Helminth co-infection in Helicobacter pylori infected INS-GAS mice attenuates gastric premalignant lesions of epithelial dysplasia and glandular atrophy and preserves colonization resistance of the stomach to lower bowel microbiota.
Whary MT1, Muthupalani S2, Ge Z2, Feng Y2, Lofgren J2, Shi HN3, Taylor NS2, Correa P4, Versalovic J5, Wang TC6, Fox JG2.Author information 1Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA. Electronic address: mwhary@mit.edu.2Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA.3Mucosal Immunology Laboratory, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.4Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.5Department of Pathology, Baylor College of Medicine and Texas Children's Hospital, Houston, TX, USA.6Division of Digestive and Liver Disease, Columbia University Medical Center, New York, NY, USA.AbstractHigher prevalence of helminth infections in Helicobacter pylori infected children was suggested to potentially lower the life-time risk for gastric adenocarcinoma. In rodent models, helminth co-infection does not reduce Helicobacter-induced inflammation but delays progression of pre-malignant gastric lesions. Because gastric cancer in INS-GAS mice is promoted by intestinal microflora, the impact of Heligmosomoides polygyrus co-infection on H. pylori-associated gastric lesions and microflora were evaluated. Male INS-GAS mice co-infected with H. pylori and H. polygyrus for 5 months were assessed for gastrointestinal lesions, inflammation-related mRNA expression, FoxP3(+) cells, epithelial proliferation, and gastric colonization with H. pylori and Altered Schaedler Flora. Despite similar gastric inflammation and high levels of proinflammatory mRNA, helminth co-infection increased FoxP3(+) cells in the corpus and reduced H. pylori-associated gastric atrophy (p < 0.04), dysplasia (p < 0.02) and prevented H. pylori-induced changes in the gastric flora (p < 0.05). This is the first evidence of helminth infection reducing H. pylori-induced gastric lesions while inhibiting changes in gastric flora, consistent with prior observations that gastric colonization with enteric microbiota accelerated gastric lesions in INS-GAS mice. Identifying how helminths reduce gastric premalignant lesions and impact bacterial colonization of the H. pylori infected stomach could lead to new treatment strategies to inhibit progression from chronic gastritis to cancer in humans.
Microbes and infection / Institut Pasteur.Microbes Infect.2014 Apr;16(4):345-55. doi: 10.1016/j.micinf.2014.01.005. Epub 2014 Feb 8.
Higher prevalence of helminth infections in Helicobacter pylori infected children was suggested to potentially lower the life-time risk for gastric adenocarcinoma. In rodent models, helminth co-infection does not reduce Helicobacter-induced inflammation but delays progression of pre-malignant gastri
Molecular characterization of the reniform nematode C-type lectin gene family reveals a likely role in mitigating environmental stresses during plant parasitism.
Ganji S1, Jenkins JN2, Wubben MJ3.Author information 1Department of Biochemistry and Molecular Biology, Mississippi State University, Mississippi State, MS 39762, USA. Electronic address: sg391@msstate.edu.2Department of Biochemistry and Molecular Biology, Mississippi State University, Mississippi State, MS 39762, USA; USDA-ARS, Crop Science Research Laboratory, Genetics and Precision Agriculture Research Unit, Mississippi State, MS 39762, USA. Electronic address: johnie.jenkins@ars.usda.gov.3Department of Biochemistry and Molecular Biology, Mississippi State University, Mississippi State, MS 39762, USA; USDA-ARS, Crop Science Research Laboratory, Genetics and Precision Agriculture Research Unit, Mississippi State, MS 39762, USA. Electronic address: martin.wubben@ars.usda.gov.AbstractThe reniform nematode, Rotylenchulus reniformis, is a damaging semi-endoparasitic pathogen of more than 300 plant species. Transcriptome sequencing of R. reniformis parasitic females revealed an enrichment for sequences homologous to C-type lectins (CTLs), an evolutionarily ancient family of Ca(+2)-dependent carbohydrate-binding proteins that are involved in the innate immune response. To gain further insight as to the potential role of CTLs in facilitating plant parasitism by R. reniformis, we performed a comprehensive assessment of the CTL gene family. 5'- and 3'-RACE experiments identified a total of 11 R. reniformis CTL transcripts (Rr-ctl-1 through Rr-ctl-11) that ranged in length from 1083 to 1,194 bp and showed 93-99% identity with one another. An alignment of cDNA and genomic sequences revealed three introns with the first intron residing within the 5'-untranslated region. BLAST analyses showed the closest homologs belonging to the parasitic nematodes Heligmosomoides polygyrus and Heterodera glycines. Rr-ctl-1, -2, and -3 were expressed throughout the R. reniformis life cycle; whereas, the remaining Rr-ctl genes showed life stage-specific expression. Quantitative real time RT-PCR determined that Rr-ctl transcripts were 839-fold higher in sedentary female nematodes than the next most abundant life stage. Predicted Rr-CTL peptides ranged from 301 to 338 amino acids long, possessed an N-terminal signal peptide for secretion, and contained a conserved CLECT domain, including the mannose-binding motifs EPN and EPD and the conserved WND motif that is required for binding Ca(+2). In addition, Rr-CTL peptides harbored repeats of a novel 17-mer motif within their C-terminus that showed similarity to motifs associated with bacterial ice nucleation proteins. In situ hybridization of Rr-ctl transcripts within sedentary females showed specific accumulation within the hypodermis of the body regions exposed to the soil environment; those structures embedded within the root during parasitism did not show Rr-ctl expression. A phylogenetic analysis of the Rr-CTL CLECT domain with homologous domains from other nematode species suggested that CTLs from animal- and plant-parasitic genera may have evolved in order to play an active role in the parasitic process.
Gene.Gene.2014 Mar 10;537(2):269-78. doi: 10.1016/j.gene.2013.12.048. Epub 2014 Jan 12.
The reniform nematode, Rotylenchulus reniformis, is a damaging semi-endoparasitic pathogen of more than 300 plant species. Transcriptome sequencing of R. reniformis parasitic females revealed an enrichment for sequences homologous to C-type lectins (CTLs), an evolutionarily ancient family of Ca(+2)-
Understanding the role of antibodies in murine infections with Heligmosomoides (polygyrus) bakeri: 35 years ago, now and 35 years ahead.
Harris NL1, Pleass R, Behnke JM.Author information 1Global Health Institute and Swiss Vaccine Research Institute, École Polytechnique Fédèrale de Lausanne (EPFL), Switzerland.AbstractThe rodent intestinal nematode H.p.bakeri has played an important role in the exploration of the host-parasite relationship of chronic nematode infections for over six decades, since the parasite was first isolated in the 1950s by Ehrenford. It soon became a popular laboratory model providing a tractable experimental system that is easy to maintain in the laboratory and far more cost-effective than other laboratory nematode-rodent model systems. Immunity to this parasite is complex, dependent on antibodies, but confounded by the parasite's potent immunosuppressive secretions that facilitate chronic survival in murine hosts. In this review, we remind readers of the state of knowledge in the 1970s, when the first volume of Parasite Immunology was published, focusing on the role of antibodies in protective immunity. We show how our understanding of the host-parasite relationship then developed over the following 35 years to date, we propose testable hypotheses for future researchers to tackle, and we speculate on how the new technologies will be applied to enable an increasingly refined understanding of the role of antibodies in host-protective immunity, and its evasion, to be achieved in the longer term.
The rodent intestinal nematode H.p.bakeri has played an important role in the exploration of the host-parasite relationship of chronic nematode infections for over six decades, since the parasite was first isolated in the 1950s by Ehrenford. It soon became a popular laboratory model providing a trac
Phylogenetic relationships of three species within the family Heligmonellidae (Nematoda; Heligmosomoidea) from Japanese rodents and a lagomorph based on the sequences of ribosomal DNA internal transcribed spacers, ITS-1 and ITS-2
… The data of Hs, Oe and Llwere compared with those of two other known species within the family Heligmonellidae,Calorinensis minutus (Dujardin, 1845) (Cm) and Nippostrogylus brasiliensis (Travassos,1914) (Nb), and with those of two species of Heligmosomidae (Heligmosomoidea),Heligmosomoides polygyrus bakeri and Ohbayashinema erbaevae. …
Enhanced Protection against Heligmosomoides polygyrus in IL-2 Receptor .BETA.-Chain Overexpressed Transgenic Mice with Intestinal Mastocytosis
Morimoto Masahiro,Utsumiya Kyoko
Journal of Veterinary Medical Science 73(6), 849-851, 2011
… IL-4 is also important in the regulation of resistance and susceptibility to Heligmosomoides polygyrus infection. … polygyrus and intestinal mastocytosis. … polygyrus infection. … polygyrus. …
Heligmosomoides polygyrus is a natural nematode parasite of mice. It pursues a direct and entirely enteric life cycle, entering through the mouth and maturing in the intestine to produce eggs which are voided with faeces. It is a ...
From V. Bryant, Journal of Helminthology, 1973, 3:263-268. Heligmosomoides polygyrus is a trichostrongylid nematode found in small rodents. It's life cycle is direct and involves both free-living and parasitic stages. Larvae Eggs ...