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Gene and protein expression of galectin-3 and galectin-9 in experimental pneumococcal meningitis.

Authors: Bellac, CL  Coimbra, RS  Simon, F  Imboden, H  Leib, SL 
Citation: Bellac CL, etal., Neurobiol Dis. 2007 Nov;28(2):175-83. Epub 2007 Jul 10.
Pubmed: (View Article at PubMed) PMID:17706429
DOI: Full-text: DOI:10.1016/j.nbd.2007.07.005

Inflammation of the subarachnoid and ventricular space contributes to the development of brain damage i.e. cortical necrosis and hippocampal apoptosis in pneumococcal meningitis (PM). Galectin-3 and -9 are known pro-inflammatory mediators and regulators of apoptosis. Here, the gene and protein expression profile for both galectins was assessed in the disease progression of PM. The mRNA of Lgals3 and Lgals9 increased continuously in the cortex and in the hippocampus from 22 h to 44 h after infection. At 44 h after infection, mRNA levels of Lgals9 in the hippocampus were 7-fold and those of Lgals3 were 30-fold higher than in uninfected controls (P<0.01). Galectin-9 protein did not change, but galectin-3 significantly increased in cortex and hippocampus with the duration of PM. Galectin-3 was localized to polymorphonuclear neutrophils, microglia, monocytes and macrophages, suggesting an involvement of galectin-3 in the neuroinflammatory processes leading to brain damage in PM.


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CRRD Object Information
CRRD ID: 9685206
Created: 2014-12-29
Species: All species
Last Modified: 2014-12-29
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.