Ageing-Induced Decline in Primary Myeloid Cell Phagocytosis Is Unaffected by Optineurin Insufficiency

Bibliographic Details
Title: Ageing-Induced Decline in Primary Myeloid Cell Phagocytosis Is Unaffected by Optineurin Insufficiency
Authors: Josip Peradinovic, Nikolina Mohovic, Katarina Bulic, Andrea Markovinovic, Raffaello Cimbro, Ivana Munitic
Source: Biology, Vol 12, Iss 2, p 240 (2023)
Publisher Information: MDPI AG, 2023.
Publication Year: 2023
Collection: LCC:Biology (General)
Subject Terms: phagocytosis, ageing, optineurin, neurodegeneration, inflammation, Biology (General), QH301-705.5
More Details: Optineurin is a ubiquitin-binding adaptor protein involved in multiple cellular processes, including innate inflammatory signalling. Mutations in optineurin were found in amyotrophic lateral sclerosis, an adult-onset fatal neurodegenerative disease that targets motor neurons. Neurodegeneration results in generation of neuronal debris, which is primarily cleared by myeloid cells. To assess the role of optineurin in phagocytosis, we performed a flow cytometry-based phagocytic assay of apoptotic neuronal debris and E. coli bioparticles in bone marrow-derived macrophages (BMDMs), and primary neonatal microglia from wild-type (WT) and optineurin-insufficient (Optn470T) mice. We found no difference in phagocytosis efficiency and the accompanying cytokine secretion in WT and Optn470T BMDMs and microglia. This was true at both steady state and upon proinflammatory polarization with lipopolysaccharide. When we analysed the effect of ageing as a major risk factor for neurodegeneration, we found a substantial decrease in the percentage of phagocytic cells and proinflammatory cytokine secretion in BMDMs from 2-year-old mice. However, this ageing-induced phagocytic decline was unaffected by optineurin insufficiency. All together, these results indicate that ageing is the factor that perturbs normal phagocytosis and proinflammatory cytokine secretion, but that optineurin is dispensable for these processes.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2079-7737
Relation: https://www.mdpi.com/2079-7737/12/2/240; https://doaj.org/toc/2079-7737
DOI: 10.3390/biology12020240
Access URL: https://doaj.org/article/de6aa34ca0474e9ca64173f7c5b97699
Accession Number: edsdoj.6aa34ca0474e9ca64173f7c5b97699
Database: Directory of Open Access Journals
More Details
ISSN:20797737
DOI:10.3390/biology12020240
Published in:Biology
Language:English