An international research team has found that bacteria can directly cause human blood and plasma to clot, something that has long been thought to have been lost during the course of vertebrate evolution.
The researchers believe that their new findings may help advance scientists' understanding of coagulation during bacterial infections, which in turn may pave the way for new clinical methods for treating serious medical conditions like sepsis and anthrax.
Blood often coagulates during sepsis or bacterial infections, but this has generally been regarded as a host's immune and inflammatory response.
The clots, once formed, can grow and propagate.
While the clotting may prevent the dissemination of the bacteria through the host, it often causes serious vascular damage due to blocked and injured blood vessels.
The researcher say that the location of the bacteria is crucial to clot formation, instead of the total number of bacteria or their level of concentration.
According to them, for those bacteria that can activate coagulation factors, coagulation occurs only when a cluster of bacteria forms.
"Our research demonstrates that coagulation can be controlled by changing the spatial distribution, or clustering, of bacteria," Nature Chemical Biology quoted study co-author Christian Kastrup, Post-Doctoral Assistant at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology, as saying.
"Therefore, considering the location of bacterial cells, instead of just their presence or absence and their total numbers, could significantly change our understanding of coagulation," Kastrup added.
The team point out that coagulation can occur if enough proteases, which activate coagulation, accumulate near the bacteria rather than diffuse away.
The researchers focused their study on Bacillus anthracis, the anthrax-causing pathogen. They used a safe strain that could not infect humans.
The researchers observed that coagulation, in the case of human blood, required the secretion of zinc metalloprotease InhA1, which activated prothrombin and factor X directly-not via factor XII or tissue-factor pathways.
"We refer to this mechanism as 'quorum acting' to distinguish it from quorum sensing, in which bacteria coordinate certain actions based, in part, on their density," said Wei-Jen Tang, Professor at the Ben-May Department for Cancer Research.
He further said that the observations made during the study opened up a new field of study.
"We will now explore the commonality of quorum acting, and how quorum acting can affect evolutionary dynamics," he added.
Ismagilov said that new findings had significant implications.
"The work emphasizes the importance of bacteria's spatial distribution, rather than just its average concentration in the functioning of nonlinear biochemical networks," he said.