CYTOTOXICITY

Nanobacteria are not nice organisms.  They don’t serve a useful purpose (except to increase my cath volume), and they are interested only in their own survival.  When stressed (e.g. when they are unroofed from their shelters by EDTA), Nanobacteria divide, at what for Nanobacteria is a rapid rate, about once every three days (fig. 1, rapidly dividing extracellular Nanobacteria).  Non-intracellular Nanobacteria elaborate a sticky biofilm (fig. 2), a carbonate apatite rich material that contains a lipopolysaccharide endotoxin.  Via this biofilm, Nanobacteria can attach to mammalian cells (fig. 3).  The binding is not random.  Nanobacteria appear to target cytoplasmic extensions (fig. 4), almost as if they are “going for” an undefended area, or regions adjacent to the cell nucleus.  The attack seems to be organized and coordinated; some cells will be targeted and others left unscathed.  The Nanobacteria can be seen to “line up” in their approach to the cell (fig. 5).  Figure 6 demonstrates nanobacteria “swarming” upon a fibroblast.

          Targeting and binding mammalian cells is a piece of cake if you are a Nanobacterium; all you need to do is use your sticky biofilm to attach to the cell. This causes an inflammatory response and before you know it, you’re in! Phagocytic white cells, NK cells, and T-Lymphocytes can ingest them, but they cannot kill the Nanobacteria. Somehow cell-bound Nanobacteria trick somatic cells into internalizing them, a sort of pathological endocytosis.  These internalized Nanobacteria were the vacuoles that Kajander and Ciftcioglu saw in their sick cell cultures in 1990 (fig. 7-Nanobacteria actively killing a Human T-6 Lymphocyte).   In cell culture experiments, inoculums of Nanobacteria will bind mammalian cells within 15 minutes, and obtain entry moments later; cell death occurs within three days.  Kajander and Ciftcioglu found that the rate and extent of cell death depended on the number of organisms in the inoculum.  The chart below shows the effects of a

standard inoculum of different cultures of N. sanguineum on the growth rate of mammalian fibroblasts.   

        If you give enough Nanobacteria, the targeted cells will die.  Nanobacteria trigger cellular apoptosis.  At   lower inoculums the targeted cells may survive, but they also won’t be able to kick out the Nanobacterial invaders.  Nanobacteria can be seen within the cells, acting, as we will see, sort of like a parasite.  The appearance of the intracellular Nanobacteria is a little different.  Instead of goey biofilm, the Nanobacteria cell body appears to be surrounded by a “hairy coating”.  This “hairy coating” is carbonate apatite (fig. 8, a Nanobacterium within polycystic kidney disease tissue). Other times, spicule like structures can be seen surrounding the cell body, where the biofilm used to be (fig. 9).  These linear structures are composed of carbonate apatite, the same stuff that we find in abnormally calcified mammalian structures.  This is an example of abnormal or pathological calcification.  The Nanobacterium, acting like a parasite, fixes the host’s calcium and phosphorus, and then spins out this carbonate apatite webbing.  I wonder why they do this?  

                                                                                                     Return to Scientific Review Index             Next Section in Scientific Review