Dataset Information

Proteomics analysis of blood neutrophils from WT and Wnt5 DKO mice under DSS treatment

ABSTRACT: Neutrophils are abundant innate immune cells with important roles in host defense and many inflammatory diseases. They possess plasticity and heterogenicity, which underlie their functional ambivalency; they can be beneficial or detrimental to host well-being depending on contexts. While bone marrow is often regarded as the primary source of neutrophil production, the roles of extramedullary production in regulating neutrophil plasticity and heterogenicity in the context of autoimmune diseases remain poorly understood. Here, we report that the lack of both WNT5A and WNT5B unleashes anti-inflammatory protection in mice from Dextran Sodium Sulfate-induced colitis, accompanied with reduced colonic CD8+ T cell activation and enhanced splenic extramedullary myelopoiesis. By using the proteomics method to analyze the blood neutrophils from WT and Wnt5 DKO mice under DSS treatment, our analysis revealed elevated CD101 expression in blood neutrophils from Wnt5 DKO mice, leading to the suppression of CD8 T cell activation in vitro. This proteomic investigation unveiled the mechanism through which neutrophils from Wnt5 DKO mice inhibit CD8 T cells activation.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Neutrophil, Blood

SUBMITTER: Wenxue Li

LAB HEAD: Yansheng Liu

PROVIDER: PXD048613 | Pride | 2026-03-16

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20220812_LuanYi_dko_1.raw	Raw
	20220812_LuanYi_dko_2.raw	Raw
	20220812_LuanYi_dko_3.raw	Raw
	20220812_LuanYi_wt_1.raw	Raw
	20220812_LuanYi_wt_2.raw	Raw

Items per page:

1 - 5 of 8

Publications

Wnt5 controls splenic myelopoiesis and neutrophil functional ambivalency during DSS-induced colitis.

Luan Yi Y Hu Jiajia J Wang Qijun Q Wang Xujun X Li Wenxue W Qu Rihao R Yang Chuan C Rajendran Barani Kumar BK Zhou Hongyue H Liu Peng P Zhang Ningning N Shi Yu Y Liu Yansheng Y Tang Wenwen W Lu Jun J Wu Dianqing D

Cell reports 20240308 3

Neutrophils are important innate immune cells with plasticity, heterogenicity, and functional ambivalency. While bone marrow is often regarded as the primary source of neutrophil production, the roles of extramedullary production in regulating neutrophil plasticity and heterogenicity in autoimmune diseases remain poorly understood. Here, we report that the lack of wingless-type MMTV integration site family member 5 (WNT5) unleashes anti-inflammatory protection against colitis in mice, accompanie ...[more]

PMID: 38461416

Similar Datasets

Project description:Lipocalin 24p3 (24p3) is a neutrophil secondary granule protein. 24p3 is also a siderocalin, which binds several bacterial siderophores. It was therefore proposed that synthesis and secretion of 24p3 by stimulated macrophages or release of 24p3 upon neutrophil degranulation sequesters iron-laden siderophores to attenuate bacterial growth. Accordingly, 24p3-deficient mice are susceptible to bacterial pathogens whose siderophores would normally be chelated by 24p3. Specific granule deficiency (SGD) is a rare congenital disorder characterized by complete absence of proteins in secondary granules. Neutrophils from SGD patients, who are prone to bacterial infections, lack normal functions but the potential role of 24p3 in neutrophil dysfunction in SGD is not known. Here we show that neutrophils from 24p3-deficient mice are defective in many neutrophil functions. Specifically, neutrophils in 24p3-deficient mice do not extravasate to sites of infection and are defective for chemotaxis. A transcriptome analysis revealed that genes that control cytoskeletal reorganization are selectively suppressed in 24p3-deficient neutrophils. Additionally, small regulatory RNAs (miRNAs) that control upstream regulators of cytoskeletal proteins are also increased in 24p3-deficient neutrophils. Further, 24p3-deficient neutrophils failed to phagocytose bacteria, which may account for the enhanced sensitivity of 24p3-deficient mice to both intracellular (Listeria monocytogenes) and extracellular (Candida albicans, Staphylococcus aureus) pathogens. Interestingly, Listeria does not secrete siderophores and additionally, the siderophore secreted by Candida is not sequestered by 24p3. Therefore, the heightened sensitivity of 24p3-deficient mice to these pathogens is not due to sequestration of siderophores limiting iron availability, but is a consequence of impaired neutrophil function. Key words: Lipocalin, 24p3, neutrophils, cell motility, chemotaxis, MIRNA-362-3p To address the role of lipocalin 2 in regulating miRNA expression profiling in neutrophils derived from mouse bone marrow, we performed microarray analysis of miRNAs in wild type (N=2) and lcn2 knockout (N=2) neutrophils.