Interactions between host and oral commensal microorganisms are key events in health and disease status

The oral cavity has sometimes been described as a mirror that reflects a person''s health. Systemic disease such as diabetes or vitamin deficiency may be seen as alterations in the oral mucosa. A variety of external factors cause changes in the oral mucosa, thus altering mucosal structure and function, and promoting oral pathologies (most frequently bacterial, fungal and viral infections). Little is known, however, about immune surveillance mechanisms that involve the oral mucosa.There is no direct contact between specific immune cells in the basal epithelium and microorganisms in the upper layers of the oral mucosa. The author''s hypothesis is that the protective immunity is conveyed through epithelial cells. The present brief review assesses the oral mucosa''s role as the main defense in the interactions between the host and the oral microbial community. A unique model was used to investigate these interactions as the cause of oral disease and to develop new treatments that exploit our knowledge of the host-microorganism relationship.Key Words: Epithelial cells, Fibroblasts, Oral mucosa, Oral pathologies, Tissue engineering     

Interactions between host and oral commensal microorganisms are key events in health and disease status.

The oral cavity has sometimes been described as a mirror that reflects a person's health. Systemic disease such as diabetes or vitamin deficiency may be seen as alterations in the oral mucosa. A variety of external factors cause changes in the oral mucosa, thus altering mucosal structure and function, and promoting oral pathologies (most frequently bacterial, fungal and viral infections). Little is known, however, about immune surveillance mechanisms that involve the oral mucosa.There is no direct contact between specific immune cells in the basal epithelium and microorganisms in the upper layers of the oral mucosa. The author's hypothesis is that the protective immunity is conveyed through epithelial cells. The present brief review assesses the oral mucosa's role as the main defense in the interactions between the host and the oral microbial community. A unique model was used to investigate these interactions as the cause of oral disease and to develop new treatments that exploit our knowledge of the host-microorganism relationship.     

Role of commensal gut bacteria in inflammatory bowel diseases

Aberrant immune responses toward commensal gut bacteria can result in the onset and perpetuation of inflammatory bowel diseases (IBD). Reduced microbiota diversity in conjunction with lower proportion of Gram positive and higher proportion of Gram negative bacteria than in healthy subjects is frequently reported in IBD patients. In a subset of IBD patients, E. coli strains with specific features trigger disease. Important molecular mechanisms underlying this effect have been identified. However, in the majority of patients the exact nature of host-microbe interactions that contribute to IBD development has so far not been defined. The application of metagenomic techniques may help to identify bacterial functions that are involved in the aggravation or alleviation of IBD. Subsequently, the relevance for disease development of bacterial candidate genes may be tested taking advantage of reductionist animal models of chronic gut inflammation. This approach may help to identify bacterial functions that can be targeted in future concepts of IBD therapy.     

Role of commensal gut bacteria in inflammatory bowel diseases

Aberrant immune responses toward commensal gut bacteria can result in the onset and perpetuation of inflammatory bowel diseases (IBD). Reduced microbiota diversity in conjunction with lower proportion of Gram positive and higher proportion of Gram negative bacteria than in healthy subjects is frequently reported in IBD patients. In a subset of IBD patients, E. coli strains with specific features trigger disease. Important molecular mechanisms underlying this effect have been identified. However, in the majority of patients the exact nature of host-microbe interactions that contribute to IBD development has so far not been defined. The application of metagenomic techniques may help to identify bacterial functions that are involved in the aggravation or alleviation of IBD. Subsequently, the relevance for disease development of bacterial candidate genes may be tested taking advantage of reductionist animal models of chronic gut inflammation. This approach may help to identify bacterial functions that can be targeted in future concepts of IBD therapy.     

Microbial-gut interactions in health and disease. Interactions between dendritic cells and bacteria in the regulation of intestinal immunity

Dendritic cells (DCs) are immunoregulatory antigen-presenting cells. DCs can be potent activators of na?ve T cells and influence the generation and homing of effector lymphocytes; they can also induce regulatory mechanisms and maintain non-responsiveness. In part, these different outcomes are influenced by exposure of the DC to microbial products. The regulatory role of DCs is of particular importance at mucosal surfaces such as the intestine, where the immune system exists in intimate association with the external antigenic environment. Much of what we know about DCs has come from studies on the cells outside the gastrointestinal tract but information about gut DCs and their contribution to the specialized immune environment of the gut is now emerging. Here, we review current knowledge on gut DCs, suggest models for interactions between DCs and the commensal microflora in health and disease, and discuss gut DCs as targets for probiotic therapies.     

Mechanisms and consequences of gut commensal translocation in chronic diseases

ABSTRACT

Humans and other mammalian hosts have evolved mechanisms to control the bacteria colonizing their mucosal barriers to prevent invasion. While the breach of barriers by bacteria typically leads to overt infection, increasing evidence supports a role for translocation of commensal bacteria across an impaired gut barrier to extraintestinal sites in the pathogenesis of autoimmune and other chronic, non-infectious diseases. Whether gut commensal translocation is a cause or consequence of the disease is incompletely defined. Here we discuss factors that lead to translocation of live bacteria across the gut barrier. We expand upon our recently published demonstration that translocation of the gut pathobiont Enterococcus gallinarum can induce autoimmunity in susceptible hosts and postulate on the role of Enterococcus species as instigators of chronic, non-infectious diseases.     

Interactions between host and gut microbiota in domestic pigs: a review

ABSTRACT

It is well established that pig gut microbiota plays a critical role in maintaining metabolic homeostasis as well as in a myriad of physiological, neurological and immunological functions; including protection from pathogens and digestion of food materials – some of which would be otherwise indigestible by the pig. A rich and diverse gut microbial ecosystem (balanced microbiota) is the hallmark of good health; while qualitative and quantitative perturbations in the microbial composition can lead to development of various diseases. Alternatively, diseases caused by stressors or other factors have been shown to negatively impact the microbiota. This review focuses primarily on how commensal microorganisms in the gastrointestinal tract of pigs influence biochemical, physiological, immunological, and metabolic processes within the host animal.     

Systemic antibody responses to gut microbes in health and disease

Gastrointestinal commensal microbes usually exist in mutualistic relationship with their mammalian host. This relationship exists even though the mammalian host immune system is equipped with exquisite sensors for microbial chemical structures which trigger powerful immune defense mechanisms. Such beneficial mutualism is specifically maintained at the gut mucosal interface by a variety of physical and bioactive barriers as well as specific immunregulatory mechanisms. In addition, there is a strict compartmentalization between systemic and gut mucosal immunity--at least in inbred mice--which focuses adaptive immunity to gut microbes specifically to the gut tissue and the gut lumen. Only in circumstances of increased gut microbial exposure due to elevated gut epithelial permeability, due to genetic deficiencies in local defense mechanisms, due to imbalances in local immune regulation or in case of gastrointestinal pathogenic bacterial infections this compartmentalization is broken and systemic immune responses to gut microbes are induced, which manifest for example as systemic antibody responses specific for gut microbial antigens. Here we briefly discuss the abundance of systemic antibody responses to commensal gut bacteria in healthy humans and how it is altered in situations with chronic enteropathies such as in inflammatory bowel disease and HIV-1 infection or infection with gut bacterial pathogens.     

Non-invasive markers of gut wall integrity in health and disease

The intestinal mucosa is responsible for the absorption of nutrients from the lumen and for the separation of the potentially toxic luminal content(external environment) from the host(internal environment).Disruption of this delicate balance at the mucosal interface is the basis for numerous(intestinal) diseases.Experimental animal studies have shown that gut wall integrity loss is involved in the development of various inflammatory syndromes,including post-operative or post-traumatic systemic inflammatory ...     

心肠对话:肠道菌群在心血管疾病中的作用

心血管疾病(CVD)是对人类健康构成极大威胁的一类疾病,其发生、发展往往受遗传与环境的多种因素影响。肠道菌群是人体内数目最大的菌群库,影响宿主的生理代谢,近年来肠道菌群与宿主间的相互作用逐渐受到重视。肠道微生物群在人类健康和疾病中发挥着重要作用,许多研究证实了肠道菌群及其代谢产物可从血脂异常、2型糖尿病、高血压、动脉粥样硬化、心力衰竭等多个方面影响CVD。因此,以肠道菌群作为CVD治疗靶点的方案值得探索。本文将对肠道菌群在CVD发病机制中的作用及通过调节肠道菌群治疗CVD的方法进行系统综述。     

Interactions between viruses and bacteria in patients with chronic bronchitis.

The possibility that viral infections of the respiratory tract might predispose to bacterial colonization or infection was studied in 120 patients with chronic obstructive pulmonary disease and 30 control subjects; these individuals were observed for seven years. The ratio of the number of observed to the number of expected associations between viruses and bacteria was 2.43 (P = 0.037) for the pair influenza virus and Streptococcus pneumoniae and was 2.06 (P = 0.056) for influenza virus and Haemophilus influenzae. Consistently positive, but not significant, associations were detected between rhinovirus and herpes simplex virus infections and isolations of S. pneumoniae and H. influenzae. In contrast, isolations of the nonpathogenic Haemophilus parainfluenzae could not be related to prior viral infections. Significant rises in titer of antibody to H. influenzae were detected on 76 occasions, and 20 (26%) of these antibody rises were associated with viral or mycoplasmal infections during the preceding 120 days. The expected number of such associations was 8.34 (ratio of number observed to number expected, 2.40; P = 0.08). These results suggest that viral infections of the respiratory tract in patients with chronic obstructive pulmonary disease are associated with increased colonization by potentially pathogenic bacteria and may also predispose to infections with H. influenzae.