Proper functioning of the immune system (IS) depends on its modulation by body associated microorganisms, in a process starting early after birth, lasting through all life time and which contributes for the shaping of microbial ecosystem itself, ultimately influencing body homeostasis. The importance of a fine-tuned microbiota-immunity balance can be illustrated by multiple human disorders having as an underlying basis defects in immune response and accompanying gut dysbiosis, such as autoimmune and inflammatory bowel diseases [
1]. The use of animal models has been essential for the works unraveling IS functions and for understanding of immune-related diseases. Examples of such models include mice lineages bi-directionally selected for high and low quantitative antibody responses to a given antigen, but whose altered response extends to antigens unrelated to those employed in the selective process [
2]. In addition to antibody production, these mice, which are represented by five selections obtained from an outbred Swiss mice foundation population (F0) [
3], show interline differences with respect to other biological features. For example, selection III low antibody producer mice (LIII) display a higher resistance to chemically induced skin tumorigenesis [
4] and to
Salmonella typhimurium infection [
5], higher susceptibility to pristane-induced arthritis (PIA) [
6] and higher longevity following intraperitoneal injection of
Mycobacterium leprae heat shock protein Hsp65 [
7]. On the other hand, selection III high responder mice (HIII) are more resistant to
Trypanosoma cruzi infection than animals of the LIII lineage, a feature which was shown to be gender-specific (females are more resistant than males) and correlated with interferon-γ and nitric oxide production by peritoneal lymph node cells [
8]. The polarity with which these traits are manifested in between the lineages is the result of selective pressure towards the accumulation of quantitative trait loci endowed with opposite modulatory effects on the antibody biosynthesis pathway [
9]. Given several examples of reciprocal influence of gut microbiota and immune system [
10], we investigated whether immunity related and other interline differences between LIII and HIII could have an impact on fecal bacteriome of these mice lineages.