Induction of Apoptosis in Normal Human Dermal Fibroblasts Infected with<i>Borrelia burgdorferi</i>Sensu Lato

RozwadowskaBeata,; Albertyńska, Marta; Okła, Hubert; JasikKrzysztof, P; Swinarew, Andrzej; Mazurek, Urszula; Dudek, Sławomir; Urbańska-JasikDanuta,; Poprawa, Izabela

doi:10.1089/vbz.2016.2057

Cited by 5 publications

(2 citation statements)

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“…Studies have indicated apoptotic cell death induced by Borrelia infection in dermal fibroblasts ( Rozwadowska et al, 2017 ), neural cells ( Myers et al, 2009 ; Ramesh et al, 2013 ), peripheral T lymphocytes ( Sandra et al, 2003 ), and monocytes ( Cruz et al, 2008 ) among others. Contradictory to previous studies, our dermal fibroblast and chondrosarcoma cells grew similarly to the untreated cells despite being infected with a high MOI (200) ( Figure 3 ).…”

Section: Discussionmentioning

confidence: 99%

“…Smaller pathogens fit inside, for instance, caveolae or clathrin-coated vesicles, while larger ones internalize via more sizeable cellular compartments and progress through such endocytosis pathways as macropinocytosis ( Cossart and Helenius, 2014 ). Borrelia have been demonstrated to invade a variety of human cells, for instance, endothelial cells ( Comstock and Thomas, 1991 ; Ma et al, 1991 ), dermal fibroblasts ( Klempner et al, 1993 ; Rozwadowska et al, 2017 ), synovial cells ( Girschick et al, 1996 ), and neural cells ( Livengood and Gilmore, 2006 ; Miklossy et al, 2008 ), among others. Furthermore, it has been demonstrated that Borrelia can be internalized by human cells without affecting cell viability, and this has been thought to play a role in host immune evasion ( Ma et al, 1991 ; Girschick et al, 1996 ; Livengood and Gilmore, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

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Distinctive Evasion Mechanisms to Allow Persistence of Borrelia burgdorferi in Different Human Cell Lines

et al. 2021

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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.

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