German dentists' websites on periodontitis have low quality of information.

BACKGROUND: The internet is an increasingly relevant source of health information. We aimed to assess the quality of German dentists' websites on periodontitis, hypothesizing that it was significantly associated with a number of practice-specific parameters. METHODS: We searched four electronic search engines and included pages which were freely accessible, posted by a dental practice in Germany, and mentioned periodontal disease/therapy. Websites were assessed for (1) technical and functional aspects, (2) generic quality and risk of bias, (3) disease-specific information. For 1 and 2, validated tools (LIDA/DISCERN) were used for assessment. For 3, we developed a criterion catalogue encompassing items on etiologic and prognostic factors for periodontitis, the diagnostic and treatment process, and the generic chance of tooth retention in periodontitis patients. Inter- and intra-rater reliabilities were largely moderate. Generalized linear modeling was used to assess the association between the information quality (measured as % of maximally available scores) and practice-specific characteristics. RESULTS: Seventy-one websites were included. Technical and functional aspects were reported in significantly higher quality (median: 71%, 25/75th percentiles: 67/79%) than all other aspects (p < 0.05). Generic risk of bias and most disease-specific aspects showed significantly lower reporting quality (median range was 0-40%), with poorest reporting for prognostic factors (9;0/27%), diagnostic process (0;0/33%) and chances of tooth retention (0;0/2%). We found none of the practice-specific parameters to have significant impact on the overall quality of the websites. CONCLUSIONS: Most German dentists' websites on periodontitis are not fully trustworthy and relevant information are not or insufficiently considered. There is great need to improve the information quality from such websites at least with regards to periodontitis.

The aryl hydrocarbon receptor in innate T cell immunity.

Recent studies highlight an important role of the aryl hydrocarbon receptor (AhR) at mucosal barriers. Surprisingly, activation of the AhR, required for the maintenance of lymphocytes as well as lymphoid architecture, can be achieved via cues derived from the external environment. This environment contains both beneficial and harmful microorganisms as well as a diverse array of compounds, and the epithelia must offer very sophisticated levels of defence. This is achieved via multifaceted immune recognition diversity and cellular complexity. Mucosal associated tissues, particularly in the gastrointestinal tract, constitute a complex immune organ for local lymphocytes and contain highly organised lymphoid structures. We will discuss the recent observations concerning the AhR in relation to the function and maintenance of innate T cells, with focus on γδ T cells found enriched at epithelial barriers.

IL-22 mediates host defense against an intestinal intracellular parasite in the absence of IFN-γ at the cost of Th17-driven immunopathology.

The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. In this study, we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-γ was the predominant cytokine during E. falciformis infection in wild-type mice, it was found to be dispensable for host defense and the development of intestinal inflammation. E. falciformis-infected IFN-γR(-/-) and IFN-γ(-/-) mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surprisingly harbored fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and intestine. CD4(+) T cells were found to be the source of IL-17A and IL-22, which drove the recruitment of neutrophils and increased tissue expression of anti-microbial peptides (RegIIIß, RegIIIγ) and matrix metalloproteinase 9. Concurrent neutralization of IL-17A and IL-22 in E. falciformis-infected IFN-γR(-/-) mice resulted in a reduction in infection-induced body weight loss and inflammation and significantly increased parasite shedding. In contrast, neutralization of IL-22 alone was sufficient to increase parasite burden, but it had no effect on body weight loss. Treatment of an E. falciformis-infected intestinal epithelial cell line with IFN-γ, IL-17A, or IL-22 significantly reduced parasite development in vitro. Taken together, to our knowledge these data demonstrate for the first time an antiparasite effect of IL-22 during an intestinal infection, and they suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-γ signaling.

CD8+ cells protect mice against reinfection with the intestinal parasite Eimeria falciformis.

We investigated cellular immune responses of mice infected with the apicomplexan parasite Eimeria falciformis in order to characterise protective immune mechanisms and effector functions. Adoptive transfer experiments with mesenterial lymph node cells (MLNC) from immune donor mice were performed, and the oocyst output monitored after challenge infection. Phenotypical analysis by fluorescence cytometry and T cell proliferation assay showed that already from day four post infection E. falciformis-specific lymphocytes were present in the MLN. The frequency of parasite-specific, IFN-gamma producing CD4+ and CD8+ cells increased in this period by 9.8% and 16.4%, respectively. Infection experiments with IFN-gamma deficient mice revealed that IFN-gamma is involved in resistance to primary and secondary infection. Transfer of total MLNC from immune donors reduced the oocyst output by 65-74%, as compared to the oocyst output of animals transferred with cells from naïve donors. Transfer of CD8+ cells inhibited parasite development resulting in a reduction of oocyst numbers by 42-64%, whereas CD4+ cells showed no influence on resistance to reinfection.

Intravital observation of Plasmodium berghei sporozoite infection of the liver.

Plasmodium sporozoite invasion of liver cells has been an extremely elusive event to study. In the prevailing model, sporozoites enter the liver by passing through Kupffer cells, but this model was based solely on incidental observations in fixed specimens and on biochemical and physiological data. To obtain direct information on the dynamics of sporozoite infection of the liver, we infected live mice with red or green fluorescent Plasmodium berghei sporozoites and monitored their behavior using intravital microscopy. Digital recordings show that sporozoites entering a liver lobule abruptly adhere to the sinusoidal cell layer, suggesting a high-affinity interaction. They glide along the sinusoid, with or against the bloodstream, to a Kupffer cell, and, by slowly pushing through a constriction, traverse across the space of Disse. Once inside the liver parenchyma, sporozoites move rapidly for many minutes, traversing several hepatocytes, until ultimately settling within a final one. Migration damage to hepatocytes was confirmed in liver sections, revealing clusters of necrotic hepatocytes adjacent to structurally intact, sporozoite-infected hepatocytes, and by elevated serum alanine aminotransferase activity. In summary, malaria sporozoites bind tightly to the sinusoidal cell layer, cross Kupffer cells, and leave behind a trail of dead hepatocytes when migrating to their final destination in the liver.