Development of an in vivo ligated loop model reveals new insight into the host immune response against Campylobacter jejuni
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ABSTRACT:
PROVIDER: PRJNA615847 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11433800_1.fastq.gz | Fastqsanger.gz | |||
| SRR11433800_2.fastq.gz | Fastqsanger.gz | |||
| SRR11433801_1.fastq.gz | Fastqsanger.gz | |||
| SRR11433801_2.fastq.gz | Fastqsanger.gz | |||
| SRR11433802_1.fastq.gz | Fastqsanger.gz |
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Project description:The symptoms of infectious diarrheal disease are mediated by the interplay between the host and pathogen. Campylobacter jejuni is the leading bacterial cause of diarrhea worldwide due to its near-ubiquitous zoonotic association with poultry. One of the outstanding questions is what factors drive the intestinal inflammation during the development of C. jejuni-mediated disease. Specifically, it is not known the extent to which the bacteria are responsible for the diarrheal symptoms via cell necrosis, or whether there is immune cell recruitment prior to tissue damage. To determine the stepwise process of inflammation that leads to diarrhea, we used a piglet ligated intestinal loop model to study the intestinal environment in response to C. jejuni. Pigs were chosen due to the anatomical similarity of the porcine intestine to the human intestine, as the basis of disease modeling is to understand the process of human disease. Using immunoassays and proteomic approaches, we found that neutrophils are most likely the predominant cell type recruited to the intestines of C. jejuni infected animals. In the lumen of the intestine, a number of neutrophil related proteins increased during C. jejuni infection, including proteins related to neutrophil migration (elastase and MMP9), actin reorganization and bacterial uptake (Cdc42, WAVE-2, and Arp2/3), and antimicrobial proteins (lipocalin-2, myeloperoxidase, S100A8, and S100A9). The appearance of neutrophils also corresponds with increases of both IL-8 and TNF-a. Compared to infection with the C. jejuni wild-type strain, infection with the noninvasive C. jejuni ∆ciaD mutant resulted in a blunted inflammatory response, with less inflammatory cytokines and neutrophil markers. These findings indicate that intestinal inflammation is driven by C. jejuni virulence, and that resident intestinal cells precipitate the inflammatory response. Using this new disease model, we have developed a platform to study the early immune events during C. jejuni infection.
2020-10-07 | GSE147629 | GEO
Project description:Proteomic data from pig ligated loops. Pig loops infected with C. jejuni F38011 and mutant; time points 3, 12, 30 hours post infection. Supernatant and pellet samples collected from loops; 6 biological replicates for supernatant samples and 5 biological replicates for pellet samples.
2020-03-10 | MSV000085078 | MassIVE
Project description:The symptoms of infectious diarrheal disease are mediated by a combination of a pathogen's virulence factors and the host immune system. Campylobacter jejuni is the leading bacterial cause of diarrhea worldwide due to its near-ubiquitous zoonotic association with poultry. One of the outstanding questions is to what extent the bacteria are responsible for the diarrheal symptoms via intestinal cell necrosis versus immune cell initiated tissue damage. To determine the stepwise process of inflammation that leads to diarrhea, we used a piglet ligated intestinal loop model to study the intestinal response to C. jejuni. Pigs were chosen due to the anatomical similarity between the porcine and the human intestine. We found that the abundance of neutrophil related proteins increased in the intestinal lumen during C. jejuni infection, including proteins related to neutrophil migration (neutrophil elastase and MMP9), actin reorganization (Arp2/3), and antimicrobial proteins (lipocalin-2, myeloperoxidase, S100A8, and S100A9). The appearance of neutrophil proteins also corresponded with increases of the inflammatory cytokines IL-8 and TNF-α. Compared to infection with the C. jejuni wild-type strain, infection with the noninvasive C. jejuni ∆ciaD mutant resulted in a blunted inflammatory response, with less inflammatory cytokines and neutrophil markers. These findings indicate that intestinal inflammation is driven by C. jejuni virulence and that neutrophils are the predominant cell type responding to C. jejuni infection. We propose that this model can be used as a platform to study the early immune events during infection with intestinal pathogens.
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Project description:Campylobacter jejuni is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis. Campylobacter jejuni is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis.
2016-10-01 | GSE73793 | GEO
Project description:The persistence of Campylobacter jejuni in the natural environment, despite its microaerophilic nature, continues to be a subject of active investigation. Its survival and persistence likely stem from a combination of factors, including interactions with amoebae. C. jejuni transiently interacts with Acanthamoebae and this is thought to provide protection against unfavourable conditions and prime the bacteria for interactions with warm-blooded hosts. Acanthamoebae play vital roles in ecosystems by preying on microorganisms and establishing ecological niches with various bacterial species, some of which are clinically important pathogens. To gain a better understanding on the role of Acanthamoebae in the persistence of C. jejuni in the natural environment, we examined their interactions at the molecular level.
2024-06-28 | GSE262802 | GEO
Project description:Campylobacter jejuni is a common cause of diarrheal disease worldwide. Human infection typically occurs through the ingestion of contaminated poultry products. We previously demonstrated that an attenuated Escherichia coli live vaccine strain expressing the C. jejuni N-glycan on its surface reduces the Campylobacter load in more than 50% of vaccinated leghorn and broiler birds to undetectable levels (responder birds), whereas the remainder of the animals were still colonized (non-responders). To understand the underlying mechanism, we conducted 3 larger scale vaccination and challenge studies using 135 broiler birds and found a similar responder/non responder effect. The submitted data were used for a genome-wide association study of the chicken responses to glycoconjugate vaccination against Campylobacter jejuni.
2021-11-01 | GSE181619 | GEO
Project description:Gene content comparison of control C. jejuni subsp. jejuni strain 11168 which colonizes and causes disease in C57BL/6 IL-10-/- mice versus C. jejuni strains D6844, D6845, D6846, D6847, D6848, D6849, D0121, D0835, D2586, D2600,33560 and NW in the C57BL/6 IL-10-/- mice. Keywords: DNA/DNA comparison
2010-10-21 | GSE24764 | GEO
Project description:Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis. Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis.
2016-03-17 | GSE73796 | GEO
Project description:The bacterial proteins of the Dsb family catalyze the formation of disulfide bridges between cysteine residues that stabilize protein structures and ensure their proper functioning. Here we report the detailed analysis of the Dsb pathway of Campylobacter jejuni. The oxidizing Dsb system of this pathogen is unique because it consists of two monomeric DsbAs (DsbA1 and DsbA2) and one dimeric bifunctional protein (C8J_1298). Previously, we showed that DsbA1 and C8J_1298 are redundant. Here we unraveled the interaction between the two monomeric DsbAs by in vitro and in vivo experiments and by solving their structures and found that both monomeric DsbAs are dispensable proteins. Their structures confirmed that they are homologs of EcDsbL. The slight differences seen in the surface charge of the proteins do not affect the interaction with their redox partner. Comparative proteomics showed that several respiratory proteins, as well as periplasmic transport proteins, are targets of the Dsb system. Some of these, both donors and electron acceptors, are essential elements of C. jejuni respiratory process under oxygen-limiting conditions in the host intestine. The data presented provides detailed information on function of the C. jejuni Dsb system, identifying it as a potential target for novel antibacterial molecules.
2022-02-22 | PXD029340 | Pride
Project description:Transcriptional profile of C. jejuni NCTC11168 while growing in MEM medium containing L-fucose. We hypothesize that certain C. jejuni strains, containing A certain genomic island, have acquired the ability to metabolize fucose. This study demonstrates the transcriptional profile C. jejuni growth while utilizing fucose.
2011-04-01 | GSE28294 | GEO