40 research outputs found
Attenuation of -induced gastric inflammation by prior strain (AM1) infection in C57BL/6 mice
No full textHelicobacter pylori, colonize in stomach of ~50% of the world population. cag pathogenicity Island of H.
pylori is one of the important virulent factors that attributed to gastric inflammation. Coinfection with H. pylori strain with different genetic makeup alters the degree of pathogenicity and susceptibility towards antibiotics. The present study investigates host immunomodulatory effects of H. pylori infection by both cag+ strain (SS1) and cag− strain (AM1). C57BL/6 mice were infected with AM1 or SS1 strain as well as AM1 followed by SS1 (AM1/SS1) and vice versa.
Results: Mice infected with AM1/SS1 strain exhibited less gastric inflammation and reduced proMMP9 and proMMP3
activities in gastric tissues as compared to SS1/SS1 and SS1/AM1 infected groups. The expression of both MMP9 and
MMP3 followed similar trend like activity in infected tissues. Both Th1 and Th17 responses were induced by SS1 strain more profoundly than AM1 strain infection which induced solely Th1 response in spleen and gastric tissues. Moreover, IFN-γ, TNF-α, IL-1β and IL-12 were significantly downregulated in mice spleen and gastric tissues infected by AM1/SS1 compared to SS1/SS1 but not with SS1/AM1 coinfection. Surprisingly, IL-17 level was dampened significantly in AM1/ SS1 compared to SS1/AM1 coinfected groups. Furthermore, number of Foxp3+ T-regulatory (Treg) cells and immunosuppressive
cytokines like IL-10 and TGF-β were reduced in AM1/SS1 compared to SS1/SS1 and SS1/AM1 coinfected
mice gastric tissues.
Conclusions: These data suggested that prior H. pylori cag− strain infection attenuated the severity of gastric pathology induced by subsequent cag+ strain in C57BL/6 mice. Prior AM1 infection induced Th1 cytokine IFN-γ, which reduced the Th17 response induced by subsequent SS1 infection. The reduced gastritis in AM1/SS1-infected mice
might also be due to enrichment of AM1- primed Treg cells in the gastric compartment which inhibit Th1 and Th17
responses to subsequent SS1 infection. In summary, prior infection by non-virulent H. pylori strain (AM1) causes reduction of subsequent virulent strain (SS1) infection by regulation of inflammatory cytokines and MMPs expressio
Comparative transcriptomics of H. pylori strains AM5, SS1 and their hpyAVIBM deletion mutants: possible roles of cytosine methylation.
No full textHelicobacter pylori is an important human pathogen and one of the most successful chronic colonizers of the human body. H. pylori uses diverse mechanisms to modulate its interaction with the host in order to promote chronic infection and overcome host immune response. Restriction-modification genes are a major part of strain-specific genes present in H. pylori. The role of N(6)--adenine methylation in bacterial gene regulation and virulence is well established but not much is known about the effect of C(5) -cytosine methylation on gene expression in prokaryotes. In this study, it was observed by microarray analysis and RT-PCR, that deletion of an orphan C(5) -cytosine methyltransferase, hpyAVIBM in H. pylori strains AM5and SS1 has a significant effect on the expression of number of genes belonging to motility, adhesion and virulence. AM5ΔhpyAVIBM mutant strain has a different LPS profile and is able to induce high IL-8 production compared to wild-type. hpyAVIBM from strain 26695 is able to complement mutant SS1 and AM5 strains. This study highlights a possible significance of cytosine methylation in the physiology of H. pylori
LPS profiles of <i>hpyAVIBM</i> deletion mutant and wild-type strains.
No full text<p>Lane 1: wild-type strain AM5, lane 2: <i>hpyAVIBM</i> deletion mutant AM5 complemented with <i>hpyAVIBM</i> from strain 26695, lane 3: <i>hpyAVIBM</i> deletion mutant. * highlights the bands different between wild type and mutant.</p
Motility assay.
No full text<p>The photograph shows a BHI 7% FBS soft agar plate after 4 days of incubation. (<b>A</b>) SS1 (<b>B</b>) AM5 (<b>C</b>) Graph showing relative change in the diameter of mutant vs wild-type strain.</p
ATF3 Stimulates IL-17A by Regulating Intracellular Ca2+/ROS-Dependent IL-1β Activation During Streptococcus pneumoniae Infection
No full textVariation in dinucleotide repeats in <i>H. pylori</i> clinical isolates.
No full text<p>Arrow indicates the substitution/deletion mutation.</p
Association of Intact dupA (dupA1) rather than dupA1 cluster with duodenal ulcer in Indian population
No full textComparative transcriptomics of <i>H. pylori</i> wild type vs <i>hpyAVIBM</i> deletion mutant of strains AM5 and SS1.
No full text<p>The genes listed are either down- or up-regulated in the <i>hpyAVIBM deletion</i> mutant of <i>H. pylori</i> strains AM5 and SS1. The identity of each gene is indicated by the Locus name as annotated in the <i>H. pylori</i> strain 26695 genome. The average ratio presented is the mean of mutant/wt ratio. P value <0.005.</p><p>ND: not determined.</p><p>- : not significant.</p
<i>hpyAVIAM</i> and <i>hpyAVIBM.</i>
No full text<p>(<b>A</b>) Schematic presentation of operon coding <i>hpyAVIAM</i> and <i>hpyAVIBM</i>. (<b>B</b>) Distribution of <i>hpyAVIBM i</i>n symptomatic and asymptomatic strains. P<0.0001.</p
Helicobacter pylori strains harboring babA2 from Indian sub population are associated with increased virulence in ex vivo study
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