| Literature DB >> 27803173 |
Jiehua Hong1, Yan Li2, Xiuguo Hua1, Yajie Bai1, Chunyan Wang1, Caixia Zhu3, Yuming Du1, Zhibiao Yang1, Congli Yuan1.
Abstract
The hallmark of Bartonella infection is long-lasting intraerythrocytic parasitism. However, the process of Bartonella bacteremia is still enigmatic. In the current study, we used Bartonella tribocorum to determine how Bartonella invasion into the bloodstream from dermal inoculation might occur. Bartonella was poorly phagocytized by peritoneal macrophages in vitro. Intracellular Bartonella survived and replicated in macrophages at an early stage of infection. Intracellular Bartonella inhibited spontaneous cell death of macrophages. They also inhibited Salmonella-induced pyroptosis and mildly reduced inflammasome activation through an unidentified mechanism. A rat model confirmed that Bartonella was also inadequately phagocytized in vivo, because numerous free-floating bacilli were observed in lymph collected from thoracic duct drainage as early as 2 hours after inoculation. Lymphatic fluid drainage in the bloodstream significantly reduced the bacterial load in the bloodstream. These findings illustrated a potential route by which Bartonella invade bloodstream from dermal inoculation before they are competent to infect erythrocytes.Entities:
Keywords: Bartonella; inflammasome; innate immunity; lymphatic circulation
Mesh:
Year: 2017 PMID: 27803173 DOI: 10.1093/infdis/jiw526
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226