finally, our current gaps in understanding of the immune response trajectory and the associated modifiable mechanisms in sepsis leave us a long way from successful immunomodulation for these patients. This article is freely available.
AB - The novel concepts within Sepsis‑3 criteria include a focus on dysregulated host responses, removal of the systemic inflammation response syndrome (SIRS) criteria from sepsis diagnosis, the use of Sepsis-related (Sequential) Organ Failure Assessment (SOFA) scores to define organ dysfunction, and the explicit recognition of the septic shock as a subset of sepsis. Protection against infection requires a surveillance system, an effector response against “perceived” pathogens, a method for regaining immune homeostasis following an immune response, and generation of immunological memory. In comparison to normally regulated responses to infection, the innate immune system shows profoundly abnormal neutrophil and macrophage function. Similarly, the adaptive immune system is typically depleted numerically of lymphocytes and functionally with T and B cell exhaustion. Although there are numerous proposed mechanisms by which these dysregulated immune responses may be associated with organ failure, it is unclear what the unifying organ failure mechanisms in sepsis are. Furthermore, in sepsis survivors, the epigenetic changes on immune cells and widespread changes to lymphocyte populations may increase the risk of adverse events such as rehospitalisation and mortality. Finally, our current gaps in understanding of the immune response trajectory and the associated modifiable mechanisms in sepsis leave us a long way from successful immunomodulation for these patients. This article is freely available.
KW - Apoptosis
KW - Exhaustion
KW - Inflammation
KW - Sepsis
KW - Suppression
UR - http://www.scopus.com/inward/record.url?scp=85083441496&partnerID=8YFLogxK
U2 - 10.1007/s00063-020-00683-2
DO - 10.1007/s00063-020-00683-2
M3 - Review article
C2 - 32291506
AN - SCOPUS:85083441496
SN - 2193-6218
VL - 115
SP - 10
EP - 14
JO - Medizinische Klinik - Intensivmedizin und Notfallmedizin
JF - Medizinische Klinik - Intensivmedizin und Notfallmedizin
ER -