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According to research, gut bacteria could continuously poison us.


Senior Member
On the translocation of bacteria and their lipopolysaccharides between blood and peripheral locations in chronic, inflammatory diseases: the central roles of LPS and LPS-induced cell death
Bacterial cell wall components, such as the endotoxin lipopolysaccharide (LPS) of Gram-negative strains, are well known as potent inflammatory agents, but should normally be cleared. Thus, their continuing production and replenishment from dormant bacterial reservoirs provides an easy explanation for the continuing, low-grade inflammation (and inflammatory cytokine production) that is characteristic of many such diseases. Although experimental conditions and determinants have varied considerably between investigators, we summarise the evidence that in a great many circumstances LPS can play a central role in all of these processes, including in particular cell death processes that permit translocation between the gut, blood and other tissues. Such localised cell death processes might also contribute strongly to the specific diseases of interest. The bacterial requirement for free iron explains the strong co-existence in these diseases of iron dysregulation, LPS production, and inflammation.
We also rehearsed the considerable evidence that minor leakages from the gut microbiome (e.g.ref. 73–75), even if only a tiny fraction of the 10–100 trillion cells involved, whether via specialised structures such as M cells or more significant breaches in the gut epithelium (as can also occur in some cancers and stroke), are more than sufficient to provide a continuing inoculum to the bloodstream. Clearly the innate and adaptive immune system will normally remove those organisms threatening growth and noticeable bacteraemia, but this statement does not account for the fraction that become dormant and hide therefrom (whether geographically in cells and/or by losing their immunogenic potential, for instance by creating L-forms). While the dormant bacteria do seem mainly to be hidden inside cells, their inflammatory products may not be.
Our central argument is that low grade inflammation is mainly effected via the continuing production and shedding of LPS (and similar molecules) as dormant bacteria periodically awaken, proliferate and produce LPS before returning to dormancy.
If this is going to be true, it is instructive to determine how much LPS and related molecules are typically found in human blood under various conditions. The potential load of LPS in the alimentary canal is ~1 g. We note, of course, that (as with serum ferritin) the basis of these assays used to estimate concentration is typically a binding reaction, whether to an antibody or (in the case of LPS) based on a Limulus amoebocyte lysate (or its recombinant factor C94). Thus these and other (e.g.ref. 95–97) assays typically measure the (thermodynamically active) free forms, while the total amounts may be very much greater if (as with LPS) they are mainly bound to LBP or ApoE of HDL/cholesterol, or even monocyte surfaces. Indeed, given that HDL–cholesterol is capable of sequestering LPS (and lipoteichoic acid[gram-positive bacteria toxin]), it is not surprising that there is considerable evidence that HDL–cholesterol is protective against sepsis and sepsis-related death, showing further the importance of free LPS levels in disease prognosis.