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Surviving sepsis with LECT2

Date:
December 17, 2012
Source:
Rockefeller University Press
Summary:
Failure to launch an adequate immune response may be at the root of septic shock, according to a new study.
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Failure to launch an adequate immune response may be at the root of septic shock, according to a study published Dec. 17 in The Journal of Experimental Medicine.

Bacterial sepsis is a potentially deadly blood infection that results in massive immune activation and inflammation. Sepsis therapies have traditionally focused on quelling this exaggerated inflammatory response. But a recent study challenged this approach by showing that patients with sepsis had abnormally low levels of an inflammatory protein called LECT2.

The new study by Jiong Chen and colleagues at Ningbo University in China shows that low LECT2 levels are indeed detrimental. Injecting LECT2 into septic mice promoted bacterial clearance by immune cells called macrophages and increased their production of survival-promoting factors. If these findings hold true in humans, boosting immunity with LECT2 may be protective by helping clear the infection.


Story Source:

The above post is reprinted from materials provided by Rockefeller University Press. Note: Materials may be edited for content and length.


Journal Reference:

  1. X.-J. Lu, J. Chen, C.-H. Yu, Y.-H. Shi, Y.-Q. He, R.-C. Zhang, Z.-A. Huang, J.-N. Lv, S. Zhang, L. Xu. LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor. Journal of Experimental Medicine, 2012; DOI: 10.1084/jem.20121466

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Rockefeller University Press. "Surviving sepsis with LECT2." ScienceDaily. ScienceDaily, 17 December 2012. <www.sciencedaily.com/releases/2012/12/121217121609.htm>.
Rockefeller University Press. (2012, December 17). Surviving sepsis with LECT2. ScienceDaily. Retrieved August 4, 2015 from www.sciencedaily.com/releases/2012/12/121217121609.htm
Rockefeller University Press. "Surviving sepsis with LECT2." ScienceDaily. www.sciencedaily.com/releases/2012/12/121217121609.htm (accessed August 4, 2015).

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