SUMMARY
In the oral cavity, indigenous bacteria are often associated with two major oral diseases, caries and periodontal diseases. These diseases seem to appear following an inbalance in the oral resident microbiota, leading to the emergence of potentially pathogenic bacteria. To define the process involved in caries and periodontal diseases, it is necessary to understand the ecology of the oral cavity and to identify the factors responsible for the transition of the oral microbiota from a commensal to a pathogenic relationship with the host. The regulatory forces influencing the oral ecosystem can be divided into three major categories: host related, microbe related, and external factors. Among host factors, secretory immunoglobulin A (SIgA) constitutes the main specific immune defense mechanism in saliva and may play an important role in the homeostasis of the oral microbiota. Naturally occurring SIgA antibodies that are reactive against a variety of indigenous bacteria are detectable in saliva. These antibodies may control the oral microbiota by reducing the adherence of bacteria to the oral mucosa and teeth. It is thought that protection against bacterial etiologic agents of caries and periodontal diseases could be conferred by the induction of SIgA antibodies via the stimulation of the mucosal immune system. However, elucidation of the role of the SIgA immune system in controlling the oral indigenous microbiota is a prerequisite for the development of effective vaccines against these diseases. The role of SIgA antibodies in the acquisition and the regulation of the indigenous microbiota is still controversial. Our review discusses the importance of SIgA among the multiple factors that control the oral microbiota. It describes the oral ecosystems, the principal factors that may control the oral microbiota, a basic knowledge of the secretory immune system, the biological functions of SIgA, and, finally, experiments related to the role of SIgA in oral microbial ecology.
Social cognition is affected in people with schizophrenia, but whether this is the case for healthy relatives of these patients is less clear. The presence of social cognition impairments in relatives would suggest a potential genetic role of social cognition in schizophrenia. To determine whether social cognition is affected in first-degree relatives of people with schizophrenia and examine the impact of potential moderator variables, a meta-analysis of studies investigating at least one domain of social cognition (mentalizing, emotional processing, social perception, social knowledge and/or attributional style) in adult first-degree relatives of patients with schizophrenia was performed. Our inclusion criteria were satisfied by 29 studies, of which 11 evaluated mentalizing, 20 emotional processing, and two social perception. Moderate mean effect sizes were obtained for these three components. Across all studies, effect sizes were significantly correlated with IQ and age differences between groups, calling for careful group matching for future studies. Overall, the results from this meta-analysis highlight that social cognition is globally affected in first-degree relatives of people with schizophrenia, suggesting that social cognition deficits in schizophrenia may be related to a genetic vulnerability for the disorder.
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