c-d) After 3 h of infection, longer #TSA HDAC randurls[1|1|,|CHEM1|]# actin projections and actin redistribution were observed, and some bacilli were found inside the B cell (c) or surrounded by actin organisations (d). Figure 8 Confocal images of B cells infected with mycobacteria. The actin filaments were labelled with rhodamine-phalloidin and the bacteria were stained with fluorescein isothiocyanate (FITC). a) M. smegmatis (MSM) infection caused evident actin

rearrangements within 1 h of infection; a mycobacterium was observed attached to the cell. b-c) After 3 h of infection with MSM, intracellular bacteria were observed (b) and long actin filaments were evident (c). d) M. tuberculosis (MTB) infection induced actin reorganisation after 1 h of infection, and bacilli attached to the cells were observed; e-f) B cells, after 3 h of infection with MTB, presented actin cytoskeletal changes in cells without any adhered or intracellular bacteria. Discussion The classical B-cell roles include the production of antibodies and cytokines and Selleckchem PXD101 the generation of immunological

memory, which are key factors in the adaptive immune response. Recently, their role in innate immunity is been increasingly recognised [27, 28]. The majority of studies that analyse B-cell specific-antigen recognition mainly focus on soluble antigens. B cells have been traditionally considered non-phagocytic cells [29]; therefore, the process of bacterial uptake by B cells has not been extensively documented. Mature B cells bind specific

soluble protein antigens through a unique and restricted BCR [30–32]. At present, it is known that the Antigen-B-cell receptor (Ag-BCR) complex is internalised check details into clathrin-coated pits, although raft signalling and actin polymerisation are required for efficient receptor mediated-endocytosis [33]. The binding of antigens to the BCR induces cell signalling and triggers changes in the actin cytoskeletal organisation, although these changes are limited to the vicinity of the Ag-bound BCR and are not generalised throughout the cellular membrane [33, 34]. The actin reorganisation after the BCR-antigen engagement is a rapid albeit transient event [34]. The internalised BCR transports the Ag to the endosomal compartments, where it is fragmented and loaded onto nascent MHC class II proteins for its presentation to T cells [31]. In contrast to BCR-mediated specific soluble-antigen uptake, we studied the features of non-specific bacterial uptake by B cells. In our study, B lymphoblast cells of the Raji cell line (Burkitt’s lymphoma) were infected with two Mycobacterium species and with S. typhimurium, and the resultant cellular membrane changes and cytoskeletal reorganisation events were analysed.