Article

Suppression of the TLR3 mediated pro-inflammatory gene expressions by PPDPF in chicken DF-1 cells

Eunmi Hwang1, Hyungkuen Kim1, Anh Duc Truong2, Sung-Jo Kim1,*, Ki-Duk Song3,4,**
Author Information & Copyright
1Division of Cosmetics and Biotechnology, College of Life and Health Sciences, Hoseo University, Asan 31499, Korea.
2Department of Biochemistry and Immunology, Vietnam National Institute of Veterinary Research, Hanoi 80000, Viet Nam.
3Department of Agricultural Convergence Technology, Jeonbuk National University, Jeonju-si 54896, Korea.
4The Animal Molecular Genetics and Breeding Center, Jeonbuk National University, Jeonju-si 54896, Korea.
**Corresponding Author: Sung-Jo Kim, Division of Cosmetics and Biotechnology, College of Life and Health Sciences, Hoseo University, Asan 31499, Korea, Republic of. Phone: +82-41-540-5571. E-mail: sungjo@hoseo.edu.
**Corresponding Author: Ki-Duk Song, Department of Agricultural Convergence Technology, Jeonbuk National University, Jeonju-si 54896, Korea, Republic of. The Animal Molecular Genetics and Breeding Center, Jeonbuk National University, Jeonju-si 54896, Korea, Republic of. Phone: +82-63-219-5523. E-mail: kiduk.song@jbnu.ac.kr.

© Copyright 2021 Korean Society of Animal Science and Technology. This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: Oct 16, 2021; Revised: Nov 27, 2021; Accepted: Nov 30, 2021

Published Online: Dec 10, 2021

Abstract

Toll-like receptors (TLRs), as a part of innate immunity, plays an important role in detecting pathogenic molecular patterns (PAMPs) which are structural components or product of pathogens and initiate host defense systems or innate immunity. Precise negative feedback regulations of TLR signaling are important in maintaining homeostasis to prevent tissue damage by uncontrolled inflammation during innate immune responses. In this study, we identified and characterized the function of the pancreatic progenitor cell differentiation and proliferation factor (PPDPF) as a negative regulator for TLR signal-mediated inflammation in chicken. Bioinformatics analysis showed that the structure of chicken PPDPF evolutionarily conserved amino acid sequences with domains, i.e., SH3 binding sites and CDC-like kinase 2 (CLK2) binding sites, suggesting that relevant signaling pathways might contribute to suppression of inflammation. Our results showed that stimulation with polyinosinic:polycytidylic acids (Poly (I:C)), a synthetic agonist for TLR3 signaling, increased the mRNA expression of PPDPF in chicken fibroblasts DF-1 but not in chicken macrophage-like cells HD11. In addition, the expression of pro-inflammatory genes stimulated by Poly(I:C) were reduced in DF-1 cells which overexpress PPDPF. Future studies warrant to reveal the molecular mechanisms responsible for the anti-inflammatory capacity of PPDPF in chicken as well as a potential target for controlling viral resistance.

Keywords: chicken; pancreatic progenitor cell differentiation and proliferation factor; DF-1; innate immunity; inflammation; Toll-like receptor 3