Upregulation of chicken TLR4, TLR15 and MyD88 in heterophils and monocyte-derived macrophages stimulated with Eimeria tenella in vitro
| Autor: | Zhiying Wang, Zhi-li Guo, Bo Qin, Zuoyong Zhou, Kui Nie, Shijun Hu, Ze Zhang, Liting Cao |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
Neutrophils
Immunology Gene Expression Biology Eimeria Microbiology Downregulation and upregulation parasitic diseases Gene expression Animals RNA Messenger Receptor Cells Cultured Innate immune system Macrophages Toll-Like Receptors General Medicine biology.organism_classification Virology Up-Regulation Toll-Like Receptor 4 Infectious Diseases Real-time polymerase chain reaction Myeloid Differentiation Factor 88 TLR4 Parasitology Signal transduction Chickens Eimeria tenella Signal Transduction |
| Zdroj: | Experimental parasitology. 133(4) |
| ISSN: | 1090-2449 |
| Popis: | Coccidiosis, caused by Eimeria parasites, is a major parasitic disease responsible for great economic losses in the poultry industry. Toll-like receptor (TLR) family is one of the most important innate immune receptors, which involved in pathogen detection by initiating host responses, and it plays important roles in the reduction and clearance of pathogens. Very little information is available about the roles of chicken TLRs (ChTLRs) during Eimeria tenella infection. In the current study, mRNA expression of ChTLRs and associated signal adaptors in heterophils and monocyte-derived macrophages stimulated with E. tenella in vitro were measured by real-time quantitative polymerase chain reaction. The results showed that ChTLR4 and ChTLR15 expression were increased significantly in heterophils and monocyte-derived macrophages following live E. tenella sporozoites stimulation. The heat-killed E. tenella sporozoites stimulated higher expression of ChTLRs and signal adaptors than live sporozoites, the expression of ChTLR4, ChTLR15 and MyD88 in heterophils and monocyte-derived macrophages stimulated with heat-killed E. tenella sporozoites were up-regulated significantly than unstimulated cells. The results suggest that ChTLR4 and ChTLR15 are involved in response to E. tenella infection, and may operate in a MyD88-dependent manner for host defense. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect