http://nova.newcastle.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 Transcutaneous immunization with novel lipid-based adjuvants induces protection against gastric Helicobacter pylori infection http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:7216 The development of vaccines to combat pathogens that infect across mucosal surfaces has been a major goal of vaccine research. Successful mucosal vaccination requires the co-administration of adjuvants that can overcome the state of immune tolerance normally associated with mucosal application of proteins. In the case of oral immunization, delivery systems are also required to protect vaccine antigens against destruction by gastric pH and digestive enzymes. Furthermore, adjuvants used for mucosal delivery must be free of neurotoxic effects like those induced by the commonly used experimental mucosal adjuvant cholera toxin. Maintenance of the “cold chain” is also essential for the effectiveness of any vaccine and adjuvants/delivery systems that enhance the stability of a vaccine would offer a significant advantage. Needle-free methods of vaccination that induce protective immunity at multiple mucosal surfaces are also desirable for rapid vaccination of large populations. In the present study we show that transcutaneous immunization (TCI) using Lipid C, a novel lipid-based matrix originally developed for oral immunization, containing soluble Helicobacter sonicate significantly reduces the gastric bacterial burden in mice following gastric challenge with live Helicobacter pylori. Protection is associated with the production of splenic gamma interferon and gastric IgA and was achieved without the co-administration of potent and potentially toxic adjuvants, although protection was further enhanced by inclusion of CpG-ODN and cholera toxin in the lipid delivery system. 2011-02-14T01:30:14.150Z ]]> Autoimmune gastritis and parietal cell reactivity in two children with abnormal intestinal permeability http://nova.newcastle.edu.au/vital/access/manager/Repository/uon:4753 Autoimmune gastritis is characterised by lymphocytic infiltration of the gastric submucosa, with loss of parietal and chief cells and achlorhydria. Often, gastritis is expressed clinically as cobalamin deficiency with megaloblastic anaemia, which is generally described as a disease of the elderly. Here, we report on two prepubertal children who developed autoimmune gastritis. One child developed autoimmune gastritis as part of a polyglandular autoimmune disease from a family with polyglandular autoimmune disease type II (PGA type II) and the other as part of a classic "thyro-gastric cluster," which may have been triggered by emotional trauma. Both children presented with normal small bowel biopsies, with abnormal gut permeability, which subsequently resolved. These patients are among the youngest reported to date. The immune systems targetted the gastric parietal cell autoantigens (ATP4A and ATP4B) in both children, similar to the elderly. The study of children with autoimmune gastritis and their families may provide additional insights into the disease's pathogenesis and may also lead to the identification of inheritable factors influencing susceptibility. This report underlines the necessity to screen paediatric patients with organ-specific autoimmune diseases for co-existent conditions. Children with polyglandular autoimmune disease are at particularly high risk. 2010-04-27T05:31:18.769Z ]]>