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. 2023 Oct;49(10):1235-1237.
doi: 10.1007/s00134-023-07130-8. Epub 2023 Jun 23.

What's new in intensive care: disease tolerance

Rachel E Powell  1   2 , Miguel P Soares  3 , Sebastian Weis  4   5
Affiliations

What's new in intensive care: disease tolerance

Rachel E Powell et al. Intensive Care Med. 2023 Oct.
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
A Early conceptual model of sepsis progression from infection to systemic inflammatory response to sepsis and death. Popularized in early sepsis definitions, criteria, and clinical practice guidelines, this model assisted clinical care but was agnostic to underlying biology [15]. B Model proposed for translational and clinical research that includes awareness of both the hyper- and hypo-inflammatory host responses in sepsis, as well as the modifying factors of host fitness and pathogens themselves. [16]. C Conceptual model of infection and host response that includes both dysfunction/damage, imposed by pathogens and/or by immune-driven resistance mechanisms as well as disease tolerance as a key regulator of sepsis progression [1, 3]. In brief, pathogenic microorganisms directly inflict damage to the host (“Virulence”) and induce the activation of the immune systems, ("Immune-driven inflammation")  that in the early phase after infection aims at pathogens elimination ("Resistance"). As a trade-off, resistence mechanisms  can inflict damage to non-immune cells of the host (“Immunopathology”). “Damage Control” mechanisms counter infection-associated stress, promote maintenance of “Homeostasis” and as such establish “Disease Tolerance” and limit disease severity
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