PMID- 36007354
OWN - NLM
STAT- MEDLINE
DCOM- 20220920
LR  - 20221019
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 150
DP  - 2022 Oct
TI  - The role of neuroplastin65 in macrophage against E. coli infection in mice.
PG  - 78-89
LID - S0161-5890(22)00390-X [pii]
LID - 10.1016/j.molimm.2022.08.003 [doi]
AB  - BACKGROUND: Innate immune response constitutes the first line of defense against 
      pathogens. Inflammatory responses involve close contact between different 
      populations of cells. These adhesive interactions mediate migration of cells to 
      sites of infection leading the effective action of cells within the lesions. Cell 
      adhesion molecules are critical to controlling immune response mediating cell 
      adhesion or chemotaxis, as well as coordinating actin-based cell motility during 
      phagocytosis and chemotaxis. Recently, a newly discovered neuroplastin (Np) 
      adhesion molecule is found to play an important role in the nervous system. 
      However, there is limited information on Np functions in immune response. To 
      understand how Np is involved in innate immune response, a mouse model of 
      intraperitoneal infection was established to investigate the effect of Np on 
      macrophage-mediated clearance of E. coli infection and its possible molecular 
      mechanisms. METHODS: Specific deficiency mice with Nptn gene controlling Np65 
      isoform were employed in this study. The expression levels of mRNA and proteins 
      were detected by qPCR and western blot, or evaluated by flow cytometry. The 
      expression level of NO and ROS were measured with their specific indicators. Cell 
      cycle and apoptosis were detected by specific detection kits. Acid phosphatase 
      activity was measured by flow cytometry after labelling with LysoRed fluorescent 
      probe. Bone marrow derived macrophages (BMDMs) were isolated from bone marrow of 
      mice hind legs. Cell proliferation was detected by CCK8 assay. Cell migration was 
      measured by wound healing assay or transwell assay. RESULTS: The lethal dose of 
      E. coli infection in Np65(-/-) mice dropped to the half of lethal dose in WT 
      mice. The bacterial load in the spleen, kidney and liver from Np65(-/-) mice were 
      significantly higher than that from WT mice, which were due to the dramatic 
      reduction of NO and ROS production in phagocytes from Np65(-/-) mice. Np65 gene 
      deficiency remarkably impaired phagocytosis and function of lysosome in 
      macrophage. Furthermore, Np65 molecule was involved in maturation and 
      proliferation, even in migration and chemotaxis of BMDM in vitro. CONCLUSION: 
      This study for the first time demonstrates that Np is involved in multi-function 
      of phagocytes during bacterial infection, proposing that Np adhesion molecule 
      plays a critical role in clearing pathogen infection in innate immunity.
CI  - Copyright (c) 2022 Elsevier Ltd. All rights reserved.
FAU - Ren, Huan
AU  - Ren H
AD  - Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, and Department of 
      Immunology and Microbiology, Tongji University School of Medicine, 1239 Siping 
      Road, Shanghai 200092, China.
FAU - Xia, Xiaoxue
AU  - Xia X
AD  - Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, and Department of 
      Immunology and Microbiology, Tongji University School of Medicine, 1239 Siping 
      Road, Shanghai 200092, China.
FAU - Dai, Xueting
AU  - Dai X
AD  - Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, and Department of 
      Immunology and Microbiology, Tongji University School of Medicine, 1239 Siping 
      Road, Shanghai 200092, China.
FAU - Dai, Yalei
AU  - Dai Y
AD  - Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, and Department of 
      Immunology and Microbiology, Tongji University School of Medicine, 1239 Siping 
      Road, Shanghai 200092, China. Electronic address: daiyl@tongji.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220822
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Actins)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (neuroplastin protein, mouse)
RN  - EC 3.1.3.2 (Acid Phosphatase)
SB  - IM
MH  - Acid Phosphatase
MH  - Actins
MH  - Animals
MH  - Cell Adhesion Molecules
MH  - *Escherichia coli/metabolism
MH  - *Escherichia coli Infections
MH  - Fluorescent Dyes
MH  - Macrophages
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Protein Isoforms
MH  - RNA, Messenger
MH  - Reactive Oxygen Species
OTO - NOTNLM
OT  - Chemotaxis
OT  - Lysosome
OT  - Macrophage
OT  - NO
OT  - Neuroplastin
OT  - ROS
COIS- Declaration of Competing Interest The authors declare no conflict of interest.
EDAT- 2022/08/26 06:00
MHDA- 2022/09/21 06:00
CRDT- 2022/08/25 18:20
PHST- 2022/04/10 00:00 [received]
PHST- 2022/07/20 00:00 [revised]
PHST- 2022/08/04 00:00 [accepted]
PHST- 2022/08/26 06:00 [pubmed]
PHST- 2022/09/21 06:00 [medline]
PHST- 2022/08/25 18:20 [entrez]
AID - S0161-5890(22)00390-X [pii]
AID - 10.1016/j.molimm.2022.08.003 [doi]
PST - ppublish
SO  - Mol Immunol. 2022 Oct;150:78-89. doi: 10.1016/j.molimm.2022.08.003. Epub 2022 Aug 
      22.