Prevention and Treatment of Autoimmune Arthritis Using IL-12 Gene-Silenced Dendritic Cells Friday, June 8 10:45 am−11:05 am
Wei‐Ping MinXiufen ZhengIgor A. PopovXusheng ZhangMu LiHongtao SunMotohiko SuzukiCostin VladauBertha GarcíaRobert D. Inman
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Hygiene hypothesis
Purpose of review Adverse reactions to food resulting in gastrointestinal symptoms are common in the general population. Although only a minority of individuals complaining of such symptoms have immune-mediated reactions to food (food allergy), gastrointestinal food allergies do exist in both children and adults. This review provides an update on the pathogenesis and clinical management of food allergy manifesting in the gut, emphasizing recent developments in the field. Recent findings Recent studies have broadened our understanding of the innate gastrointestinal defense systems and the role of the gut flora for protection against allergy. These findings support the hygiene theory in which microbial challenge in early life is thought to protect against the development of allergic disease. New insights into the regulation of mast cells and eosinophils, their homing to the intestine, and their interaction with the specific immune system and the enteric nervous system have been given. In parallel, the molecular structure of major food allergens is being unraveled, and new therapies that focus largely on modulating the immune response to food antigens have been developed. Summary These new findings have important implications for the diagnosis and management of food allergies. The availability of recombinant allergens will improve methods to diagnose and treat food allergy, and genetic engineering will allow future therapies such as vaccination against food allergy. Emerging knowledge of the role of the gut flora in mucosal immunity will enhance strategies to prevent and treat food allergy using probiotics such as Lactobacillus GG. Such new approaches will extend existing options for managing food allergy and preventing anaphylaxis.
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Introduction: Based on the hygiene hypothesis, a low prevalence of Helicobacter pylori (H. pylori) infection may explain the recent high prevalence of allergic diseases including food allergy. However, there are very few studies that investigate the relationship between H. pylori and food allergy. Summary: We searched for PubMed, Ovid Medline and the Cochrane library for relevant articles published in English from inception to November 2015. The inverse relationship between H. pylori and food allergy remains unproven because of contradictory and limited evidence at the moment. Likewise, only limited studies have examined the relationship between CagA; one of H. pylori virulence factor and food allergy. On the other hand, in vitro evidence seems to point out a role of H. pylori in the causation of food allergy. The inconsistent results from epidemiological data may be due to small sample size, heterogeneous populations and unstandardised methods or food allergens. Conclusions: Available studies do not support the role of H. pylori in food allergy.
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Spirillaceae
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Cell mediated immunity
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Several epidemiologic studies indicate that the increased prevalence of allergic diseases is associated with a reduced microbial stimulation of the immune system, thus providing a consistent evidence-based support to the hypothesis proposed by Strachan that hygienic conditions represent a risk factor for development of allergy (hygiene hypothesis). Personal data in this expanding area of research seem to confirm the hygiene hypothesis in both European (1) and American (2) large population samples. However, they also suggest that the time and type of infection represent crucial factors in determining the susceptibility for allergic diseases that are also influenced by other genetic and environmental factors related to population sample and style of life considered. It has been suggested that microbial stimulation or hygiene influence the susceptibility of allergic diseases by modulating the Th1/Th2 balance (3). However, since the reduced prevalence of infectious diseases seems to be associated not only with an increased prevalence of Th2 allergic diseases but also with an increased prevalence of typical Th1-mediated diseases (4), the Th1-Th2 hypothesis seems too simplistic to completely explain the hygiene hypothesis. Additional factors such as defects in regulatory T cell (Treg) number or function probably play a relevant role in modulating the complex immune response to a combined microbial, allergenic and autoantigenic stimulation. Certainly, the studies of the relationships between infections and allergic-immunologic diseases should open new perspectives in the approaches to treatment of these frequent, chronic and invalidating conditions (Fig. 1)(5).FIG. 1: Schematic representation of the putative microbial and immunologic events underlying the hygiene hypothesis.Key Questions 1) What kind of epidemiologic studies should be performed to provide further understanding and support for the hygiene hypothesis? 2) Which experimental studies should be triggered by epidemiologic studies? 3) Is there enough background information to indicate the use of bacterial products in humans to prevent allergies?
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フェノサフラニンによる減感作用を通して還元増感乳剤の写真性を検討し,イオウ増感と比較した。その結果,イオウ増感と同様,還元増感もフェノサフラニンの減感作用を促進し,ともにフェノサフラニンの減感作用に対し同様の挙動を示すことがわかった。また,フェノサフラニンを添加した化学増感乳剤の青感度は,化学増感の程度に依存しない。したがって,フェノサフラニンの減感作用は, フェノサフラニン未添加の化学増感乳剤の青感度が高いほど強い。一方,ホール・トラップとして還元性物質を添加した場合には減感は抑制され, 還元増感およびイオウ増感とは異なる挙動を示す。これらの事実から, 還元増感およびイオウ増感により形成された感光核は,ホール・トラップではなく,エレクトロン・トラップとして写真感度の上昇に寄与していることが示される。またイオウ増感感光核が銀核よりなることが示唆される。
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Background. Rhinitis and asthma are common comorbidities. The aim of this study was to determine the risk factors for asthma and other allergic diseases in seasonal rhinitis (SR) patients. Methods. Records of 922 patients diagnosed as SR between 1991 and 2005 were evaluated retrospectively. Patients were grouped according to the results of our standard skin prick tests as follows: I-No sensitization: no sensitization to any allergen; II-Mono-pollen sensitization: sensitization to only one pollen allergen; III-Poly-pollen sensitization: sensitization to more than one pollen allergen; IV-Mite sensitization: sensitization to mite with or without any other allergen sensitization. Results. The mean age of the patients was 29.5 ± 9.6 and 587 patients (63.2%) were females. Age at onset of SR was median 21 years (16–29 years). Of the 922 patients, 99 had no sensitization, 335 had poly-pollen sensitization, 346 had mono-pollen sensitization, and 142 had mite sensitization. The most prevalent allergens were P. pratense (85.3%) and O. europae (31.5%). No sensitization group as compared to poly-pollen sensitization group had significantly higher prevalence of asthma as a single accompanying disease (14.1%, p < 0.05). Mono-pollen sensitization was significantly associated with lower risk of any accompanying allergic disease (OR: 0.7, 95% CI 0,5–0,9) while no sensitization group (OR: 2.8, 95% CI 1.3–5.9) and mite sensitization were associated with asthma (OR: 2.3, 95% CI 1.2–4.4). Conclusion. SR is a condition that presents with different phenotypes. The group with no sensitization and mite sensitization has the highest prevalence of asthma while SR patients with mono-pollen sensitization are unlikely to have an accompanying allergic disease, including asthma.
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Hay fever
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Abstract Repeated administrations of methamphetamine (2 mg/kg, s.c), 10 times at 3‐day intervals, induced ambulatory sensitization in all groups of mice that were 13‐, 15‐, 19‐, 23‐ and 36‐weeks‐old at the start of methamphetamine administration. The most prominent sensitization was observed in the 19‐week‐old mice. Among five groups of mice, even though the mice of 36 weeks old showed the highest sensitivity to methamphetamine at the first administration, they exhibited the lowest sensitization during the latter stage of repeated methamphetamine administration. Methamphetamine sensitization once established was well reproduced by the post‐sensitization period of 8 weeks. Furthermore, the group of mice given methamphetamine with post‐sensitization interval of 8 weeks (19‐week‐old mice) exhibited further enhancement of the sensitization. In contrast, the groups of mice given methamphetamine with post‐sensitization intervals of 12 and 25 weeks (the 23‐ and 36‐week‐old, respectively) showed a significant reduced sensitization, and the latter group failed to reach the level of sensitization previously established. These results suggest that the induction of and maintenance of methamphetamine sensitization are dependent on the age of the mice, and that methamphetamine sensitization once established completely persists for up to 8 weeks.
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