While demonstrated associations between the human microbiome and health or disease were an overarching theme of the workshop, with most speakers at least touching on the topic, some speakers homed in on it. Josef Neu, professor of pediatrics in the Division of Neonatology at the University of Florida, provided an overview of recent microbiome-disease research in pediatric populations. First, he described evidence suggesting that a fetal microbiome exists; that is, babies are born with microbiomes acquired during the last trimester of pregnancy (DiGiulio et al., 2008; Goldenberg et al., 2000; Koenig et al., 2011). The existence of a fetal microbiome has clinical implications, with greater microbial diversity being associated with prematurity (DiGiulio et al., 2008; Mshvildadze et al., 2010). Then he summarized recent evidence of associations between microbiome composition and two diseases prevalent among babies in neonatal intensive care units (ICUs): necrotizing enterocolitis and late-onset sepsis (Alexander et al., 2011; Mai et al., 2011). Neu also explored in more detail a topic that Lita Proctor had mentioned, that is, microbiome differences between babies born vaginally and babies born via C-section (Dominguez-Bello et al., 2010). The differences are important not only because of the increasing prevalence of C-section deliveries in many countries, but also because of the wide range of immune-related diseases associated with C-section delivery (Neu and Rushing, 2011). Finally, he remarked on other recent evidence indicating associations between microbial ecology in children and the onset of type 1 diabetes (Brown et al., 2011; Vaarala et al., 2008). Together, these various avenues of research suggest that the early microbiome, from fetal development through childhood, can influence both short- and long-term health.
Researchers have made significant headway in understanding how the oral microbiome contributes to health and disease. Richard Darveau, professor and chair in the Department of Periodontics at the University of Washington Dental School, described evidence indicating that unlike many other human pathogens, the periopathogen Porphyromonas gingivalis triggers disease not by inducing inflammation but by intervening with host immunity in a more subversive manner. In fact, inflammation is a normal part of a healthy oral environment, with neutrophil movement being a sign of healthy “immune surveillance” and cytokine production contributing to healthy tissue development and function (Roberts and Darveau, 2002). Eventually, over time, even a healthy mouth experiences bone loss. However, P. gingivalis accelerates the process. The bacteria interferes with innate immunity in a way that prevents the host from detecting and clearing not just P. gingivalis, but other oral microbes as well (Burns et al., 2010; Coats et al., 2005, 2007; Hajishengallis et al., 2008a,b, 2011; Liang et al.,