Jack, RS and Fan, XL and Bernheiden, M and Rune, G and Ehlers, M and Weber, A and Kirsch, G and Mentel, R and Furll, B and Freudenberg, M and Schmitz, G and Stelter, F and Schutt, C (1997) Lipopolysaccharide-binding protein is required to combat a murine Gram-negative bacterial infection. NATURE, 389 (6652). pp. 742-745. ISSN 0028-0836,
Full text not available from this repository.Abstract
An invading pathogen must be held in check by the innate immune system until a specific immune response can be mounted. In the case of Gram-negative bacteria, the principal stimulator of the innate immune system is Lipopolysaccharide (LPS), a component of the bacterial outer membrane(1). In vitro, LPS is bound by lipopolysaccharide-binding protein (LBP)(2) and transferred to CD14-the LPS receptor on the macrophage surface(3,4)-or to high-density lipoprotein (HDL) particles(5,6). Transfer to CD14 triggers an inflammatory response which is crucial for keeping an infection under control. Here we investigate how LBP functions in vivo by using LBP-deficient mice. Surprisingly, we find that LBP is not required in vivo for the clearance of LPS from the circulation, but is essential for the rapid induction of an inflammatory response by small amounts of LPS or Gram-negative bacteria and for survival of an intraperitoneal Salmonella infection.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | FREE-FLOW ISOTACHOPHORESIS; CD14; ENDOTOXIN; MICE; LPS; LIPOPROTEINS; MONOCYTES; RECEPTOR; SHOCK; |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:31 |
| URI: | https://pred.uni-regensburg.de/id/eprint/50478 |
Actions (login required)
 |
View Item |
