The Bacterium Frischella perrara Causes Scab Formation in the Gut of its Honeybee Host.

UNLABELLED: Honeybees harbor well-defined bacterial communities in their guts. The major members of these communities appear to benefit the host, but little is known about how they interact with the host and specifically how they interface with the host immune system. In the pylorus, a short region between the midgut and hindgut, honeybees frequently exhibit scab-like structures on the epithelial gut surface. These structures are reminiscent of a melanization response of the insect immune system. Despite the wide distribution of this phenotype in honeybee populations, its cause has remained elusive. Here, we show that the presence of a common member of the bee gut microbiota, the gammaproteobacterium Frischella perrara, correlates with the appearance of the scab phenotype. Bacterial colonization precedes scab formation, and F. perrara specifically localizes to the melanized regions of the host epithelium. Under controlled laboratory conditions, we demonstrate that exposure of microbiota-free bees to F. perrara but not to other bacteria results in scab formation. This shows that F. perrara can become established in a spatially restricted niche in the gut and triggers a morphological change of the epithelial surface, potentially due to a host immune response. As an intermittent colonizer, this bacterium holds promise for addressing questions of community invasion in a simple yet relevant model system. Moreover, our results show that gut symbionts of bees engage in differential host interactions that are likely to affect gut homeostasis. Future studies should focus on how these different gut bacteria impact honeybee health. IMPORTANCE: As pollinators, honeybees are key species for agricultural and natural ecosystems. Their guts harbor simple communities composed of characteristic bacterial species. Because of these features, bees are ideal systems for studying fundamental aspects of gut microbiota-host interactions. However, little is known about how these bacteria interact with their host. Here, we show that a common member of the bee gut microbiota causes the formation of a scab-like structure on the gut epithelium of its host. This phenotype was first described in 1946, but since then it has not been much further characterized, despite being found in bee populations worldwide. The scab phenotype is reminiscent of melanization, a conserved innate immune response of insects. Our results show that high abundance of one member of the bee gut microbiota triggers this specific phenotype, suggesting that the gut microbiota composition can affect the immune status of this key pollinator species.

Early life host-microbe interactions : implications for the development of asthma

Plus de 300 millions de personnes dans le monde souffrent de l'asthme. L'asthme est une maladie inflammatoire chronique des voies respiratoires caractérisée par des symptômes variables et récurrents, une obstruction bronchique réversible et des bronchospasmes. Les symptômes communs incluent une respiration sifflante, de la toux, une oppression thoracique et de la dyspnée. Normalement, la maladie commence à se manifester pendant l'enfance. Pourtant, facteurs génétiques héréditaires et événements environnementaux survenant au cours de la petite enfance sont responsables de sa manifestation, indiquant que le développement de la maladie est lié à des événements qui se produisent bien avant son déclenchement. L'infection respiratoire virale aiguë constitue un de ces facteurs environnementaux jouant un rôle prépondérant. Un des virus les plus communs est le virus respiratoire syncytial (VRS), qui infecte presque tous les enfants avant l'âge de 2 ans. Ce virus, s'il infecte des tout-petits, peut en effet provoquer une bronchiolite aiguë, un phénomène qui a été épidémiologiquement lié à l'apparition d'asthme plus tard dans la vie. Dans le premier chapitre de cette thèse, nous avons étudié, chez la souris, comment une infection avec le VRS influe sur l'asthme allergique. Nous avons constaté que seule l'infection des souris à l'état de nouveau-né prédispose à un asthme allergique plus sévère chez l'adulte. En effet, si des souris adultes étaient infectées, elles étaient protégées contre l'apparition des symptômes asthmatiques. Cela nous a mené à investiguer les mécanismes immunitaires spécifiques durant cette courte période du début de la vie. Deux événements se produisent en parallèle au cours de la petite enfance: (1) Le système immunitaire, qui est encore immature immédiatement après la naissance, commence à se développer pour être en mesure de jouer son rôle protecteur contre les agents infectieux. (2) Le corps, y compris les poumons, est colonisé par des bactéries commensales, qui vivent en symbiose avec leur hôte humain. Chez l'adulte, ces bactéries sont connues pour influencer notre système immunitaire, l'éduquant à générer des réponses immunitaires adéquates et efficaces. Dans la deuxième partie de cette thèse, nous avons voulu déterminer si ces bactéries symbiotiques étaient impliquées dans l'éducation du système immunitaire du nouveau-né et quelles conséquences cela pourrait avoir sur les réponses immunitaires engendrées par ce dernier. Pour étudier l'effet de ces bactéries symbiotiques, nous avons utilisé des souris stériles, en d'autres termes des souris qui n'hébergent pas ces bactéries symbiotiques. En comparant ces souris stériles à des souris qui abritent une flore microbienne normale, nous avons constaté que les bactéries symbiotiques sont vitales pour la bonne éducation du système immunitaire du nouveau-né. Nous avons démontré que le contact direct des cellules immunitaires avec la flore microbienne dans les poumons modifie le phénotype de ces cellules immunitaires, ce qui change probablement leur réaction au cours de réponses immunitaires. Nous avons donc vérifié si l'éducation immunitaire induite par cette microflore est importante pour prévenir les maladies pulmonaires telles que l'asthme allergique, affections qui sont causées par une réaction excessive du système immunitaire envers des agents inoffensifs. En effet, nous avons observé que le processus de maturation du système immunitaire néonatal, lequel a été déclenché et façonné par la flore microbienne, est important pour éviter une réaction asthmatique exagérée chez la souris adulte. Ce phénomène est dû aux lymphocytes T régulateurs. Ces cellules, dont la présence est induite dans les poumons, ont des capacités immunosuppressives et atténuent donc les réponses immunitaires pour prévenir une inflammation excessive. En conclusion, nous avons montré dans cette thèse que la colonisation par des bactéries symbiotiques tôt dans la vie est un événement décisif pour la maturation du système immunitaire et pour prévenir le développement de l'asthme. Dans l'avenir, il serait intéressant de découvrir quelles bactéries sont présentes dans les poumons du nouveau-né et lesquelles sont directement impliquées dans ce processus de maturation immunitaire. Une prochaine étape serait alors de favoriser la présence de ces bactéries au début de la vie au moyen d'un traitement avec des agents pré- ou probiotiques, ce qui pourrait éventuellement contribuer à une prévention précoce du développement de l'asthme. -- L'asthme est une maladie chronique inflammatoire des voies respiratoires affectant près de 300 millions d'individus dans le monde. Bien que les traits caractéristiques du phénotype asthmatique s'établissent généralement pendant l'enfance, la prédisposition au développement de la maladie est intimement liée à des événements survenant durant la petite enfance, comme le sont par exemple les infections virales respiratoires aiguës. Les mécanismes par lesquels ces événements provoquent un dysfonctionnement immunitaire et, par conséquent, conduisent au développement de l'asthme n'ont pas encore été entièrement décelés. La dysbiose du microbiote des voies respiratoires a été récemment associes au phénotype asthmatique, touisTcis, la cuûoboiatioî! d un lien cause à effet entre la dysbiose microbienne et l'apparition des symptômes asthmatiques reste à être démontrée. Dans cette thèse, nous avons étudié le rôle que joue la colonisation microbienne des voies respiratoires au cours de la petite enfance dans la maturation du système immunitaire ainsi que dans la protection contre l'inflammation pulmonaire de type allergique. Nous avons de surcroît développé un modèle expérimental pour comprendre comment les infections virales respiratoires interfèrent avec ce processus. Dans la première partie de cette thèse, nous avons évalué l'effet d'infections causées par le virus respiratoire syncytial (VRS) sur le développement de l'asthme. En accord avec des études épidémiologiques, nous avons constaté qu'une infection au VRS lors de la période néonatale exacerbait les réponses pulmonaires allergiques ultérieures. Par contraste, une infection à l'âge adulte avait un effet protecteur. Nous avons ainsi démontré que l'influence d'une infection à VRS sur l'issue et la sévérité de l'asthme respiratoire était strictement dépendante de l'âge. Ces résultats nous ont conduit à émettre l'hypothèse que des différences dans le phénotype homéostatique des cellules immunitaires pourraient être responsables de ces disparités liées à l'âge. Par conséquent, dans la deuxième partie de cette thèse, nous avons suivi et caractérisé le processus de maturation des cellules immunitaires dans les poumons du nouveau-né en condition d'homéostasie. Nous avons découvert que leur phénotype change de façon dynamique pendant le développement néonatal et que la colonisation par des microbes était déterminante pour la maturation des cellules immunitaires dans les poumons. Dans la dernière partie de cette thèse, nous avons démontré comment le microbiote pulmonaire éduque le développement immunitaire durant la période néonatale l'orientant de manière à induire une tolérance face aux aéroallergènes. Nous avons découvert que la colonisation microbienne des voies respiratoires provoque une expression transitoire de PD-L1 sur les cellules dendritiques (CD) pulmonaires du type CD11b+ dans les deux premières semaines de la vie. Cet événement engendre par la suite la génération de lymphocytes T régulateurs (TREG) dans les poumons, lesquels sont responsables de la protection contre une réponse inflammatoire allergique exagérée chez la souris adulte. Par conséquent, nous proposons un rôle pivot de la maturation immunitaire induite par le microbiote pulmonaire dans l'établissement de la tolérance aux aéroallergènes. En conclusion, les résultats présentés dans cette thèse fournissent de nouveaux indices révélant comment des événements se produisant lors de la petite enfance peuvent façonner les réponses du système immunitaire dirigées contre les allergènes et soulignent le rôle central joué par le microbiote pulmonaire dans l'édification d'une réponse immunitaire équilibrée. En résumé, notre travail met en évidence le microbiote pulmonaire comme étant une cible potentielle pour la prévention de certaines maladies respiratoires. -- Asthma is a chronic inflammatory disorder of the respiratory tract and affects approximately 300 million individuals world-wide. Although the asthmatic phenotype commonly establishes during childhood, predisposition towards disease development has been linked to events in early infancy, such as severe respiratory viral infections. However, the mechanisms by which these events cause immune dysfunction and, therefore, lead to the development of asthma have yet to be fully deciphered. Dysbiosis of the airway microbiota has recently been associated with the asthmatic phenotype; however, conclusive evidence for a causal link between microbial dysbiosis in the ail ways and asthma development is still missing. In this thesis we investigated the role of early-life microbial airway colonization in immune maturation and the protection against allergic airway inflammation and established an experimental model to address how respiratory viral infections interfere in this process. In the first part of this thesis we evaluated the effect of Respiratory syncytial virus (RSV) infections on the development of asthma. In concurrence with epidemiological studies, we found that neonatal infection exacerbated subsequent allergic airway inflammation. In contrast, adult infection was protective in the same context. Thus, we could demonstrate that the influence of RSV infection on subsequent allergic airway responses was strictly age-dependent. These findings led us to the hypothesis that differences in the homeostatic phenotype of immune cells could be responsible for the age-related disparities seen within the context of RSV. Therefore, in a second part of this thesis, we followed the process of homeostatic immune cell maturation in the neonatal lung. Immune cell phenotypes changed dynamically during neonatal development. We discovered that the colonization with microbes was central to the maturation of immune cells in the lung. In the last part of this thesis, we demonstrated how microbiota-driven immune development during the neonatal period induces tolerance against aeroallergens. We discovered that microbial colonization led to a transient programmed death-ligand (PD-L) 1 expression on CD11b+ pulmonary dendritic cells (DCs) during the first two weeks of life. This in turn induced regulatory T (TREG) cells in the lung, which were responsible for the protection against exaggerated allergic airway inflammation in adult mice. Thus, we propose a key role for microbiota-driven immune maturation in the establishment of tolerance towards aeroallergens. In conclusion, the results presented in this thesis provide new insights into how early-life events shape pulmonary immune responses towards allergens and suggest the airway microbiota as a key player in establishing a balanced immune response. Overall, our work highlights the airway microbiota as potential target for disease prevention.

The effects of cocoa on the immune system

Cocoa is a food relatively rich in polyphenols, which makes it a potent antioxidant. Due to its activity as an antioxidant, as well as through other mechanisms, cocoa consumption has been reported to be beneficial for cardiovascular health, brain functions, and cancer prevention. Furthermore, cocoa influences the immune system, in particular the inflammatory innate response and the systemic and intestinal adaptive immune response. Preclinical studies have demonstrated that a cocoa-enriched diet modifies T-cell functions that conduce to a modulation of the synthesis of systemic and gut antibodies. In this regard, it seems that a cocoa diet in rats produces changes in the lymphocyte composition of secondary lymphoid tissues and the cytokines secreted by T cells. These results suggest that it is possible that cocoa could inhibit the function of Th2 cells, and in line with this, the preventive effect of cocoa on IgE synthesis in a rat allergy model has been reported, which opens up new perspectives when considering the beneficial effects of cocoa compounds. On the other hand, cocoa intake modifies the functionality of gut-associated lymphoid tissue by means of modulating IgA secretion and intestinal microbiota. The mechanisms involved in these influences are discussed here. Further research may elucidate the cocoa compounds involved in such an effect and also the possible medical approaches to these repercussions

Microbis per combatre els excessos de sucre

La microbiota intestinal dels diabètics és diferent. L'absència i l'excés d'alguns bacteris podrien estar darrere de la malaltia, indica un estudi a 'Nature'

Evidencia existente sobre la influencia de la ingesta de prebióticos sobre el riesgo de cáncer colorrectal

El cáncer colorrectal es uno de los cánceres más comunes a nivel mundial. Entre el riesgo a desarrollarlo y la microbiota intestinal existe una relación compleja que puede ser modificada por la alimentación. El efecto de los prebióticos sobre la composición y la actividad de la microbiota colónica pueden producir cambios beneficiosos en la flora alterada de los pacientes con cáncer de colon. De todos los prebióticos, se sospecha que la inulina HP y el sinergil (30% oligofructosa y 70% de inulina) son los que mantienen una relación más estrecha con la neoplasia. Este fenómeno podría ser explicado por la longitud de las cadenas de los fructanos. Los estudios realizados en animales observan que la administración de prebióticos reduce el número y la multiplicidad de focos de criptas aberrantes, reduce el número y la vida media de los tumores, inhibe el crecimiento de éstos y potencia el efecto de diferentes fármacos quimioterapéuticos. Los resultados obtenidos en roedores que pretenden simular la predisposición genética no son homogéneos. Algunos de los estudios realizados en humanos, mayoritariamente sanos, observan cambios en la composición de la microbiota, en el perfil de los ácidos biliares y en los ácidos grasos de cadena corta, pero los resultados obtenidos difieren entre los diferentes estudios y no obtienen resultados concluyentes.

Microbiome influences on allergy in mice and humans.

The microbiota plays a pivotal role in the development and calibration of host immunity. Over many millennia, finely balanced interactions between the microbiota and host tissue compartments have evolved, imparting metabolic advantages and protection against pathogens, while restricting deleterious immune responses against innocuous antigens. Perturbations in host-microbiota crosstalk at critical developmental windows in early life may underlie allergy and chronic inflammation. Although the microbiota's of the gut and skin have been extensively characterized, the lung microbiota has also, in recent years, received considerable attention. This ever-expanding field is pushing the boundaries of pulmonary research, with potential implications for novel strategies in the treatment and prevention of chronic lung diseases. In this article, we provide a summary of the development of the microbiota in early life, and describe the evidence from human and murine studies of how microbial dysbiosis in early life can alter the trajectory of immune development and provide the setting for allergic disorders in later life.

Mutations in the heat-shock protein A9 (HSPA9) gene cause the EVEN-PLUS syndrome of congenital malformations and skeletal dysplasia.

We and others have reported mutations in LONP1, a gene coding for a mitochondrial chaperone and protease, as the cause of the human CODAS (cerebral, ocular, dental, auricular and skeletal) syndrome (MIM 600373). Here, we delineate a similar but distinct condition that shares the epiphyseal, vertebral and ocular changes of CODAS but also included severe microtia, nasal hypoplasia, and other malformations, and for which we propose the name of EVEN-PLUS syndrome for epiphyseal, vertebral, ear, nose, plus associated findings. In three individuals from two families, no mutation in LONP1 was found; instead, we found biallelic mutations in HSPA9, the gene that codes for mHSP70/mortalin, another highly conserved mitochondrial chaperone protein essential in mitochondrial protein import, folding, and degradation. The functional relationship between LONP1 and HSPA9 in mitochondrial protein chaperoning and the overlapping phenotypes of CODAS and EVEN-PLUS delineate a family of "mitochondrial chaperonopathies" and point to an unexplored role of mitochondrial chaperones in human embryonic morphogenesis.

DLL4 promotes continuous adult intestinal lacteal regeneration and dietary fat transport.

The small intestine is a dynamic and complex organ that is characterized by constant epithelium turnover and crosstalk among various cell types and the microbiota. Lymphatic capillaries of the small intestine, called lacteals, play key roles in dietary fat absorption and the gut immune response; however, little is known about the molecular regulation of lacteal function. Here, we performed a high-resolution analysis of the small intestinal stroma and determined that lacteals reside in a permanent regenerative, proliferative state that is distinct from embryonic lymphangiogenesis or quiescent lymphatic vessels observed in other tissues. We further demonstrated that this continuous regeneration process is mediated by Notch signaling and that the expression of the Notch ligand delta-like 4 (DLL4) in lacteals requires activation of VEGFR3 and VEGFR2. Moreover, genetic inactivation of Dll4 in lymphatic endothelial cells led to lacteal regression and impaired dietary fat uptake. We propose that such a slow lymphatic regeneration mode is necessary to match a unique need of intestinal lymphatic vessels for both continuous maintenance, due to the constant exposure to dietary fat and mechanical strain, and efficient uptake of fat and immune cells. Our work reveals how lymphatic vessel responses are shaped by tissue specialization and uncover a role for continuous DLL4 signaling in the function of adult lymphatic vasculature.

Tabagisme et système digestif: une relation complexe. Partie 2: Microbiote intestinal et tabagisme [Smoking and digestive tract: a complex relationship. Part 2: Intestinal microblota and cigarette smoking].

Le système digestif est colonisé dès la naissance par une population bactérienne, le microbiote, qui influence le développement du système immunitaire. Des modifications dans sa composition sont associées à des pathologies comme l'obésité et les maladies inflammatoires chroniques de l'intestin. Outre les antibiotiques, des facteurs environnementaux comme le tabagisme semblent aussi avoir une influence sur la composition de la flore intestinale, pouvant en partie expliquer la prise de poids à l'arrêt du tabac avec une modification de la composition du microbiote proche de celle observée chez des personnes obèses (profil microbiotique montrant des capacités accrues d'extraction calorique des aliments ingérés). Ces découvertes permettent d'imaginer de nouvelles approches diagnostiques et thérapeutiques via la régulation de ce microbiome. The digestive tract is colonized from birth by a bacterial population called the microbiota which influences the development of the immune system. Modifications in its composition are associated with problems such as obesity or inflammatory bowel diseases. Antibiotics are known to influence the intestinal microbiota but other environmental factors such as cigarette smoking also seem to have an impact on its composition. This influence might partly explain weight gain which is observed after smoking cessation. Indeed there is a modification of the gut microbiota which becomes similar to that of obese people with a microbiotical profile which is more efficient to extract calories from ingested food. These new findings open new fields of diagnostic and therapeutic approaches through the regulation of the microbiota.

Facteurs impliqués dans le développement et la progression de la maladie aLcoolique du foie [Factors influencing development and progression of alcoholic liver disease].

Only a minority ot excessive drinkers develop cirrhosis. The main cofactors implicated in the pathophysiology of alcoholic liver disease are obesity, diabetes or the metabolic syndrome. Several genetic polymorphisms have been associated with a higher risk of alcoholic cirrhosis. Recent data indicate that gut microbiota could play a role in the pathogenesis of alcoholic liver disease. The aim of this review is to summarize the factors that influence development and progression of alcoholic liver disease.

Mechanisms involved in down-regulation of intestinal IgA in rats by high cocoa intake

Previous studies have shown that rat intestinal immunoglobulin A (IgA) concentration and lymphocyte composition of the intestinal immune system were influenced by a highly enriched cocoa diet. The aim of this study was to dissect the mechanisms by which a long-term high cocoa intake was capable of modifying gut secretory IgA in Wistar rats. After 7 weeks of nutritional intervention, Peyer's patches, mesenteric lymph nodes and the small intestine were excised for gene expression assessment of IgA, transforming growth factor ß, C-C chemokine receptor-9 (CCR9), interleukin (IL)-6, CD40, retinoic acid receptors (RAR¿ and RARß), C-C chemokine ligand (CCL)-25 and CCL28 chemokines, polymeric immunoglobulin receptor and toll-like receptors (TLR) expression by real-time polymerase chain reaction. As in previous studies, secretory IgA concentration decreased in intestinal wash and fecal samples after cocoa intake. Results from the gene expression showed that cocoa intake reduced IgA and IL¿6 in Peyer's patches and mesenteric lymph nodes, whereas in small intestine, cocoa decreased IgA, CCR9, CCL28, RAR¿ and RARß. Moreover, cocoa-fed animals presented an altered TLR expression pattern in the three compartments studied. In conclusion, a high-cocoa diet down-regulated cytokines such as IL-6, which is required for the activation of B cells to become IgA-secreting cells, chemokines and chemokine receptors, such as CCL28 and CCR9 together with RAR¿ and RARß, which are involved in the gut homing of IgA-secreting cells. Moreover, cocoa modified the cross-talk between microbiota and intestinal cells as was detected by an altered TLR pattern. These overall effects in the intestine may explain the intestinal IgA down-regulatory effect after the consumption of a long-term cocoa-enriched diet.

Environmental factors in multiple sclerosis [Environmental factors in multiple sclerosis]

Although multiple sclerosis (MS) is recognized as a disorder involving the immune system, the interplay of environmental factors and individual genetic susceptibility seems to influence MS onset and clinical expression, as well as therapeutic responsiveness. Multiple human epidemiological and animal model studies have evaluated the effect of different environmental factors, such as viral infections, vitamin intake, sun exposure, or still dietary and life habits on MS prevalence. Previous Epstein-Barr virus infection, especially if this infection occurs in late childhood, and lack of vitamin D (VitD) currently appear to be the most robust environmental factors for the risk of MS, at least from an epidemiological standpoint. Ultraviolet radiation (UVR) activates VitD production but there are also some elements supporting the fact that insufficient UVR exposure during childhood may represent a VitD-independent risk factor of MS development, as well as negative effect on the clinical and radiological course of MS. Recently, there has been a growing interest in the gut-brain axis, a bidirectional neuro-hormonal communication system between the intestinal microbiota and the central nervous system (CNS). Indeed, components of the intestinal microbiota may be pro-inflammatory, promote the migration of immune cells into the CNS, and thus be a key parameter for the development of autoimmune disorders such as MS. Interestingly most environmental factors seem to play a role during childhood. Thus, if childhood is the most fragile period to develop MS later in life, preventive measures should be applied early in life. For example, adopting a diet enriched in VitD, playing outdoor and avoiding passive smoking would be extremely simple measures of primary prevention for public health strategies. However, these hypotheses need to be confirmed by prospective evaluations, which are obviously difficult to conduct. In addition, it remains to be determined whether and how VitD supplementation in adult life would be useful in alleviating the course of MS, once this disease has already started. A better knowledge of the influence of various environmental stimuli on MS risk and course would certainly allow the development of add-on therapies or measures in parallel to the immunotherapies currently used in MS.

Importance of amoebae as a tool to isolate amoeba-resisting microorganisms and for their ecology and evolution: the Chlamydia paradigm.

Free-living amoebae are distributed worldwide and are frequently in contact with humans and animals. As cysts, they can survive in very harsh conditions and resist biocides and most disinfection procedures. Several microorganisms, called amoeba-resisting microorganisms (ARMs), have evolved to survive and multiply within these protozoa. Among them are many important pathogens, such as Legionella and Mycobacteria, and also several newly discovered Chlamydia-related bacteria, such as Parachlamydia acanthamoebae, Estrella lausannensis, Simkania negevensis or Waddlia chondrophila whose pathogenic role towards human or animal is strongly suspected. Amoebae represent an evolutionary crib for their resistant microorganisms since they can exchange genetic material with other ARMs and develop virulence traits that will be further used to infect other professional phagocytes. Moreover, amoebae constitute an ideal tool to isolate strict intracellular microorganisms from complex microbiota, since they will feed on other fast-growing bacteria, such as coliforms potentially present in the investigated samples. The paradigm that ARMs are likely resistant to macrophages, another phagocytic cell, and that they are likely virulent towards humans and animals is only partially true. Indeed, we provide examples of the Chlamydiales order that challenge this assumption and suggest that the ability to multiply in protozoa does not strictly correlate with pathogenicity and that we should rather use the ability to replicate in multiple and diverse eukaryotic cells as an indirect marker of virulence towards mammals. Thus, cell-culture-based microbial culturomics should be used in the future to try to discover new pathogenic bacterial species.

Complications following an accidental sodium hypochlorite extrusion: A report of two cases

Sodium hypochlorite (NaOCl) is the most commonly used solution in root canal treatments, as it is a low-cost method that displays a very effective antimicrobial activity against microbiota of infected root canals. However, this solution can cause complications especially due to its cytotoxic features. When this solution is injected into the adjacent tissues, the patient usually experiences intense pain, and an urgent treatment should be implemented in order to prevent a long-term sequelae. This paper describes the clinical features of two patients that experienced an accidental extrusion of NaOCl after endodontic treatment of varying severity and with different treatments. Furthermore, it shows the long-term neurologic injuries that this type of accidents may cause and a treatment protocol for these situations will be suggested.

Probiotic lactobacilli and bifidobacteria in the mouth – in vitro studies on saliva-mediated functions and acid production

Probiotic lactobacilli and bifidobacteria in the mouth – in vitro studies on saliva-mediated functions and acid production Probiotics are viable bacteria which, when used in adequate amounts, are beneficial to the health of the host. Although most often related to intestinal health, probiotic bacteria can be found also in the mouth after consumption of products that contain them. This study aimed at evaluating the oral effects of probiotic bacteria already in commercial use. In a series of in vitro studies, the oral colonisation potential of different probiotic bacteria, their acid production and potential saliva-mediated effects on oral microbial ecology were investigated. The latter included effects on the salivary pellicle, the adhesion of other bacteria, and the activation of the peroxidase system. Streptococcus mutans, Streptococcus gordonii, Aggregatibacter actinomycetemcomitans and Helicobacter pylori were used as bacterial indicators of the studied phenomena. There were significant differences between the probiotic strains in their colonisation potential. They all were acidogenic, although using different sugars and sugar alcohols. However, their acid production could be inhibited by the peroxidase system. Based on the results, it can be suggested that probiotic bacteria might influence the oral microbiota by different, partly species or strain-specific means. These include the inhibition of bacterial adhesion, modification of the enamel pellicle, antimicrobial activity, and activation of the peroxidase system. To conclude, probiotic strains differed from each other in their colonisation potential and other oral effects as evaluated in vitro. Both positive and potentially harmful effects were observed, but the significance of the perceived results needs to be further evaluated in vivo.