In addition, no evident filopodia formation was observed during M. tuberculosis infection, and the protrusions were more similar to ruffles. The TPCA-1 ic50 actin cytoskeleton sustained these membrane protrusions (C188-9 supplier Figures 8e and 8f), although the actin filaments were shorter compared to those formed during PMA treatment and M. smegmatis

or S. typhimurium infection. Of the three bacteria utilised for the infection of B cells, only M. tuberculosis was able to survive and multiply intracellularly (Figure 1). In an earlier study of M. tuberculosis uptake by human-transformed B cells [14], the authors described the formation of membrane protrusions during mycobacterial infection that were similar to those described by our group. The authors also demonstrated the presence of mycobacteria in spacious vacuoles and the presence of abundant mitochondria in infected cells. The authors indicated that the internalisation of live M. tuberculosis by B cells results in the presentation of the mycobacterial antigen to T cells. A number of characteristic structures were observed in B cells that were infected I-BET-762 clinical trial with M. tuberculosis, including “curved vacuoles” with arched or crescent shapes (Figures 5d and 5e), which contain amorphous material. Because these structures were not observed with the other

infections, they appear to be characteristic of M. tuberculosis infection. In our study, we were unable to observe Salmonella-induced

Adenosine filaments (SIFs), which are the hallmark organelles in which the bacteria multiply in epithelial cells [41, 42]. This observation might be the result of the rapid elimination of Salmonella from the B cells. To our knowledge, there is currently no description of SIF formation in Salmonella-infected B cells. B-cell infection by S. typhimurium has been previously reported [29, 43, 44]. It is known that S. typhimurium is internalised through macropinocytosis in several cell models, such as epithelial cells and macrophages [45, 46]. It was recently demonstrated that S. typhimurium can infect B cells by macropinocytosis [20]. Thus, we utilised the Salmonella infection of B cells as a positive control to corroborate that the process induced during mycobacterium internalisation by B cells was macropinocytosis. All of the features observed during B cell infection by Salmonella were consistent with the phenomenon of macropinocytosis, including the membrane protrusion formation (Figure 6j), actin involvement (Figures 7b, 7c and 7d), and spacious vacuole formation (Figure 4e and 4f) [46–48]. Therefore, due the morphological evidence and the inhibition of bacterial internalisation by amiloride, we can conclude that S. typhimurium induced macropinocytosis for its internalisation into the Raji B cell, which confirms the recent findings on the internalisation of S. typhimurium into mouse primary B cells [20].