Muscle fiber characteristics and expression level of Troponin T3, Toll-like receptor 2, and Toll-like receptor 4 genes in chicken meat with white striping.

Background and Aim: The poultry industry faces an emerging muscular defect in chicken meat called white striping (WS). The biological processes associated with WS myopathy are immune system activation, angiogenesis, hypoxia, cell death, and striated muscle contraction. We examined the Troponin T3 (TNNT3), Toll-like receptor 2 (TLR2), and Toll-like receptor 4 (TLR4) genes based on their functions related to muscle contraction and the innate immune system. This study aimed to determine the muscle fiber characteristics (MFCs) and expression level of TNNT3, TLR2, and TLR4 genes in white striping chicken meat (WSCM). Materials and Methods: A total of 428 breast samples were randomly collected from a commercial poultry processing plant. The samples were classified into four levels: 0 (normal), 1 (moderate WS), 2 (severe WS), and 3 (extreme WS). Five samples per group were selected to evaluate MFCs, including total number of muscle fibers, muscle fiber diameter, cross-sectional area, endomysium thickness, and perimysium thickness. Five samples per group were selected for ribonucleic acid (RNA) isolation to evaluate the messenger RNA (mRNA) expression levels of TNNT3, TLR2, and TLR4 genes related to WS. Results: Statistical analysis revealed that the total number of fibers, endomysium thickness, and perimysium thickness significantly differed between groups (p < 0.05). Muscle fiber diameter and cross-sectional area did not significantly differ (p > 0.05). The expression of the TNNT3 gene did not significantly differ among groups (p > 0.05). Toll-like receptor 2 and TLR4 mRNA expression significantly differed among groups (p < 0.05). Conclusion: These detailed MFCs will provide baseline information to observe WS in chicken meat. Toll-like receptor 2 and TLR4 genes may play a role in the occurrence of WS in chicken meat through non-specific immune reactions.

Quercetin enhances and modulates the fungal killing efficacy of chicken heterophils through immunological recognition, effector functions, and resolution.

Herbal compound, quercetin, has previously been shown its modulatory effects on mammalian neutrophils and avian counterpart. However, at this instance it is not clear how quercetin promotes its effects on fungal and yeast killing in chicken heterophils. In the present study, we have proved that quercetin exerts the significant modulatory effects against pathogenic yeast (Candida albicans) in freshly isolated heterophils from Thai native broiler chicken. This substance is shown to facilitate heterophil effector functions through the reduction of ROS generation, and promotion of phagocytosis and candidacidal killing. The quercetin effects on zymosan recognition and migration of cells toward zymosan are subtle, but insignificant differed from control, whereas cell migration towards live Candida is markedly differed. We also find the abundant release of heterophil extracellular traps (HETs) from quercetin-primed cells. From a gene expression standpoint, cells received quercetin display the up-regulation of fungal recognition and migratory genes. The quercetin shows anti-inflammatory function by suppression of pro-inflammatory cytokine genes as well as most of ROS-related genes. Collectively, our findings highlight and provide clues for a promising utilization of quercetin in chicken innate immunity to further combat the fungal infections.