Dey Somrita, Bishayi Biswadev
Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, 92 A.P.C. Road, Calcutta, 700009 West Bengal India.
J Inflamm (Lond). 2016 Nov 28;13:36. doi: 10.1186/s12950-016-0145-0. eCollection 2016.
Macrophages serve as intracellular reservoirs of . Recent in vitro studies have confirmed high level resistance by to macrophage mediated killing and the intracellular persistence of Staphylococci may play an important role in the pathogenesis. Since this localization protects them from both cell-mediated and humoral immune responses, therefore, a successful anti-staphylococcal therapy should include the elimination of intracellular bacteria, further protecting the host cells from staphylococci-induced cell death. So, only antibiotic therapy may not be helpful, successful therapy needs combination of drugs not only for elimination of pathogen but also for rescuing the host cell for induced cell death.
In keeping with this idea an in vitro study has been done to examine the effect of Riboflavin along with antibiotics on phagocytosis, hydorgen peroxide, superoxide production, antioxidant enzyme levels, and cytokine levels in mouse macrophages for amelioration of the burden. The immune boosting effects of Riboflavin have been validated through perturbations of redox homeostasis and pro-inflammatory cytokines measurements.
It was observed that the supplementation of Vitamin B-2 (Riboflavin) not only enhances macrophage function as previously reported but also decreases pro-inflammatory responses in infected macrophages. The observed influence of Riboflavin on enhanced antimicrobial effects such as enhanced phagocytosis of macrophages exposed to , hydrogen peroxide or superoxide production when combined with either ciprofloxacin (CIP) or Azithromycin (AZM) and decrease in pro-inflammatory responses of IFN-γ, IL-6, IL-1β. Riboflavin treatment also decreased NO and TNF-α level possibly by inhibiting the NF-κβ pathway. The increased antioxidant enzymes like glutathione reductase, SOD and GSH level helped in maintaining a stable redox state in the cell.
Riboflavin plus antibiotic pretreatment not only enhances macrophage functions but also decreases proinflammatory responses in infected macrophages indicating better bacterial clearance and regulated inflammation which may be considered as a novel and important therapeutic intervention.
巨噬细胞是……的细胞内储存库。最近的体外研究证实,……对巨噬细胞介导的杀伤具有高度抗性,葡萄球菌在细胞内的持续存在可能在发病机制中起重要作用。由于这种定位保护它们免受细胞介导和体液免疫反应的影响,因此,成功的抗葡萄球菌治疗应包括消除细胞内细菌,进一步保护宿主细胞免受葡萄球菌诱导的细胞死亡。所以,仅抗生素治疗可能无济于事,成功的治疗需要联合使用药物,不仅用于消除病原体,还用于挽救宿主细胞免受……诱导的细胞死亡。
基于这一想法,进行了一项体外研究,以检查核黄素与抗生素联合使用对小鼠巨噬细胞吞噬作用、过氧化氢、超氧化物产生、抗氧化酶水平和细胞因子水平的影响,以减轻……负担。通过氧化还原稳态的扰动和促炎细胞因子测量验证了核黄素的免疫增强作用。
观察到补充维生素B-2(核黄素)不仅如先前报道的那样增强巨噬细胞功能,而且还降低感染……的巨噬细胞中的促炎反应。观察到核黄素对增强抗菌作用的影响,例如与环丙沙星(CIP)或阿奇霉素(AZM)联合使用时,暴露于……的巨噬细胞的吞噬作用增强、过氧化氢或超氧化物产生增加,以及IFN-γ、IL-6、IL-1β的促炎反应降低。核黄素治疗还可能通过抑制NF-κβ途径降低NO和TNF-α水平。谷胱甘肽还原酶、超氧化物歧化酶和谷胱甘肽等抗氧化酶水平的增加有助于维持细胞内稳定的氧化还原状态。
核黄素加抗生素预处理不仅增强巨噬细胞功能,而且降低感染……的巨噬细胞中的促炎反应,表明细菌清除效果更好且炎症得到调节,这可被视为一种新的重要治疗干预措施。