期刊
JOURNAL OF INFECTIOUS DISEASES
卷 215, 期 2, 页码 303-311出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiw526
关键词
Bartonella; lymphatic circulation; innate immunity; inflammasome
资金
- National Natural Science Foundation of China [31400124, 81372098, 31572525]
- Open Foundation of State Key Laboratory of Veterinary Etiological Biology (Agri-X project Shanghai Jiaotong university)
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.
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