My understanding is that, in healthy humans, gut bacteria are not presented in huge numbers to the immune system because the intestinal barrier (tight junctions) prevent most of them from migrating into the blood stream.
Are then not antibodies against gut bacteria a clear sign of a damaged gut barrier?
(FWIW there seem to be suspicions that Ankylosing Spondylitis is also caused by a certain type of bacteria being present _and_ getting into places such that antibodies against them are formed.)
There is a lot of literature that supports the role of gut bacteria inducing Tregs, and now there is also some evidence of epitope transport from the gut into the thymus.
Hence, I think these events might matter even if they are not very frequent.
But you could be right, and perhaps there's not really a relevant mutualistic relationship between host and commensals in terms of epitope crossreactivity.
Are then not antibodies against gut bacteria a clear sign of a damaged gut barrier?
(FWIW there seem to be suspicions that Ankylosing Spondylitis is also caused by a certain type of bacteria being present _and_ getting into places such that antibodies against them are formed.)