Allium sativum-derived allitridin inhibits treg amplification in cytomegalovirus infection
| Autor: | Yong-jian Huang, Fei Huang, Xing-lou Liu, Feng Fang, Huanji Cheng, Ya-nan Li, Sai-nan Shu |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Muromegalovirus
Regulatory T cell T cell medicine.medical_treatment chemical and pharmacologic phenomena Sulfides Biology T-Lymphocytes Regulatory Placebos Mice Immune system T-Lymphocyte Subsets In vivo Virology medicine Animals Immunologic Factors IL-2 receptor Garlic Mice Inbred BALB C Gene Expression Profiling FOXP3 Forkhead Transcription Factors Immunosuppression Herpesviridae Infections Viral Load Allyl Compounds Disease Models Animal Infectious Diseases medicine.anatomical_structure Immunology Cytokines Female Viral load |
| Zdroj: | Journal of Medical Virology. 85:493-500 |
| ISSN: | 0146-6615 |
| DOI: | 10.1002/jmv.23480 |
| Popis: | This study investigated the effects of allitridin compound on murine cytomegalovirus (MCMV)-induced regulatory T cell (Treg; CD4(+) CD25(+) Foxp3(+) ) amplification in vivo and in vitro. One hundred twenty MCMV-infected mice were allocated at random into two groups for treatment with allitridin or placebo. Another 120 mock-infected mice were randomly allocated as controls for the allitridin treatment and placebo treatment groups. The mice were euthanized at various time points after infection (out to 120 days) to evaluate the effects of treatment on Treg presence and function, as well as MCMV infective load. Co-culture with mouse embryo fibroblasts (MEF) and MCMV was performed to evaluate allitridin-mediated Treg and anti-CMV effects. The maximum tolerance concentration (MTC) of allitridin was used to treat cells for 3 days. Changes in Foxp3 mRNA and protein levels, percentages of T cell subsets, and Treg-related cytokines (IL-10 and TGF-β) were measured. Allitridin treatment did not influence Foxp3 expression and Treg proportion in uninfected mice, but did down-regulate each in infected mice during the chronic infection period. Additionally, allitridin treatment reduced the MCMV load in salivary glands. MTC allitridin treatment of co-cultures partially blocked MCMV induction of Foxp3 mRNA and protein expression. In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-β1, and significantly suppressed viral loads. In conclusion, allitridin can promote MCMV-induced Treg expansion and Treg-mediated anti-MCMV immunosuppression. Therefore, allitridin may be useful as a therapeutic agent to enhance the specific cellular immune responses against CMV. |
| Databáze: | OpenAIRE |
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