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. 2022 Nov;48(11):1617-1620.
doi: 10.1007/s00134-022-06871-2. Epub 2022 Sep 1.

Compartmentalisation of immune responses in critical illness: does it matter?

Affiliations

Compartmentalisation of immune responses in critical illness: does it matter?

Andrew Conway Morris et al. Intensive Care Med. 2022 Nov.
No abstract available

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Conflict of interest statement

ACM has received payment for speaking on behalf of Boston Scientific and sits on the Scientific Advisory Board of Cambridge Infection Diagnostics, a start-up seeking to develop novel diagnostics for infectious diseases. The other authors declare no conflicts of interest.

Figures

Fig. 1
Fig. 1
Diagrammatic representation of some of the mechanisms which lead to compartmentalised inflammatory responses in critical illness. A indicates the summary of the hypothesis that discordant immune responses in blood and tissue compartments may lead to inappropriate therapies. *Refers to the immune state assessment based on either blood or tissue-based biomarker. B illustrates how distant insults and systemic spill-over of damage-associated molecular patterns (DAMPS) can lead to inflammatory and thrombotic changes in the blood, which damage the endothelium and lead to secondary damage at distal sites such as the lungs. C illustrates how direct tissue injury, in this example from pneumonia, produces systemic overspill of inflammatory mediators into both the lymphatic and blood compartments. In both situations, cross-talk between tissue resident and infiltrating immune cells, stromal and epithelial cells influences tissue responses and makes them qualitatively distinct from responses in circulating cells. Within luminal organs with communication with the external environment the added complexity of the microbial inhabitants (microbiome) further influences mucosal immunity. Conversely, soluble plasma proteins, such as complement, coagulation cascade components and colloidal proteins, may be largely restricted to, or in far higher abundance, in the blood compartment. Notably, in both compartments, the presence of inflammatory mediators does not automatically indicate cellular hyper-function, and indeed such mediators may drive impaired antimicrobial functions [7, 15]. pbN peripheral blood neutrophil, iN interstitial neutrophil, tN tissue neutrophil, iMφ interstitial macrophage, AMφ Alveolar macrophage, Mo infiltrating monocyte, DC dendritic cell

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