Abstract :
[en] In a way, the microbiome has been on earth long before we humans appeared in any evolution theory. This ethereal “organ” has grabbed the attention of biological research and will continue to expand in the years to come. Growing evidence supports that its presence is vital to the host and particularly to us humans. Although largest part of the mirobiome research focuses on the gut microbiome, the microbial communities actually stretch in the farthest off body sites. The last few years, oral microbiome (OM) has started to steal some light. Despite of the geolocation, the microbiome maintains an intimate relationship with its host. Our long term health appears to be closely linked and sustained by a “happy”, healthy and symbiotic microbiome.Disease and state of illness, whether it is of physiological or psychological nature or both can result from many different causes and routes. Remarkably, about a third of the adult population worldwide seems to become ill as concequence of certain difficult, stressful and intense experiences during their childhood. The field of social, biological, medical and environmental sciences describes these experiences as “Early Life Adversity (ELA)” and the marrow of the “Developmental Origins of Health and Disease (DOHaD)” . Since the 80s that this sociobiological theory was introduced and described, research revealed that ELA factors could be anything from pregnancy complications, medication, birth complications, infections, social isolation, socioeconomic status, orphanhood, toxic environment and any other event that is capable of inducing extreme stress to an individual. Concequences of ELA experiences have also been introduced as wide range of common later life diseases. An institutionalisation cohort as a model of ELA, the EPIPATH, which was initially established to study the longterm immune and cardiometabolic effect of institutionalisation was used for this Thesis. At first, I aimed to investigate what was the effect of institutionalisation on the OM of these individuals using their oral taxonomic composition. Secondly, I aimed to identify a link between this composition and the immune profiles of the participants. Thirdly, knowing the stress signatures of the cohort following pre-existing cortisol and glucose measurements, I aimed to detect plausible interaction between the microbiome and those data. Lastly, I aimed to find mechanistic evidence of our prior observed associations by looking into the metabolome of the oral microbiome. Altogether our data revealed observations of a complex system of bidirectional interactions between ELA, the OM and the immune markers of cytotoxicity and immune senescence together with a particular profile of glucose and cortisol kinetics following exposure to social stress. Besides, our data expanded to the exposure of the first mechanistic cues of ELA traces on the OM metabolome. The research conducted for this thesis brings to light important evidence on how ELA interacts with the OM leading to a certain disease phenotype.
