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Therefore, considering that B lymphocytes have been recognised as classical non-phagocytic cells [29], we sought to establish whether mycobacteria were able to induce

macropinocytic internalisation in B cells. In our design, the infections were conducted with B cells in suspension; to avoid the spreading feature that is commonly observed in these cells, we did not plate Raji cells on any cell surface that was either uncovered or covered with any extracellular matrix ligands or antibodies [36, 37]. Our observations revealed that the B cells were readily infected by the three bacteria that were studied and that the infections mTOR inhibitor induced relevant changes in the cellular membrane during bacterial internalisation (Figure 6). M. smegmatis is considered a non-pathogenic mycobacteria; however, it was able to induce important membrane changes that were characterised by abundant filopodia and lamellipodia formation (Figure 6e LY3023414 and 6f) and were similar to those triggered by PMA (Figures 6c and 6d). B cells that were treated with the supernatant from the bacterial cultures (mycobacteria were removed by centrifugation and filtration) exhibited the same ultrastructural changes (data not shown). M.

smegmatis was readily internalised; in fact, some cells internalised a large number of the mycobacteria (Figure 5a). M. smegmatis exhibited a transient multiplication, which was revealed by the counting of CFU 12 and 24 h post-infection (Figure 1a). However, by 48 and 72 h, the mycobacteria were eliminated. After 24 h of infection, no evident selleck chemical intracellular mycobacteria were observed on the TEM images, and the B cell

morphology was similar to that of uninfected cells (Figure 5c). Intravacuolar mycobacteria destruction was clearly observed, and partial destruction of the bacterial cell wall was evident (Figure 5b). The results from the analysis of mycobacterial intracellular elimination, membrane protrusion formation, and cytoskeleton rearrangements during bacterial uptake resemble those observed in the infection of epithelial and endothelial cells by Palmatine M. smegmatis[19, 35], although M. smegmatis induced significantly fewer changes in endothelial cells. To our knowledge, there are no other reports of B cell infection by M. smegmatis; therefore, this study is the first description of this subject. The M. tuberculosis infection of B cells showed some differences with the effect of M. smegmatis and S. typhimurium infections. M. tuberculosis has previously demonstrated the capability to invade several cell types, including epithelial [18, 38], fibroblast [39], and endothelial cells [35, 40]. The cellular membrane protrusions formed during M. tuberculosis internalisation have been described in some of these cells [18, 35, 40]. In B cells, membrane protrusions were also observed during M. tuberculosis uptake. However, these protrusions were different from those observed with M. smegmatis and S.

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