{"title":"Morphine's role in macrophage polarization: Exploring M1 and M2 dynamics and disease susceptibility.","authors":"Jonaid Ahmad Malik, Javed N Agrewala","doi":"10.1016/j.jneuroim.2025.578534","DOIUrl":null,"url":null,"abstract":"<p><p>Morphine is a globally prevalent substance of misuse, renowned for its immunosuppressive effects mediated through opioid receptors expressed on immune cells. Macrophages are crucial antigen-presenting cells that fulfill diverse roles, such as antigen presentation, phagocytosis, wound healing, and disease protection. They are typically classified based on their activation states: M1 (proinflammatory), M2 (anti-inflammatory), and M0 (resting). Morphine significantly modulates immune responses and neuroinflammation, further complicating the landscape of opioid dependency and disease susceptibility. The association of macrophages under the influence of morphine needs to be understood under various diseased conditions. Several studies have been focused on investigating the impact of morphine on macrophage function and its implications in infectious diseases and brain-associated diseases. To light this subject, we have discussed recent advancements in understanding the influences between morphine, macrophage function, polarization, infection, brain tumors, and drug dependency. This article explores the complex relationship between morphine, macrophages, and related pathologies. Consequently, discussing deeper insights into these dynamics could guide effective treatments for substance abuse disorders.</p>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"400 ","pages":"578534"},"PeriodicalIF":2.9000,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of neuroimmunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.jneuroim.2025.578534","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Morphine is a globally prevalent substance of misuse, renowned for its immunosuppressive effects mediated through opioid receptors expressed on immune cells. Macrophages are crucial antigen-presenting cells that fulfill diverse roles, such as antigen presentation, phagocytosis, wound healing, and disease protection. They are typically classified based on their activation states: M1 (proinflammatory), M2 (anti-inflammatory), and M0 (resting). Morphine significantly modulates immune responses and neuroinflammation, further complicating the landscape of opioid dependency and disease susceptibility. The association of macrophages under the influence of morphine needs to be understood under various diseased conditions. Several studies have been focused on investigating the impact of morphine on macrophage function and its implications in infectious diseases and brain-associated diseases. To light this subject, we have discussed recent advancements in understanding the influences between morphine, macrophage function, polarization, infection, brain tumors, and drug dependency. This article explores the complex relationship between morphine, macrophages, and related pathologies. Consequently, discussing deeper insights into these dynamics could guide effective treatments for substance abuse disorders.
期刊介绍:
The Journal of Neuroimmunology affords a forum for the publication of works applying immunologic methodology to the furtherance of the neurological sciences. Studies on all branches of the neurosciences, particularly fundamental and applied neurobiology, neurology, neuropathology, neurochemistry, neurovirology, neuroendocrinology, neuromuscular research, neuropharmacology and psychology, which involve either immunologic methodology (e.g. immunocytochemistry) or fundamental immunology (e.g. antibody and lymphocyte assays), are considered for publication.