Epithelial-resident T lymphocytes, such as intraepithelial lymphocytes (IELs) located at the intestinal barrier, can offer swift protection against invading pathogens. Lymphocyte activation is strictly regulated because of its potential harmful nature and metabolic cost, and most lymphocytes are maintained in a quiescent state. However, IELs are kept in a heightened state of activation resembling effector T cells but without cytokine production or clonal proliferation. We show that this controlled activation state correlates with alterations in the IEL mitochondrial membrane, especially the cardiolipin composition. Upon inflammation, the cardiolipin composition is altered to support IEL proliferation and effector function. Furthermore, we show that cardiolipin makeup can particularly restrict swift IEL proliferation and effector functions, reducing microbial containment capability. These findings uncover an alternative mechanism to control cellular activity, special to epithelial-resident T cells, and a novel role for mitochondria, maintaining cells in a metabolically poised state while enabling rapid progression to full functionality.

Infections with parasitic worms are often long lasting and associated with modulated immune responses. We analyzed the influence of the nematode Heligmosomoides polygyrus bakeri dwelling in the small intestine on concurrent protozoan infection with Eimeria falciformis residing in the cecum. To dissect the effects of a nematode infection in the early versus chronic phase, we infected animals with E. falciformis 6 or 28 days post H. p. bakeri infection. Only a concurrent early nematode infection led to an increased replication of the protozoan parasite, whereas a chronic worm infection had no influence on the control of E. falciformis. Increased protozoan replication correlated with the reduced production of IFN-c, IL-12/23, CCL4, CXCL9 and CXCL10, reduced migration of T cells and increased expression of Foxp3 at the site of protozoan infection. This was accompanied by a stronger nematode-specific Th2 response in gut-draining LN. Protection of mice against challenge infections with the protozoan parasite was not altered. Hence, the detrimental effect of a nematode infection on the control of a concurrent protozoan infection is transient and occurs only in the narrow time window of the early phase of infection. Here, we analyzed the impact of a concurrent worm infection in the early phase versus chronic phase on the outcome of a concurrent enteric protozoan infection. We find that only early infections with H.p.b. result in an increased protozoan replication. The protozoan replication was not influenced in chronically worm-infected mice, despite signs of immunosuppression and sharply decreased IFN-g responses to Eimeria Ag in gut-draining mesenteric LN (mLN). Suppression of anti-Eimeria protective immunity during early nematode coinfection was found to be a result of a strong nematode-induced Th2 response and a reduced chemokine-mediated chemotaxis and migration of T cells to the site of Eimeria infection. Results Early phase nematode infection negatively affects the control of a primary Eimeria infectionTo test whether an infection with H.p.b. affects the course of infection with E. falciformis (E.f.) in a distinct part of the intestinal tract, mice were infected according to two protocols (Fig. 1A). E.f. was applied to mice in the early (histotrophic) phase (6 days post-H.p.b. infection, named eHpb/Ef) or chronic phase of adult worm infection (4 wk post-H.p.b. infection, named cHpb/Ef). Control mice were single infected only. Eimeria oocyst output was monitored on days 6-16 post-Eimeria infection.Interestingly, eHpb/Ef mice shed significantly more E.f. oocysts in comparison to controls infected with E.f. only (Fig. 1B and C) and had a significantly prolonged patency period (Fig. 1D). Conversely, an established chronic worm infection did not significantly alter the course of E.f. infection despite similar worm burdens (data not shown). Compared with Eimeria single-infected controls, cHpb/Ef mice had similar kinetics for oocyst output (Fig. 1B) as well as similar total numbers of shed oocysts ( Fig. 1C) and paten...

BackgroundThe 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.MethodsWe 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.ResultsSeventy-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.ConclusionsMost 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.

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