Indeed, levels of IL-10 and cortisol are known to correlate with disease severity [8,40,41]. Furthermore, it is worth mentioning that PGN and PGN-derived structures are known to prime cells and enhance a further response to LPS [42], to synergize with cytokines [43], TREM-1 ligand [44], and other PAMPs [45] to favor inflammation, and AG-014699 to induce shock and organ dysfunction in vivo [46,47].ConclusionsIn numerous clinical settings, microbial products derived from the gut are thought to worsen the disease. However, systemic bacterial translocation was rarely proven and rather endotoxin translocation has been measured. Endotoxins are only derived from Gram-negative bacteria and measuring PGN, which derives from both Gram-negative and Gram-positive bacteria could be more accurate.

We report that in patients undergoing abdominal aortic surgery, most patients were positive for circulating NOD2 agonist, indicating that microbial translocation can be more frequent than previously thought when circulating endotoxin was measured. Furthermore, our data suggest that the presence of NOD2 agonist also contributes to the inflammatory response. Although the present test remains time consuming, we expect in the near future to develop a stable permanent transfected cell line that would allow us to perform the test within six hours. Furthermore, our results suggest that any other strategies that would be aimed to recognize the presence of PGN-like structure could be very useful.

Key messages? We developed a test able to detect PGN-like (NOD2 agonist) structure in plasma? Gut manipulation is sufficient to induce translocation of microbial products? Detection of NOD2 agonist is more reliable to detect translocation than measurement of endotoxin? Among abdominal aortic surgery patients, levels of circulating NOD2 agonist positively correlated with that of cortisol and IL-10AbbreviationsAAS: abdominal aortic surgery; CAS: carotid artery surgery; CRP: C-reactive protein; ELISA: enzyme linked immunosorbent assay; fsNOD2: a frameshift mutant of NOD2; HEK: human embryonic kidney; IL: interleukin; LAL: limulus amebocyte lysate; LPS: lipopolysaccharide; MDP: muramyldipeptide; NF: nuclear factor; NOD: nucleotide-binding oligomerization domain; PAMPs: pathogen-associated molecular patterns; PBMC: peripheral blood mononuclear cells; PCT: procalcitonin; PGN: peptidoglycan; POD: postoperative day; SD: standard deviation; SEM: standard error of the mean; SIRS: systemic inflammatory response syndrome; TNF: tumor necrosis factor.

Competing interestsThe authors declare that they have no competing interests.Authors’ contributionsOYK performed the measurements, analyzed the raw data, performed statistical analysis, drafted and contributed to the writing of the paper. AM included patients, collected the clinical information, performed statistical analysis and contributed Brefeldin_A to the writing of the paper.