Effect of TSP-2 antibody against a single epitope of mouse Toll-like receptor 2 extracellular domain on nuclear factor-kappa B and cytokine expression in the intestine of septic mice.
- Author:
En-ping HUANG
1
;
Jun YAO
;
Cui-lan YANG
;
Shen-qiu LUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antibodies; pharmacology; Immunodominant Epitopes; immunology; Interleukin-6; genetics; metabolism; Intestinal Mucosa; metabolism; Male; Mice; Mice, Inbred BALB C; NF-kappa B; genetics; metabolism; Random Allocation; Receptors, Cell Surface; immunology; Sepsis; metabolism; Thrombospondins; immunology; Toll-Like Receptor 2; immunology; Tumor Necrosis Factor-alpha; genetics; metabolism
- From: Journal of Southern Medical University 2011;31(2):272-276
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of the antibody TSP-2 against a single epitope of mouse Toll-like receptor 2 extracellular domain (mTLR2ECD) on the expression of nuclear factor-kappa B (NF-κB) and cytokines in the intestinal tissue of septic mice.
METHODSMale BALB/c mice were randomly divided into 4 groups, namely the sham-operated group, model group, TSP-2 treatment group and rabbit IgG treatment group. Sepsis was induced by cecal ligation and puncture (CLP), and at 6, 12 or 24 h after the operation, the ileal tissues were harvested from the mice for HE staining. NF-κB expression was detected with immunohistochemistry. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA expressions were detected with qRT-PCR and their protein expressions by ELISA.
RESULTSThe NF-κB expression in the intestinal tissue significantly increased in the model group as compared with that in the sham- operated group, and decreased after TSP-2 treatment. The model group also showed significantly increased expression levels of TNF-α and IL-6 mRNA and protein in the intestinal tissue (P<0.05), which were lowered by TSP-2 (P<0.05) but not by rabbit IgG treatment (P>0.05).
CONCLUSIONThe TSP-2 antibody can protect the intestine and delay the development of sepsis by inhibiting NF-κB activation and down-regulating TNF-α and IL-6 expressions in mice.
