Differential expression of Toll-like receptor 4 signaling pathway genes in Escherichia coli F18-resistant and – sensitive Meishan piglets

Abstract

The Toll-like receptor 4 (TLR4) signaling pathway is an important inflammatory pathways associated with the progression of numerous diseases. The aim of the present study was to investigate the relationship between TLR4 signaling and resistance to Escherichia coli F18 in locally weaned Meishan piglets. Using a real-time PCR approach, expression profiles were determined for key TLR4 signaling pathway genes TLR4, MyD88, CD14, IFN-α, IL-1β and TNF-α in the spleen, thymus, lymph nodes, duodenum and jejunum of E. coli F18-resistant and -sensitive animals. TLR4 signaling pathway genes were expressed in all the immune organs and intestinal tissues, and the expression was generally higher in the spleen and lymph nodes. TLR4 transcription was higher in the spleen of sensitive piglets (p<0.05), but there was no significant difference in TLR4 mRNA levels in other tissues. Similarly, CD14 transcription was higher in lymph nodes of sensitive animals (p<0.05) but not in other tissues. IL-1β expression was higher in the spleen and in the duodenum of resistant piglets (p<0.05, p<0.01, respectively), and there were no significant differences in other tissues. There were also no significant differences in the expression of MyD88, TNF-α and IFN-α between sensitive and resistant piglets (p>0.05). These results further confirm the involvement of the TLR4 signaling pathway in resistance to E. coli F18 in Meishan weaned piglets. The resistance appeared to be mediated via downregulation of TLR4 and CD14, and upregulation of MyD88 that may promote the release of cytokines TNF-α, IL-1β, IFN-α and other inflammatory mediators which help to fight against E. coli F18 infection.

Dietary Supplementation With Chinese Herbal Residues or Their Fermented Products Modifies the Colonic Microbiota, Bacterial Metabolites, and Expression of Genes Related to Colon Barrier Function in Weaned Piglets

“…A melting temperature (T m ) peak of 85 ± 0.8°C was used to determine the specificity of amplification. T m values are reported as the mean of three replicates (Liu et al, 2016).…”

“…Weaning is a critical stage for piglets, as this process is associated with alterations in the architecture and function of the gut and changes in the enteric microbiota (Boudry et al, 2004). Weaned piglets often exhibit underdeveloped immune systems, digestive disorders, and post-weaning diarrhea (Liu et al, 2016), all these events decreasing growth performance and causing economic loss for the swine industry (Amezcua et al, 2002). Antibiotics and the pharmacological addition of ZnO in the diets have long been used to solve post-weaning problems (Barton, 2000).…”

New Insight into the Molecular Mechanism of the FUT2 Regulating Escherichia coli F18 Resistance in Weaned Piglets

“…For the IPEC-J2 control, Lenti-RFUT2-n, and pcDNA3.1-FUT2 cells, the in vitro evaluation of F18 fimbriae adhesion was performed as previously described [ 45 ]. A relative quantification method [ 49 ], in addition to bacteria enumeration, was used to establish an efficient and accurate method for the detection of E. coli adhesion to small intestinal epithelial cells in pigs.…”

“…Furthermore, we identified the differential expression of the FUT2 , FUT3 , TLR5 , TAP2 , IL1β genes in the duodenum, indicating that these genes probably play a crucial role in the resistance to E. coli F18. Our previous studies concentrated on the relationship of immune gene expression and E. coli F18 resistance in pigs [ 4 , 5 , 6 , 7 , 8 ], only a few reports directly on receptor formation showing the effect of the α(1,2) fucosyltransferase 1 ( FUT1 ) gene M307 G/A mutation on the adhesion of E. coli F18 to pig intestinal epithelial cells [ 9 ], but its polymorphism distribution in more than 20 Chinese local pig breeds and wild boar population is extremely skewed [ 10 , 11 , 12 ]. The smallest antigenic determinant of the E. coli F18 receptor is the type 1 H-antigen of the ABO blood group antigens [ 13 ].…”

Genetic polymorphisms associated with diabetic foot ulcer: A review article

“…Ligand-binding capacity with TLR4 may be disturbed by SNPs in the extracellular domain of TLR4 that leads to deregulation of the TLR4 signaling modifying the risk of chronic inflammation, thus prolonging wound healing (Liu et al, 2016).…”