Inflammation Related with Surgical Infections

The inflammatory response related to surgery is a systemic reaction considered as the expression of three overlapping trophic phases during which the oxygen consumption progressively increases. However, surgical inflammation could induce old functions in which life on the Earth has based on the expression of two hypothetical extraembryonic trophic axes i.e. coelomic-amniotic and trophoblastic-yolk sac related, when integrated in the interstitium of the injured tissues and organs to induce a gastrulation-related phenotype. This later phenotype would repair the tissues by fibrosis and/or regeneration. A coupling of this recapitulated extraembryonic axis would cause hyperacute or acute–on-chronic inflammation or sepsis. The mechanisms of this systemic inflammatory response could be reminiscences of some phylogenetic mechanisms that ultimately would favor a metabolic cross-talk between the eukaryotic cell and gut microbiome. These ontogenic and phylogenic hypotheses of the surgical inflammatory and septic responses could open new research pathways about the ancient co-evolution of humans with their microbiota.

Keywords: Eukaryotes, surgical infections, gut microbiome, fibrosis, regeneration, sepsis, intestinal bacterial translocation, multiorgan dysfunction syndrome, compensatory anti-inflammatory response syndrome, multiple organ failure, cholesterol, glucocorticoids, mineralocorticoids, postcapillary venules, biofilms, quorum sensing.