This family of proteins has been implicated in nodule development but their role in pathogenesis remains elusive, in depth studies may reveal the specific advantage that this protein may provide to host cells in host-pathogen interaction.
Yet given the study site, we suggest that these genes, likely mobilized via gene cassettes, may provide their host(s) with duplicates of these catabolic enzymes.
Thus, the host modifiers examined in our study – especially those that have small effects on bacterial action and lead to reduced prevalence, not extinction of Wolbachia – may provide a host-mediated pathway between different CI-types.
On the one hand, fever may provide the host with a mechanism for parasite clearance.
As a consequence B. cuenoti may provide its host with this metabolite, suggesting another case of possible metabolic complementation.
Alternatively, the influx of inflammatory cells to the site of infection may provide additional host cells for H. parasuis infection.
As has been discussed above, BC is an important source of Ig that may provide the host with passive immunity against infectious pathogens.
Plausibly, the symbiont may provide the host with nutritional supplements, such as essential amino acids and vitamins, as has been demonstrated in other plant-sucking insects [ 3, 8].
The human gut Melainabacteria may provide their host with B and K vitamins and fill a niche based on carbon fermentation in the large intestine, analogous to that of the Firmicutes.
However, the increased MIC may provide the host bacterium a selective advantage in an environment of low concentrations of quinolones, increasing the bacterial numbers and therefore the absolute chance of a chromosomal mutation encoding resistance (7, 25).
