Publications

4373

AbstractBackground:  “Candidatus Helicobacter heilmannii” induce chronic gastritis, which eventually leads to gastric B‐cell type mucosa‐associated lymphoid tissue (MALT) lymphoma. This study was performed using an animal model of infection with “Candidatus Helicobacter heilmannii” to elucidate how this chronic inflammation is induced or maintained.Materials and Methods:  BALB/c mice were infected with the “Candidatus Helicobacter heilmannii” isolate SH4. The animals were examined at 8, 26, 54, and 83 weeks after the infection. The stomach of the animals was resected and immunostained for peripheral lymph node addressin (PNAd) and mucosal addressin cell adhesion molecule 1 (MAdCAM‐1), “Candidatus Helicobacter heilmannii,” and CD45R/B220. An in vitro binding assay with L‐ and E‐selectin·IgM chimeric proteins was performed. Real‐time polymerase chain reaction was used to evaluate transcripts of N‐acetylglucosamine‐6‐O‐sulfotransferases (GlcNAc6STs), which direct the expression of the PNAd and MAdCAM‐1.Results:  Chronic gastritis developed in the infected animals, and its severity increased with the duration of the infection. B‐cell type MALT lymphoma developed in some animals at 54 and 83 weeks after infection. PNAd‐ and MAdCAM‐1‐expressing high endothelial venule (HEV)‐like vessels were induced in infected animals which developed chronic gastritis and MALT lymphoma. The number of HEV‐like vessels increased as chronic inflammation progressed. The induced HEV‐like vessels were bound by L‐ and E‐selectin·IgM chimeric protein. mRNA expressions of GlcNAc6ST‐1 and MAdCAM‐1 increased in the infected animals.Conclusions:  HEV‐like vessels expressing GlcNAc6ST‐1‐mediated L‐selectin ligand carbohydrate and MAdCAM‐1 may play a crucial role in the pathogenesis of “Candidatus Helicobacter heilmannii”‐induced chronic gastritis and MALT lymphoma.

Changes in carbohydrate metabolism in sweet orange ( Citrus sinensis ) infected with ‘ Candidatus Liberibacter asiaticus’, a purported cause of citrus Huanglongbing (HLB), were investigated. Starch levels in HLB‐infected leaves with and without symptoms increased 3·1‐ and 7·9‐fold, respectively, compared to healthy controls. In symptomless leaves, sucrose and fructose accumulated significantly ( P  <   0·05) in both midribs and lobes, and glucose only in the midribs (greater than fivefold); whereas maltose levels were reduced to 64·6% and 86·8% in the midribs and foliar lobes, respectively, of the values in healthy leaves. In leaves with symptoms, sucrose and glucose remained at high levels compared to healthy leaves, whilst no accumulation of fructose was observed; by contrast, the maltose content decreased to as low as 49·6% of that in healthy leaves. Fourfold induction of cell‐wall‐bound invertase activity was detected in both types of leaves on diseased plants. Additionally, the expression profiles of starch breakdown genes suggested that the transcription of DPE2 and MEX1 was down‐regulated. Together with the reduction of maltose, it is suggested that the impairment of starch breakdown may contribute to the starch accumulation in infected leaves. The imbalance of carbohydrate partitioning and its relation to disease physiology are discussed.