They experimentally infected birds from Alabama with a local Mycoplasma strain. As a comparison,
they also infected house finches from Arizona, a region where house finches have never experienced the disease. As expected, Alabama birds harboured a lower bacterial load in the conjunctivae compared with Arizona finches (Figure 4b). Between-population differences in bacterial load were mirrored by a differential pattern of gene expression in response to the experimental infection. Among the 52 identified genes with known function, 38% and 21% showed a post-infection expression change in Arizona and Alabama, respectively. This post-infection expression change was due to genes in Arizona birds being more down-regulated (80% of 20 genes) compared with Alabama individuals (27% of 11 genes). DAPT supplier When focusing on experimentally infected birds only and looking at the post-infection gene expression changes, all 52 genes were differentially expressed in
birds from the two populations and again this was due to Arizona individuals having 90% of these genes down-regulated post-infection (10% in Alabama birds). Among the different genes with differential expression, 10 were directly linked with immunity (Figure 4c). Nine of these 10 immune genes were down-regulated in birds from Arizona. The tenth gene (complement factor H) was up-regulated in Arizona birds. However, this gene restricts the activation of the complement check details cascade and is therefore enough functionally consistent with the expression pattern of the other immune genes. Overall, birds from Arizona showed a pattern of down-regulation of their immune response. This pattern nicely fits with the known immunosuppressive action of Mycoplasma on their chicken hosts. After 12 years of exposure to the pathogen, house finches were thus able to overcome the infection-induced immunosuppression
and restore an effective immune protection. To further confirm this view, Bonneaud et al.  also compared the pattern of gene expression between birds from Alabama sampled in 2000, after only 5 years of exposure to the bacterium. The gene expression of these birds resembled the 2007 Arizona birds more than the 2007 Alabama individuals, strongly suggesting that the observed pattern was due to a microevolutionary change that occurred with time rather than a geographical (environmental-based) variation. A further study comparing the pattern of gene expression in birds from Alabama and Arizona at 3 and 14 days post-infection  concluded a possible role of innate immunity in Mycoplasma resistance.