Mouse GAL3(Galectin 3) ELISA Kit

Chronic Chagas disease cardiomyopathy (CCC) is the most frequent and severe form of this parasitic disease. CCC is caused by a progressive inflammation in the heart, resulting in alterations that can culminate in heart failure and death. The use of dendritic cells (DCs) appears as an option for the development of treatments due to their important role in regulating immune responses. Here, we investigated whether tolerogenic cells (tDCs) could interfere with the progression of CCC in an experimental model of Chagas disease. The tDCs were generated and characterized as CD11b(+) CD11c(+) cells, low expression of MHC-II, CD86, CD80, and CD40, and increased expression of PD-L. These cells produced low levels of IL-6 and IL-12p70 and higher levels of IL-10, compared to mature DCs (mDCs). Interestingly, tDCs inhibited lymphoproliferation and markedly increased the population of FoxP3(+) Treg cells in vitro, compared to mature DCs. In a mouse model of CCC, treatment with tDCs reduced heart inflammation and fibrosis. Furthermore, tDCs treatment reduced the gene expression of pro-inflammatory cytokines (Ifng and Il12) and of genes related to cardiac remodeling (Col1a2 and Lgals3), while increasing the gene expression of IL-10. Finally, administration of tDCs, increased the percentage of Treg cells in the hearts and spleens of chagasic mice. Ours results show that tolerogenic dendritic cells have therapeutic potential on CCC, inhibiting disease progression.

Background and Purpose: Galectin-3, a P-galactoside binding lectin, acts as a strong pro-inflammatory signal. Many immunomodulatory drugs affect signaling pathways that comprise transcription factors involved in the regulation of galectin-3 gene (LGALS3) expression. The aim of our study was to investigate the effects of steroidal anti-inflammatory drugs (hydrocortisone - HC and dexamethasone - Dex) on the expression of galectin-3, both at the mRNA and the protein level. Materials and Methods: The human monocytic cell line THP-1 was exposed to various concentrations of HC (0.1, 1, 5 and 10 mu M) and Dex (0.1, 1, 10 and 100 nM) during 1, 3, 5,24, 48 or 72 hrs. Relative RT-PCR method and GeneScan analysis software were used for assessing galectin-3 mRNA level and chemiluminescent-western blot analysis for measuring galectin-3 level. Results: The results showed that both drugs in all applied concentrations halved the galectin-3 mRNA level already after I h of exposure. The decrease continued and after 72 hours the mRNA level dropped to 3.8-15.4% of the initial value. The protein expression of galectin-3 did not follow the same pattern; although both drugs in all applied concentration provoked the reduction in galectin-3 level, the decrease was observed not until 48 and 72 hours of exposure, when galectin-3 level fell to 7176 to 38% of the initial value, respectively. Conclusion: Steroidal anti-inflammatory drugs cause the reduction in both gene and protein expression of galectin-3, but the intensity of changes and the time of their appearance strongly depend on the type and concentration of the drug.