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.
