ABSTRACT SUPPLEMENT Abstract Supplement Table of Contents Categories Aging and Mucosal Immunology ............................................................................ 2 Antigen Uptake ....................................................................................................... 3 Celiac Disease .......................................................................................................... 4 Dendritic Cells ......................................................................................................... 8 Effector T Cells and Cytokines ............................................................................... 14 Epithelial Cells and Innate Immunity .................................................................... 26 Food Allergy .......................................................................................................... 48 HIV ......................................................................................................................... 52 Host‐Microbiota Interactions ............................................................................... 57 Immune Cell Migration ......................................................................................... 84 Immunology of Asthma – Basic ............................................................................ 86 Immunology of Asthma – Clinical ......................................................................... 93 Immunology of the Eye ......................................................................................... 93 Immunology of the UG Tract ................................................................................ 94 Inflammatory Bowel Disease – Basic .................................................................... 98 Inflammatory Bowel Disease – Clinical ............................................................... 128 Innate Lymphoid Cells ......................................................................................... 131 Monocytes and Macrophages ............................................................................ 140 Mucosal B Cells ................................................................................................... 146 Mucosal Immunology in the Neonate ................................................................ 151 Mucosal Infections .............................................................................................. 160 Mucosal Tolerance .............................................................................................. 175 Mucosal Vaccines ................................................................................................ 182 Respiratory Virus Infections ................................................................................ 191 Index Abstract Index by Author………………………...195 Abstract Index by Category……………………...200 1 ICMI 2017 Aging and Mucosal Immunology W01. Analysis of Immunization in Outbred Mice with W04. Gram-Positive Bacteria Regulates Analgesic Diferent Adjuvants: Interference in Production and Tolerance to Morphine Maternal-Fetal Transfer of Antibodies Li Zhang, Jingjing Meng, Santanu Banerjee, and Sabita Adriana Freitas de Almeida and Elizabeth De Gaspari. Roy. University of Miami, Miami, FL Adolfo Lutz Institute, São Paulo, Brazil Morphine, as a naturally occurring opioid, is an Neisseria meningitidis is a gram-negative diplococcus. integral component of pain relievers. Clinical use of Its incidence is bigger in mainly children under two morphine is limited by undesired side effects including years. Newborns and children are particularly analgesic tolerance, withdrawal, and addiction. susceptible to this type of infection, so further studies Previous data in our lab showed that chronic on the use of the maternal immunization are needed. morphine treatment induced bacterial translocation Our objective was to analyze the interference of from gut, which led to chronic systemic inflammation. adjuvants in the production of antibodies produced Body of literature showed that chronic inflammation and transferred on maternal-fetal immunization. The was correlated with tolerance to analgesic effect of outer membrane vesicles (OMVs) of N. meningitidis morphine. Microbiome analysis demonstrated that were used for the production of the antigenic morphine treatment induced an expansion of gram- preparations, with alum (HA) or DODAB-BF. Outbred positive bacteria and the translocated bacteria in the mice females were immunized with these systemic system belonged to Firmicutes phyla. The preparations by the prime-boost and then the purpose of this study was to investigate the role of gut offspring was bled with 3, 6, 9 and 12 weeks of life gram-positive bacteria in the analgesic tolerance of and the antibodies were analyzed by ELISA. Offspring morphine. Morphine induced bacteria translocation of mothers immunized with OMV+DODAB-BF by and systemic inflammation were significantly subcutaneous administration presents significant attenuated in the TLR2KO mice. However, depletion of antibodies, as OMV+HA immunization by the gram-positive bacteria by vancomycin disrupted the subcutaneous route, therefore, the DODAB-BF can be gut homeostasis and exacerbated analgesic tolerance an alternative. The antibodies from offspring seem to to morphine. Moreover, VSL#3 probiotics, which fall from the sixth week of life of these animals. IgG1 consisted of eight beneficial gram-positive bacteria, seems to be the best isotype that crosses the alleviated the analgesic tolerance to morphine and placental barrier. Intranasal route of immunization chronic inflammation induced by repeated morphine seems to present no significant antibody placental administration. Our study indicated the function of transfer. The use of adjuvant DODAB-BF is being gram-positive bacteria in analgesic tolerance to analysed for the first time in an antigenic preparation morphine. Future studies will elucidate and with OMVs of N. meningitidis compared to OMV+HA characterize the gram-positive bacterial communities on immunization by subcutaneous administration. that are critical to maintain gut homeostasis and When the female mice are immunized by the contribute to analgesic tolerance to morphine. intranasal route, it has been seen that the antibodies appear not be transferred properly to the offspring. So, further studies are needed to conclude whether immunization with DODAB-BF is effective by intranasal route. 2 Abstract Supplement Antigen Uptake W05. Goblet Cell Associated Antigen Passages Form W06. Increased Abundance of M Cells in the Gut via Bulk Endocytosis Following Compound Exocytosis Epithelium Dramatically Enhances Oral Prion Disease Jenny Gustafsson1, Keely G. McDonald1, Kathryn Susceptibility Knoop1, Matthew Jones1, James Fitzpatrick1, Wayne David S. Donaldson1, Anuj Sehgal1, Daniel Rios2, Ifor Lencer2 and Rodney Newberry2. 1Washington Williams3 and Neil Mabbott1. 1Roslin Institute, University School of Medicine, St. Louis, MO; 2 Harvard University of Edinburgh, Edinburgh, Scotland, United Medical School, Boston, MA Kingdom; 2Broad Institute of MIT and Harvard, Cambridge, MA; 3 Emory University School of Small intestinal goblet cells (GCs) form goblet cell associated antigen passages (GAPs) to deliver luminal Medicine, Atlanta, GA substances to lamina propria dendritic cells. The Antigen-sampling M cells, present in the follicle process by which GCs form GAPs has been enigmatic. associated epithelium of gut associated lymphoid GAP formation is linked to GC secretion by compound tissues can be exploited by pathogens to gain entry to exocytosis (CE), an event resulting in rapid expulsion the host. Many natural prion diseases of humans and of multiple mucin granules and resultant membrane animals are acquired through the consumption of tears, suggesting that GAP formation results from contaminated food or pasture. It has been suggested uptake of luminal contents via tears and basolateral that oral prion infectivity may depend on M cell- secretion. Using super-resolution microscopy, we mediated transcytosis of prions across the gut observed that luminal fluorescent antigens taken up epithelium. Therefore, alterations to the M cell by GCs localized in a network of vesicular appearing density, for example during aging or as a consequence structures at the periphery and base of the GCs. of pathogen co-infection, could affect M cell uptake of Focused ion beam scanning electron microscopy (FIB- prions and alter disease susceptibility. To confirm that SEM) was used to construct a 3D ultrastructural model oral prion infection depends on M cells, we utilised a of GAP formation. FIB-SEM revealed that luminal conditional model of M cell deficiency in which RANK, antigen was located in endosomes, multi vesicular a receptor necessary for M cell development, is only bodies (MVBs), the transgolgi network, newly formed absent on intestinal epithelium cells. In the specific mucin granules, and vesicles at the basolateral surface absence of M cells, the accumulation of prions within of the GC. Disruption of endocytosis, microtubules, Peyer’s patches and the spread of disease to the brain actin filaments, and microtubule motor proteins, was blocked, demonstrating a critical role for M cells blocked GAP formation without affecting the ability of in the initial transfer of prions across the gut GCs to secrete by CE. Vesicles containing luminal epithelium. Mice were also treated with RANKL to antigens did not have markers of early endosomes, enhance