Abstract
Lyme borreliosis is a multisystemic disease caused by the pleomorphic bacteria of the Borrelia burgdorferi sensu lato complex. The exact mechanisms for the infection to progress into a prolonged sequelae of the disease are currently unknown, although immune evasion and persistence of the bacteria in the host are thought to be major contributors. The current study investigated B. burgdorferi infection processes in two human cell lines, both non-immune and non-phagocytic, to further understand the mechanisms of infection of this bacterium. By utilizing light, confocal, helium ion, and transmission electron microscopy, borrelial infection of chondrosarcoma (SW1353) and dermal fibroblast (BJ) cells were examined from an early 30-min time point to a late 9-days post-infection. Host cell invasion, viability of both the host and B. burgdorferi, as well as, co-localization with lysosomes and the presence of different borrelial pleomorphic forms were analyzed. The results demonstrated differences of infection between the cell lines starting from early entry as B. burgdorferi invaded BJ cells in coiled forms with less pronounced host cell extensions, whereas in SW1353 cells, micropodial interactions with spirochetes were always seen. Moreover, infection of BJ cells increased in a dose dependent manner throughout the examined 9 days, while the percentage of infection, although dose dependent, decreased in SW1353 cells after reaching a peak at 48 h. Furthermore, blebs, round body and damaged B. burgdorferi forms, were mostly observed from the infected SW1353 cells, while spirochetes dominated in BJ cells. Both infected host cell lines grew and remained viable after 9 day post-infection. Although damaged forms were noticed in both cell lines, co-localization with lysosomes was low in both cell lines, especially in BJ cells. The invasion of non-phagocytic cells and the lack of cytopathic effects onto the host cells by B. burgdorferi indicated one mechanism of immune evasion for the bacteria. The differences in attachment, pleomorphic form expressions, and the lack of lysosomal involvement between the infected host cells likely explain the ability of a bacterium to adapt to different environments, as well as, a strategy for persistence inside a host.
Highlights
Borrelia burgdorferi, the causative agent of Lyme borreliosis (LB), is a pleomorphic bacterium transmitted via Ixodes ticks (Burgdorfer et al, 1982)
With helium ion microscopy the surfaces of biological samples can be examined without any additional metallic coating procedures of samples, which might affect and distort results
Spirochetes were located on top of the infected SW1353 cell (Figures 1E,G), while both spirochetal and coiled forms were observed on the BJ cells (Figures 1F,G) 30 min post-infection
Summary
The causative agent of Lyme borreliosis (LB), is a pleomorphic bacterium transmitted via Ixodes ticks (Burgdorfer et al, 1982). Borrelia is found in the parental spirochete form with a length varying from 10 to 30 μm, as well as, forming vesicles or blebs, as a metabolically inactive round body (RB) and even in biofilms (Meriläinen et al, 2015) These pleomorphic forms can be induced by unfavorable culture conditions such as changes in pH, osmotic pressure, temperature, and even with antibiotic treatment (Kersten et al, 1995; Murgia and Cinco, 2004; Srivastava and De Silva, 2009; Meriläinen et al, 2015; Sharma et al, 2015). The exact mechanisms resulting in the long-term sequelae of the disease are currently undetermined
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
