Lymphatic Circulation Disseminates Bartonella Infection Into Bloodstream

<span class="paragraphSection"><div class="boxTitle">Abstract</div>The hallmark of <span style="font-style:italic;">Bartonella</span> infection is long-lasting intraerythrocytic parasitism. However, the process of <span style="font-style:italic;">Bartonella</span> bacteremia is still enigmatic. In the current study, we used <span style="font-style:italic;">Bartonella tribocorum</span> to determine how <span style="font-style:italic;">Bartonella</span> invasion into the bloodstream from dermal inoculation might occur. <span style="font-style:italic;">Bartonella</span> was poorly phagocytized by peritoneal macrophages in vitro. Intracellular <span style="font-style:italic;">Bartonella</span> survived and replicated in macrophages at an early stage of infection. Intracellular <span style="font-style:italic;">Bartonella</span> inhibited spontaneous cell death of macrophages. They also inhibited <span style="font-style:italic;">Salmonella</span>-induced pyroptosis and mildly reduced inflammasome activation through an unidentified mechanism. A rat model confirmed that <span style="font-style:italic;">Bartonella</span> 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 <span style="font-style:italic;">Bartonella</span> invade bloodstream from dermal inoculation before they are competent to infect erythrocytes.</span>

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