Microbiome in acute appendicitis
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB49215 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR7616240_1.fastq.gz | Fastqsanger.gz | |||
| ERR7616240_2.fastq.gz | Fastqsanger.gz | |||
| ERR7616250_1.fastq.gz | Fastqsanger.gz | |||
| ERR7616250_2.fastq.gz | Fastqsanger.gz | |||
| ERR7616260_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: The diagnosis of acute appendicitis can be surprisingly difficult without computed tomography, which carries significant radiation exposure. Genome-wide expression profiling was applied to whole blood RNA of acute appendicitis patients versus patients with other abdominal disorders, in order to identify biomarkers of appendicitis. From a large cohort of emergency patients, a discovery set of patients with surgically confirmed appendicitis, or abdominal pain from other causes, was identified. RNA from whole blood was profiled by microarrays, and RNA levels were filtered by a combined fold-change (>2) and p value (<0.05). A separate set of patients, including patients with respiratory infections, was used to validate a partial least squares discriminant (PLSD) prediction model. Results: Transcript profiling identified 37 differentially expressed genes (DEG) in appendicitis versus abdominal pain patients. The DEG list contained 3 major ontologies: infection-related, inflammation-related, and ribosomal processing. Appendicitis patients had lower level of neutrophil defensin mRNA (DEFA1,3), but higher levels of alkaline phosphatase (ALPL) and interleukin-8 receptor-ß (IL8RB), which was confirmed in a larger cohort of 60 patients using droplet digital PCR (ddPCR). Conclusions: Patients with acute appendicitis have detectable changes in the mRNA expression levels of factors related to neutrophil inate defense systems. The low defensin mRNA levels suggest that appendicitis patient's immune cells are not directly activated by pathogens, but are primed by diffusible factors in the microenvironment of the infection. The detected biomarkers are consistent with prior evidence that biofilm-forming bacteria in the appendix may be an important factor in appendicitis.
2016-06-08 | GSE83091 | GEO
Project description:Gene expression was evaluated in 9 appendix samples removed from patients who went to the operating room with the diagnosis of acute appendicitis and 4 samples removed for non-inflammatory reasons. A circumferential piece of tissue was obtained at the distal aspect of each specimen. The tissue was flash frozen at -80 degrees for later processing. Frozen specimens were homogenized into TriReagent and RNA was isolated according to the manufacturer's instruction. RNA was processed and hybridized to Affymetrix microarray. Keywords: Disease state analysis
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Project description:Gene expression profiling of pediatric patients with simple appendicitis (SA) compared to perforated appendicitis (PA) and non-appendicitis abdominal pain (NAAP).
2024-02-20 | GSE225466 | GEO
Project description:Appendicitis is the most common condition necessitating emergency abdominal surgery. While most cases are localized, 20% are complicated and result in appendix perforation. The management of non-complicated appendicitis varies across different medical centers, encompassing both surgical and non-surgical options, whereas complicated appendicitis is predominantly managed surgically. Differentiating them poses a clinical challenge, especially in pediatric patients, crucial for guiding appropriate treatment strategies. Therefore, there is an unmet need for biomarkers to distinguish the two entities. Here we examined the utility of epigenetic liquid biopsies in appendicitis. We used DNA methylation markers specific to immune and gastrointestinal epithelial cells to assess the tissue origins of plasma cell-free DNA (cfDNA) in patients with appendicitis. Appendix epithelium cfDNA was not detected in plasma samples from children with appendicitis relative to patients with abdominal pain and controls. In contrast, neutrophil and regulatory T-cell cfDNA were elevated in appendicitis enhancing the specificity and sensitivity of appendicitis diagnosis beyond the information provided by neutrophil counts. Notably, eosinophil cfDNA was most significantly elevated in children with perforated compared with non-perforated appendicitis. This finding was cross-validated using a machine-learning approach. In conclusion, eosinophil cfDNA can serve as a non-invasive biomarker for diagnosing perforated appendicitis.
2025-04-30 | GSE275452 | GEO
Project description:Gene expression was evaluated in 9 appendix samples removed from patients who went to the operating room with the diagnosis of acute appendicitis and 4 samples removed for non-inflammatory reasons. A circumferential piece of tissue was obtained at the distal aspect of each specimen. The tissue was flash frozen at -80 degrees for later processing. Frozen specimens were homogenized into TriReagent and RNA was isolated according to the manufacturerâs instruction. RNA was processed and hybridized to Affymetrix microarray. Experiment Overall Design: 9 patients and 4 controls
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2025-01-13 | PXD044477 | Pride
Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
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Project description:Transcriptional profiling was utilized to define the biological pathways of gingival epithelial cells modulated by mono- and complex co-culture with oral commensal S. gordonii and pathogenic P. gingivalis. We used microarrays to detail the global programme of gene expression underlying infection and identified distinct classes of up- and down-regulated genes during this process. Keywords: infection state
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Project description:To gain a comprehensive view of the host response to pathogens within these tissues, we determined the transcriptional profiles of intestinal lymphatic tissue infected with Y. enterocolitica. Expression analysis using Affymetrix GeneChips revealed a complex host response in the Peyer’s patches (PP) and mesenteric lymph nodes (MLN) following oral infection with Y. enterocolitica. Keywords: Disease state analysis
2006-05-04 | GSE4764 | GEO
Project description:Background Alterations of the gut microbiome have been linked to multiple chronic diseases. However, the drivers of such changes remain largely unknown. The oral cavity acts as a major route of exposure to exogenous factors including pathogens, and processes therein may affect the communities in the subsequent compartments of the gastrointestinal tract. Here, we perform strain-resolved, integrated multi-omic analyses of saliva and stool samples collected from eight families with multiple cases of type 1 diabetes mellitus (T1DM). Results We identified distinct oral microbiota mostly reflecting competition between streptococcal species. More specifically, we found a decreased abundance of the commensal Streptococcus salivarius in the oral cavity of T1DM individuals, which is linked to its apparent competition with the pathobiont Streptococcus mutans. The decrease in S. salivarius in the oral cavity was also associated with its decrease in the gut as well as higher abundances in facultative anaerobes including Enterobacteria. In addition, we found evidence of gut inflammation in T1DM as reflected in the expression profiles of the Enterobacteria as well as in the human gut proteome. Finally, we were able to follow transmitted strain-variants from the oral cavity to the gut at the metagenomic, metatranscriptomic and metaproteomic levels, highlighting not only the transfer, but also the activity of the transmitted taxa along the gastrointestinal tract. Conclusions Alterations of the oral microbiome in the context of T1DM impact the microbial communities in the lower gut, in particular through the reduction of “oral-to-gut” transfer of Streptococcus salivarius. Our results indicate that the observed oral-cavity-driven gut microbiome changes may contribute towards the inflammatory processes involved in T1DM. Through the integration of multi-omic analyses, we resolve strain-variant “mouth-to-gut” transfer in a disease context.
2022-10-05 | PXD031579 | Pride