Oral Enrichment of Streptococcus and its Role in Systemic Inflammation Related to Monocyte Activation in Humans with Cocaine Use Disorder.
Oral Enrichment of Streptococcus and its Role in Systemic Inflammation Related to Monocyte Activation in Humans with Cocaine Use Disorder.
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DOI：
10.1007/s11481-021-10007-6
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发表时间：
2022-06
期刊：
影响因子：
--
通讯作者：
Jiang W
中科院分区：
文献类型：
--
作者：
Fu X;Cheng D;Luo Z;Wagner A;Fitting S;Cong X;Xu W;Maas K;Wan Z;Zhu J;Zhou Z;Stoops WW;McRae-Clark A;Jiang W
可卡因的使用通常与慢性全身性炎症增加有关。然而，可卡因使用介导的全身性炎症的驱动因素尚未完全了解。在目前的研究中，我们招募了可卡因使用障碍的个体和不使用可卡因的健康个体，并收集了配对的唾液和血液样本。唾液样本用于评估口腔微生物组，血浆样本用于评估33种细胞因子和趋化因子。与非使用者相比，使用者表现出唾液微生物菌群减少。链球菌是可卡因使用者唾液中唯一增加的属，而可卡因使用者中的几个属与非使用者相比有所减少。值得注意的是，可卡因使用者表现出几种单核细胞活化标志物的血浆水平增加，包括单核细胞趋化蛋白（MCP）-4，巨噬细胞炎性蛋白（MIP）-3，4，巨噬细胞衍生趋化因子（MDC），胸腺和活化调节趋化因子（TARC），所有这些都与三种链球菌的唾液水平增加有关。此外，与对照相比，用链球菌或其脂磷壁酸处理优先活化原代人单核细胞以在体外产生促炎细胞因子和趋化因子，如MIP-3 β和TARC。然而，与单独的培养基或细菌相比，单核细胞在暴露于可卡因或可卡因加细菌后未能产生这些趋化因子。这项研究表明，慢性可卡因使用相关的血液炎症可能是由于口腔链球菌增加及其对骨髓细胞活化的影响，但不是直接由可卡因引起的。通过口腔微生物组的可卡因相关全身性炎症模型。在目前的研究中，我们提出了一个可卡因使用相关的全身炎症模型。单独的皮质醇不诱导单核细胞活化和炎症。随着链球菌和系统性易位的增加，可卡因的使用改变了口腔微生物组。链球菌或其产物的系统性易位通过细菌或细菌产物的受体激活单核细胞（例如，Toll样受体2）产生促炎细胞因子或趋化因子。
Cocaine use is commonly associated with increased chronic systemic inflammation. However, the drivers for cocaine use-mediated systemic inflammation are not fully understood. In the current study, we recruited individuals with cocaine use disorder and healthy individuals who did not use cocaine and collected paired saliva and blood samples. The saliva samples were used to assess the oral microbiome, and the plasma samples were evaluated for 33 cytokines and chemokines. Cocaine users exhibited decreased saliva microbial diversities compared to non-users. Streptococcus was the only increased genus in the saliva from cocaine users, whereas several genera were decreased in cocaine users compared to non-users. Notably, cocaine users exhibited increased plasma levels of several monocyte activation markers, including monocyte chemoattractant protein (MCP)-4, macrophage inflammatory protein (MIP)-3✓, macrophage-derived chemokine (MDC), and thymus and activation-regulated chemokine (TARC), all of which were correlated with increased saliva levels of three Streptococcus species. Furthermore, treatment with Streptococcus or its lipoteichoic acid preferentially activated primary human monocytes to produce proinflammatory cytokines and chemokines, such as MIP-3✓ and TARC, in vitro compared to controls. However, monocytes failed to produce these chemokines after exposure to cocaine or cocaine plus bacteria compared to medium or bacteria alone. This study revealed that chronic cocaine use-associated inflammation in the blood may result from increased oral Streptococcus and its effects on myeloid cell activation, but does not result from cocaine directly. A model for cocaine-associated systemic inflammation via oral microbiome. In the current study, we propose a model of cocaine use-associated systemic inflammation. Cocaine alone does not induce monocyte activation and inflammation. Cocaine use altered oral microbiome with the increases in Streptococcus and systemic translocation. The systemic translocation of Streptococcus or its products activate monocytes via receptors for bacteria or bacterial products (e.g., toll-like receptor 2) to produce proinflammatory cytokines or chemokines.
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影响因子：
1.7
作者：
Fox, Helen C.;D'Sa, Carrol;Kimmerling, Anne;Siedlarz, Kristen M.;Tuit, Keri L.;Stowe, Raymond;Sinha, Rajita
通讯作者：
Sinha, Rajita
影响因子：
6.2
作者：
Cabral, Guy A.
通讯作者：
Cabral, Guy A.
DOI：
10.1164/rccm.201210-1913oc
发表时间：
2013-05-15
影响因子：
24.7
作者：
Morris, Alison;Beck, James M.;Weinstock, George M.
通讯作者：
Weinstock, George M.
影响因子：
15.5
作者：
Luo, Zhenwu;Li, Min;Jiang, Wei
通讯作者：
Jiang, Wei
影响因子：
4.6
作者：
Chivero, Ernest T.;Ahmad, Rizwan;Buch, Shilpa
通讯作者：
Buch, Shilpa