Damri Odeya, Agam Galila
Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Zlotowski Center for Neuroscience and Zelman Center-The School of Brain Sciences and Cognition, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel.
Int J Mol Sci. 2024 Dec 11;25(24):13277. doi: 10.3390/ijms252413277.
This narrative review examines lithium's effects on immune function, inflammation and cell survival, particularly in bipolar disorder (BD) in in vitro studies, animal models and clinical studies. In vitro studies show that high lithium concentrations (5 mM, beyond the therapeutic window) reduce interleukin (IL)-1β production in monocytes and enhance T-lymphocyte resistance, suggesting a protective role against cell death. Lithium modulates oxidative stress in lipopolysaccharide (LPS)-activated macrophages by inhibiting nuclear factor (NF)-ƙB activity and reducing nitric oxide production. At therapeutically relevant levels, lithium increased both pro-inflammatory [interferon (INF)-γ, IL-8 and tumor necrosis factor (TNF)-α)] and anti-inflammatory (IL-10) cytokines on whole blood supernatant culture in healthy volunteers, influencing the balance of pro- and anti-inflammatory responses. Animal models reveal lithium's potential to alleviate inflammatory diseases by reducing pro-inflammatory cytokines and enhancing anti-inflammatory responses. It also induces selective macrophage death in atherosclerotic plaques without harming other cells. In primary rat cerebellum cultures (ex vivo), lithium prevents neuronal loss and inhibits astroglial growth, impacting astrocytes and microglia. Clinical studies show that lithium alters cytokine profiles and reduces neuroinflammatory markers in BD patients. Chronic treatment decreases IL-2, IL-6, IL-10 and IFN-γ secretion from peripheral blood leukocytes. Lithium response correlates with TNF-α levels, with poor responders showing higher TNF-α. Overall, these findings elucidate lithium's diverse mechanisms in modulating immune responses, reducing inflammation and promoting cell survival, with significant implications for managing BD and other inflammation-related conditions. Yet, to better understand the drug's impact in BD and other inflammatory/neuroinflammatory conditions, further research is warranted to appreciate lithium's therapeutic potential and its role in immune regulation.
本叙述性综述考察了锂对免疫功能、炎症和细胞存活的影响,尤其是在双相情感障碍(BD)中的影响,涵盖体外研究、动物模型和临床研究。体外研究表明,高浓度锂(5 mM,超出治疗窗)可降低单核细胞中白细胞介素(IL)-1β的产生,并增强T淋巴细胞抗性,提示其对细胞死亡具有保护作用。锂通过抑制核因子(NF)-ƙB活性和减少一氧化氮产生,调节脂多糖(LPS)激活的巨噬细胞中的氧化应激。在治疗相关水平上,锂可增加健康志愿者全血上清液培养中的促炎细胞因子[干扰素(INF)-γ、IL-8和肿瘤坏死因子(TNF)-α]和抗炎细胞因子(IL-10),影响促炎和抗炎反应的平衡。动物模型显示锂有潜力通过减少促炎细胞因子和增强抗炎反应来减轻炎症性疾病。它还可诱导动脉粥样硬化斑块中的选择性巨噬细胞死亡,而不损害其他细胞。在原代大鼠小脑培养物(体外)中,锂可防止神经元丢失并抑制星形胶质细胞生长,对星形胶质细胞和小胶质细胞产生影响。临床研究表明,锂可改变BD患者的细胞因子谱并降低神经炎症标志物。长期治疗可减少外周血白细胞分泌IL-2、IL-6、IL-10和IFN-γ。锂反应与TNF-α水平相关,反应不佳者TNF-α水平较高。总体而言,这些发现阐明了锂在调节免疫反应、减轻炎症和促进细胞存活方面的多种机制,对BD和其他炎症相关病症的管理具有重要意义。然而,为了更好地理解该药物在BD和其他炎症/神经炎症病症中的作用,有必要进行进一步研究以了解锂的治疗潜力及其在免疫调节中的作用。