| Literature DB >> 34448131 |
Xiaoyu Fu1,2, Da Cheng1,2, Zhenwu Luo1, Amanda Wagner3, Sylvia Fitting4, Xiaomei Cong5, Wanli Xu6, Kendra Maas6, Zhuang Wan1, Jian Zhu7, Zejun Zhou8, William W Stoops9, Aimee McRae-Clark3,10, Wei Jiang11,12.
Abstract
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)-3α, 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-3α 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.Entities:
Keywords: Cocaine use disorder; Monocyte activation; Plasma inflammation; Saliva microbiome; Streptococcus
Year: 2021 PMID: 34448131 PMCID: PMC8881519 DOI: 10.1007/s11481-021-10007-6
Source DB: PubMed Journal: J Neuroimmune Pharmacol ISSN: 1557-1890 Impact factor: 7.285