A global reduction in the capacity to cope with a variety of stressors and a concomitant progressive increase in proinflammatory status are major characteristics of the aging process. This phenomenon, named inflamm-aging, is provoked by a continuous antigenic load and stress (Franceschi et al., 2000).
The initial conceptualization of infamm-aging is due to inflammatory stimuli. One of the most important system responsible for the inflamm-aging is the immune system. It seems that the immosenescence, the aging of the immune system, derives from a lifelong exposure to antigens, as well to persistent viral infections, that contribute to the accumulation of effector memory cells producing high amounts of pro-inflammatory mediators (Ostan et al., 2008; Pawelec, 2012; Salvioli et al., 2013).
A lot of inflammatory stimuli also derive from the gut microbiota. Several studies have showed that the microbial composition and diversity of the gut ecosystem of centenarians is different from a young individuals (Franceschi et al., 2007).
This difference is explained as an alteration of the microbiota of the elderly associated with an increased inflammatory status, represented by high levels of IL-6 and IL-8 cytokins (Biagi et al., 2010).
The gastrointestinal tract is sterile in utero and then rapidly colonized at birth via maternal contact. The composition as number and as diversity of bacteria increases throughout early childhood. The adult colon contains 1012 bacteria per gram of colonic content (Dominguez-Bello et al., 2011).
This complex and organized system (intestinal microbiome) plays a crucial role in imprinting the mucosal immune system and in maintaining normal gut physiology. The intestinal microbiome influences the host functions well beyond the gut. It seems to be also implicated in a variety of diseases such as obesity, diabetes, nonalcoholic fatty liver disease, autism, multiple sclerosis, and cardiovascular disease (De Vos, 2012).
The influence of the intestinal microbiome on the brain function is based on the fact that oral administration of antibiotics improves the cognitive decline in patients with hepatic encephalopathy (Riordan et al., 1997). Recent works have shown that the cognitive decline in hepatic encephalopathy is associated with the presence of specific bacteria (Bajaj et al., 2012).
Changes in brain chemistry in germ-free mice include a decrease in the N-methyl- D-aspartate (NMDA) receptor subunit, NR2BmRNA expression in amygdala, up-regulation of brain-derived neurotrohic factor (BDNF), and decreased expression of the serotonin receptor 1A (5HT1A) in the hippocampus (Neufeld et al., 2011).
Another study in mice has demonstrated similar changes in brain chemistry with reduced expression of the synaptic plasticity-related genes PSD-95 and synaptophysin in the striatum (Diaz Heijtz et al., 2011).
These studies show that the presence of commensal bacteria in the gut is critical for the normal development of the brain, focusing the attention about the possibility that the intestinal bacteria may influence brain plasticity later in life.
After the postnatal colonization and the expansion of whole intestinal microbiome, the microbiological composition of the gut remains stable under normal conditions (no particular stress, no specific pathologies, etc.), with transient variations caused by diet and/or antimicrobial drugs (Dominguez-Bello et al., 2011). But, always in mice, these variations induced by diet and/or antimicrobial drugs may produce a mild shift in the microbial composition of the gut and may be sufficient to cause changes in brain chemistry and brain functionality (Bercik et al., 2011; Li et al., 2009).
A recent study has shown that probiotics improved impaired spatial memory in diabetic rats (Davari et al., 2013). This effect of probiotic bacteria shows an important role on the brain-gut axis.