Project description:The objectives of this study were to establish a microbiome profile for oral epithelial dysplasia using archival lesion swab samples to characterize the community variations and the functional potential of the microbiome using 16S rRNA gene sequencing
Project description:Interventions: Two period cross-over trial. Intervention with mouth-rinsing will commence at the start of either induction, consolidation, or re-induction chemotherapy phase. Group 1 will be rinse with 10 mL of 0.12% chlorhexidine gluconate mouthwash twice daily, and Group 2 will rinse with 15 mL of 1% povidone iodine mouthwash twice daily, for 14 days during the first period of study. Alkaline saline mouthrinse will be used by the subjects during the 2 week ‘washout’ time between the two periods of study. The two groups will then switch mouthrinses during the second study period. The occurrence of ulcerative lesions and severity of mucositis will be measured at baseline and twice weekly of each study period, using the Oral Mucositis Assessment Scale and World Health Organization Grading Scale. If oral mucositis/ulceration develops during either period and persists beyond 14 days, the subjects will continue to use the mouthwash assigned to their group until lesions heal. A participant diary on the use of mouthwash and other oral care hygiene measures such as toothbrushing and flossing will be used to monitor adherence to treatment.
Primary outcome(s): determining whether there is a difference in effect of 0.12% chlorhexidine and 1% povidone iodine mouthrinses that are both accepted as standard of care for oral mucositis in pediatric cancer patients using the Oral Mucositis Assessment Scale and World Health Organization Grading Scale[2 weeks]
Study Design: Purpose: Prevention; Allocation: Randomised controlled trial; Masking: Open (masking not used);Assignment: Crossover;Type of endpoint: Efficacy
Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
