Abstract
BackgroundMastitis, an infection caused by Gram-positive bacteria, produces udder inflammation and oxidative injury in milk-producing mammals. Toll-like receptor 2 (TLR2) is important for host recognition of invading Gram-positive microbes. Over-expression of TLR2 in transgenic dairy goats is a useful model for studying various aspects of infection with Gram-positive bacteria, in vivo.MethodsWe over-expressed TLR2 in transgenic dairy goats. Pam3CSK4, a component of Gram-positive bacteria, triggered the TLR2 signal pathway by stimulating the monocytes-macrophages from the TLR2-positive transgenic goats, and induced over-expression of activator protein-1 (AP-1), phosphatidylinositol 3-kinase (PI3K) and transcription factor nuclear factor kappa B (NF-κB) and inflammation factors downstream of the signal pathway.ResultsCompared with wild-type controls, measurements of various oxidative stress-related molecules showed that TLR2, when over-expressed in transgenic goat monocytes-macrophages, resulted in weak lipid damage, high level expression of anti-oxidative stress proteins, and significantly increased mRNA levels of transcription factor NF-E2-related factor-2 (Nrf2) and the downstream gene, heme oxygenase-1 (HO-1). When Pam3CSK4 was used to stimulate ear tissue in vivo the HO-1 protein of the transgenic goats had a relatively high expression level.ConclusionsThe results indicate that the oxidative injury in goats over-expressing TLR2 was reduced following Pam3CSK4 stimulation. The underlying mechanism for this reduction was increased expression of the anti-oxidation gene HO-1 by activation of the Nrf2 signal pathway.
Highlights
Mastitis, an infection caused by Gram-positive bacteria, produces udder inflammation and oxidative injury in milk-producing mammals
Toll-like receptor 2 (TLR2) expression levels in the transgenic group were significantly higher than those of the Wt group at 1 and 8 h post-stimulation (P < 0.05) (Fig. 1e). These results confirmed that TLR2 expression of the monocytes-macrophages of the transgenic group was upregulated after Pam3CSK4 stimulation
These results show that TLR2 triggered activation of the NF-κB signal pathway, with NFκB expression levels decreasing at an earlier stage than those of Wt
Summary
An infection caused by Gram-positive bacteria, produces udder inflammation and oxidative injury in milk-producing mammals. Over-expression of TLR2 in transgenic dairy goats is a useful model for studying various aspects of infection with Gram-positive bacteria, in vivo. An inflammatory and oxidative stress disease of udders, is caused by pathogenic bacteria. The disease is common in goats and other dairy animals. TLR2 activation relies mainly on the MyD88 signaling pathway, which activates the NF-κB pathway and mitogen-activated protein kinase (MAPK) pathway. Phosphorylated MAPK activates the transcription factor activator protein-1 (AP-1) and activation of the PI3K/Akt signaling pathway. Expression of inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, IL-8, chemokines and nitrous oxide (NO) can all induce immune responses
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
