In an endotoxaemic mouse model of sepsis, a tissue-based proteomics approach for 
biomarker discovery identified long pentraxin 3 (PTX3) as the lead candidate for 
inflamed myocardium. When the redox-sensitive oligomerization state of PTX3 was 
further investigated, PTX3 accumulated as an octamer as a result of 
disulfide-bond formation in heart, kidney, and lung-common organ dysfunctions 
seen in patients with sepsis. Oligomeric moieties of PTX3 were also detectable 
in circulation. The oligomerization state of PTX3 was quantified over the first 
11 days in critically ill adult patients with sepsis. On admission day, there 
was no difference in the oligomerization state of PTX3 between survivors and 
non-survivors. From day 2 onward, the conversion of octameric to monomeric PTX3 
was consistently associated with a greater survival after 28 days of follow-up. 
For example, by day 2 post-admission, octameric PTX3 was barely detectable in 
survivors, but it still constituted more than half of the total PTX3 in 
non-survivors (p < 0.001). Monomeric PTX3 was inversely associated with cardiac 
damage markers NT-proBNP and high-sensitivity troponin I and T. Relative to the 
conventional measurements of total PTX3 or NT-proBNP, the oligomerization of 
PTX3 was a superior predictor of disease outcome.