OK Good!
The bacteria may not even exist at the oral tolerance induction sites in the GI-tract (e.g. Peyer's patches), so I still think that ingesting antigens in small amounts that aren't immunostimulatory seems risky in theory. I can't see how it could be effective anyway.
so - if i am understanding your reasoning correctly - you are considering the body to be virgin to antigens of the offending organisms - and so by adding a small amount of antigens of them - you concern is that this small level of antigens might promote immune tolerance to the very bacteria we are hoping to treat. NOT GOOD!
i am not sure if immunotolerance is based only on levels of antigens - i suspect the immune system has other criteria by which it senses foes vs friends - but lets assume it is quantity-dependent for the purposes of this discussion
Then, if Markov is correct and bacterial biofilm colonies are located inside the kidney and making people ill (or there are biofilm infections located anywhere inside the body for that matter) - then the immune system is already exposed to these antigens at some level.
The level cannot be zero as white blood cells or their equivalents go everywhere in the body to some extent - including the kidney.
indeed the theory is that it is these very chemicals that are circuiting in the blood stream and causing illness symptoms.
as such it wouldn't actually matter if the start point was below the threshold of immune activation or above it - more antigen exposure is always moving the host away from immune tolerance and towards more activation
also - if what you are proposing were a real issue - wouldn't people be becoming immunotolerant to the low levels of pathogens all around us - in the air we breath, the food we eat, the water we drink, the surfaces we touch and then touch our eyes, nose mouth etc
I think it much more likely that biofilm colonies - if present - are not sealed in some kind of 100% impervious barrier inside the body making them invisible to the immune system - but instead exist in a state exposed to the immune system - but in a kind of stalemate with the it.
we know the biofilm colony has lots of tools to wage the war against the host defences,
as described in the paper you posted above :
-redundancy of adhesins and structural elements - so even if the immune system makes antibodies to some, it always has others
-ability to kill macrophages with pore forming toxins - preventing them from chewing it up
-ability to disrupt host immune signalling pathways - dysregulating them
-etc
this is exactly what happens in other well studied biofilm infections - like diabetic wound infections, surgical implant infections etc.
I think this is the sheep auto-inoculation paper -
https://vetjournal.it/images/archive/pdf_riviste/4672.pdf