4.7 Article

AjTGF? alleviates V. splendidus-induced inflammation through SMADs pathway in Apostichopus japonicus

Journal

FISH & SHELLFISH IMMUNOLOGY
Volume 134, Issue -, Pages -

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fsi.2023.108593

Keywords

Transforming growth factor beta (TGF-?); Inflammatory response; SMADs; Collagens

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Inhibition of inflammatory response is crucial in controlling inflammation development and protecting organisms from excessive damage. Transforming growth factor beta (TGF-beta) plays a role in inhibiting inflammation in vertebrates. In this study, the role of TGF-beta in regulating inflammation in invertebrates was investigated using sea cucumbers. The results showed that AjTGF-beta negatively regulated inflammation and promoted damage repair through AjSMADs and collagen expression.
The inhibition of inflammatory response is an essential process to control the development of inflammation and is an important step to protect the organism from excessive inflammatory damage. As a pleiotropic cytokine, transforming growth factor beta (TGF-beta) plays a regulatory role in inhibiting inflammation in vertebrates. To investigate the role of TGF-beta in the regulation of inflammation in invertebrates, we cloned and characterized the TGF-beta gene from Apostichopus japonicus via rapid amplification of cDNA ends, and the sample was designated as AjTGF-beta. For Vibrio splendidus-challenged sea cucumbers, the expression of AjTGF-beta mRNAs in coelomocytes decreased at 96 h (0.27-fold), which was contrary to the trend of inflammation. AjTGF-beta was expressed in all tissues with the highest expression in the body wall. When AjTGF-beta was knocked down by using small interfering RNA (siRNA-KD) to 0.45-fold, AjSMAD 2/3 and AjSMAD6 were downregulated to 0.32- and 0.05-fold compared with the control group, respectively. Furthermore, when the damaged sea cucumber was challenged by V. splendidus co-incubated with rAjTGF-beta, the damage area had no extensive inflammation, and damaged repair appeared at 72 h compared with the Vs + BSA group, in which the expression of AjSMAD 2/3 was upregulated by 1.35-fold. Under this condition, AjSMAD 2/3 silencing alleviated rAjTGF-beta-induced damage recovery. Moreover, rAjTGF-beta slightly induced the collagen I expression from 6.13 ng/mL to 7.84 ng/mL, and collagen III was upregulated from 6.23 ng/mL to 6.89 ng/mL compared with the Vs + BSA group. This finding indicates that AjTGF-beta negatively regulated the inflammatory progress and accelerated the repair of damage by AjSMADs to regulate the collagens expression.

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