Miles Brodie, Abdel-Ghaffar Khaled A, Gamal Ahmed Y, Baban Babak, Cutler Christopher W
Department of Periodontics, College of Dental Medicine, Georgia Regents University Augusta, GA, USA.
Ain Shams University Cairo, Egypt.
Front Microbiol. 2014 Jan 27;5:6. doi: 10.3389/fmicb.2014.00006. eCollection 2014.
The majority of risk factors for chronic inflammatory diseases are unknown. This makes personalized medicine for assessment, prognosis, and choice of therapy very difficult. It is becoming increasingly clear, however, that low-grade subclinical infections may be an underlying cause of many chronic inflammatory diseases and thus may contribute to secondary outcomes (e.g., cancer). Many diseases are now categorized as inflammatory-mediated diseases that stem from a dysregulation in host immunity. There is a growing need to study the links between low-grade infections, the immune responses they elicit, and how this impacts overall health. One such link explored in detail here is the extreme sensitivity of myeloid dendritic cells (mDCs) in peripheral blood to chronic low-grade infections and the role that these mDCs play in arbitrating the resulting immune responses. We find that emerging evidence supports a role for pathogen-induced mDCs in chronic inflammation leading to increased risk of secondary clinical disease. The mDCs that are elevated in the blood as a result of low-grade bacteremia often do not trigger a productive immune response, but can disseminate the pathogen throughout the host. This aberrant trafficking of mDCs can accelerate systemic inflammatory disease progression. Conversely, restoration of dendritic cell homeostasis may aid in pathogen elimination and minimize dissemination. Thus it would seem prudent when assessing chronic inflammatory disease risk to consider blood mDC numbers, and the microbial content (microbiome) and activation state of these mDCs. These may provide important clues ("the canary in the coal mine") of high inflammatory disease risk. This will facilitate development of novel immunotherapies to eliminate such smoldering infections in atherosclerosis, cancer, rheumatoid arthritis, and pre-eclampsia.
大多数慢性炎症性疾病的风险因素尚不清楚。这使得针对评估、预后和治疗选择的个性化医疗变得非常困难。然而,越来越清楚的是,低度亚临床感染可能是许多慢性炎症性疾病的潜在原因,因此可能导致继发性后果(如癌症)。现在许多疾病被归类为炎症介导的疾病,其源于宿主免疫失调。越来越需要研究低度感染、它们引发的免疫反应以及这如何影响整体健康之间的联系。本文详细探讨的一个这样的联系是外周血中的髓样树突状细胞(mDCs)对慢性低度感染的极端敏感性以及这些mDCs在仲裁由此产生的免疫反应中所起的作用。我们发现,新出现的证据支持病原体诱导的mDCs在慢性炎症中发挥作用,导致继发性临床疾病风险增加。由于低度菌血症而在血液中升高的mDCs通常不会引发有效的免疫反应,但可以将病原体传播到整个宿主体内。mDCs的这种异常运输可以加速全身性炎症疾病的进展。相反,恢复树突状细胞的内环境稳定可能有助于消除病原体并尽量减少传播。因此,在评估慢性炎症性疾病风险时,考虑血液中mDCs的数量以及这些mDCs的微生物含量(微生物组)和激活状态似乎是谨慎的做法。这些可能提供高炎症性疾病风险的重要线索(“煤矿中的金丝雀”)。这将有助于开发新的免疫疗法,以消除动脉粥样硬化、癌症、类风湿性关节炎和先兆子痫中的这种隐匿性感染。