PUBLICATION

Loss of Ripk3 attenuated neutrophil accumulation in a lipopolysaccharide-induced zebrafish inflammatory model

Authors: Wen, W., Chen, J., Zhou, Y., Li, G., Zhang, Y.
ID: ZDB-PUB-220302-5
Date: 2022
Source: Cell death discovery 8: 88 (Journal)
Registered Authors: Zhang, Yiyue
Keywords: none
MeSH Terms: none
PubMed: 35220408 Full text @ Cell Death Discov

Abstract

Neutrophils are important effector cells during inflammation, which play complex roles. Therefore, investigating the regulation of neutrophil accumulation during inflammation might provide targets for treating related diseases. In the present study, we generated a ripk3-deficient zebrafish line to study the roles of Ripk3 in neutrophil-related inflammation. The homeostatic hematopoiesis and cytokine expression of the ripk3-deficient larvae were unaltered. The ripk3-deficient larvae with caudal fin fold injury exhibited similar neutrophil enrichment with wild-type larvae, suggesting that Ripk3 is not essential for non-infectious inflammatory responses. When challenged with lipopolysaccharide (LPS), the ripk3-deficient larvae showed significantly less neutrophil accumulation in the injection site and differential expression of several key cytokines. Ripk3 inhibitors could also attenuate neutrophil accumulation in wild-type larvae, indicating that Ripk3 could serve as a candidate target for inflammation treatment. In summary, our study indicated that Ripk3 has an essential role in LPS-induced inflammatory responses. It was suggested that the ripk3-deficient zebrafish might be applied in developing infectious disease models, while Ripk3 also has potential as an inflammation-treatment target.

Genes / Markers

Marker	Marker Type	Name
cxcl8a	GENE	chemokine (C-X-C motif) ligand 8a
hbbe1.1	GENE	hemoglobin beta embryonic-1.1
il10	GENE	interleukin 10
il13	GENE	interleukin 13
il1b	GENE	interleukin 1, beta
il4	GENE	interleukin 4
il6	GENE	interleukin 6 (interferon, beta 2)
mfap4.1	GENE	microfibril associated protein 4, tandem duplicate 1
rag1	GENE	recombination activating 1
ripk3	GENE	receptor-interacting serine-threonine kinase 3

1 - 10 of 10

Show

Figures

Show all Figures

Expression

Phenotype

Fish	Conditions	Stage	Phenotype	Figure
AB	chemical treatment by injection: lipopolysaccharide	Protruding-mouth	neutrophil increased accumulation yolk, abnormal	Fig. 5
AB	chemical treatment by injection: lipopolysaccharide	Protruding-mouth	whole organism il13 expression decreased amount, abnormal	Fig. 5
AB	chemical treatment by injection: lipopolysaccharide	Protruding-mouth	whole organism il1b expression increased amount, abnormal	Fig. 5
AB	chemical treatment by injection: lipopolysaccharide	Protruding-mouth	whole organism il4 expression decreased amount, abnormal	Fig. 5
AB	chemical treatment by injection: lipopolysaccharide	Protruding-mouth	whole organism il6 expression increased amount, abnormal	Fig. 5
AB	transection: caudal fin	Protruding-mouth	whole organism cxcl8a expression increased amount, abnormal	Fig. 4
AB	transection: caudal fin	Protruding-mouth	whole organism il10 expression increased amount, abnormal	Fig. 4
AB	transection: caudal fin	Protruding-mouth	whole organism il1b expression increased amount, abnormal	Fig. 4
AB	transection: caudal fin	Protruding-mouth	whole organism il4 expression increased amount, abnormal	Fig. 4
AB	transection: caudal fin	Protruding-mouth	whole organism il6 expression increased amount, abnormal	Fig. 4

1 - 10 of 28

Show

Mutations / Transgenics

Allele	Construct	Type	Affected Genomic Region
szy12		Small Deletion	ripk3

Human Disease / Model

Sequence Targeting Reagents

Target	Reagent	Reagent Type
ripk3	CRISPR3-ripk3	CRISPR

Fish

Fish
AB
ripk3^szy12/szy12

Antibodies

Orthology

Engineered Foreign Genes

Mapping

Wen et al., 2022 ZDB-PUB-220302-5 PMID:35220408

Loss of Ripk3 attenuated neutrophil accumulation in a lipopolysaccharide-induced zebrafish inflammatory model

Wen et al., 2022

ZDB-PUB-220302-5
PMID:35220408