{"id":{"repo_id":"uic","oai_identifier":"oai:figshare.com:article/32994116"},"canonical_url":"https://search.dev.ndltd.org/etd/uic/oai:figshare.com:article/32994116","repository":{"repo_id":"uic","name":"University of Illinois - Chicago","base_url":"https://api.figshare.com/v2/oai"},"display":{"title":"Host Immune-Microbial Interactions in Inflammatory States","abstract":"Chronic inflammation is a seemingly paradoxical state characterized by both persistent immune activation and immune suppression. Patients afflicted with chronic inflammatory diseases such as end-stage renal disease and sarcoidosis face increased susceptibility to infection as well as mixed responses to vaccination. Thus, the extent to which the immune system of these patient populations remain operational versus compromised warrants further investigation. We examined (1) the immune response of end-stage renal disease patients undergoing hemodialysis (HD) when stimulated with the SARS-CoV-2 mRNA vaccine, as well as (2) associations between the immune transcriptome with gut microbiome in sarcoidosis patients. Given the complexity of the immune system, we employed omics technologies and approaches that would span the gene, protein, and metabolite levels. To assess the functional component of the HD immune response to vaccine stimulation, anti-spike IgG and neutralizing antibody titers were measured at time points before and after vaccination and revealed antibody responses on par with healthy control subjects. However, RNA-seq and differential gene expression analysis of the immune transcriptome revealed that the innate immune response in HD, while intact, was delayed compared to controls. Network analysis of differential gene module co-expression and transcription factor-gene interactions further implicated weakened transcriptional regulation of dendritic cell activation pathways. To characterize the gut microbiome in sarcoidosis, taxonomic and functional profiles were constructed from metagenomic shotgun sequencing of stool, differential abundance analysis of microbial species, and functional annotation of the taxonomic profile, yielding 12 microbial species and 79 metabolic pathways that were significantly differentially abundant in sarcoidosis. KEGG enrichment analysis of these pathways revealed overall decreased activity in pathways related to microbial energy metabolism and HIF-1 signaling. Since these pathways are important for intestinal epithelial cells to maintain hypoxia in the gut environment, their widespread loss indicates this hypoxic homeostasis is disrupted in sarcoidosis. Moreover, previous studies reported HIF-1 overexpression in sarcoidosis macrophages and granulomas, further implicating its involvement in sarcoidosis pathogenesis. Our work demonstrates the power of omics approaches in unraveling multilayered insights into immune dysregulation in chronic inflammatory states that may inform clinical interventions for managing these diseases.","abstract_html":"Chronic inflammation is a seemingly paradoxical state characterized by both persistent immune activation and immune suppression. Patients afflicted with chronic inflammatory diseases such as end-stage renal disease and sarcoidosis face increased susceptibility to infection as well as mixed responses to vaccination. Thus, the extent to which the immune system of these patient populations remain operational versus compromised warrants further investigation. We examined (1) the immune response of end-stage renal disease patients undergoing hemodialysis (HD) when stimulated with the SARS-CoV-2 mRNA vaccine, as well as (2) associations between the immune transcriptome with gut microbiome in sarcoidosis patients. Given the complexity of the immune system, we employed omics technologies and approaches that would span the gene, protein, and metabolite levels. To assess the functional component of the HD immune response to vaccine stimulation, anti-spike IgG and neutralizing antibody titers were measured at time points before and after vaccination and revealed antibody responses on par with healthy control subjects. However, RNA-seq and differential gene expression analysis of the immune transcriptome revealed that the innate immune response in HD, while intact, was delayed compared to controls. Network analysis of differential gene module co-expression and transcription factor-gene interactions further implicated weakened transcriptional regulation of dendritic cell activation pathways. To characterize the gut microbiome in sarcoidosis, taxonomic and functional profiles were constructed from metagenomic shotgun sequencing of stool, differential abundance analysis of microbial species, and functional annotation of the taxonomic profile, yielding 12 microbial species and 79 metabolic pathways that were significantly differentially abundant in sarcoidosis. KEGG enrichment analysis of these pathways revealed overall decreased activity in pathways related to microbial energy metabolism and HIF-1 signaling. Since these pathways are important for intestinal epithelial cells to maintain hypoxia in the gut environment, their widespread loss indicates this hypoxic homeostasis is disrupted in sarcoidosis. Moreover, previous studies reported HIF-1 overexpression in sarcoidosis macrophages and granulomas, further implicating its involvement in sarcoidosis pathogenesis. Our work demonstrates the power of omics approaches in unraveling multilayered insights into immune dysregulation in chronic inflammatory states that may inform clinical interventions for managing these diseases.","abstract_has_math":false,"creators":["Jessica Lee (733479)"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2026,"date_issued":"2026-05-01T00:00:00Z","date_published":"2026-05-01T00:00:00Z","updated_at":"2026-07-27T21:33:42Z","subjects":["Biology, Microbiology","Health Sciences, Immunology"],"languages":[],"rights":["In Copyright"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://doi.org/10.25417/uic.32994116.v1","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Jessica Lee (733479)"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2026-05-01T00:00:00Z"]},{"key":"dc:relation","label":"Dc Relation","values":["https://figshare.com/articles/thesis/Host_Immune-Microbial_Interactions_in_Inflammatory_States/32994116"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Microbiology","Health Sciences, Immunology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["In Copyright"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["10.25417/uic.32994116.v1"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Chronic inflammation is a seemingly paradoxical state characterized by both persistent immune activation and immune suppression. Patients afflicted with chronic inflammatory diseases such as end-stage renal disease and sarcoidosis face increased susceptibility to infection as well as mixed responses to vaccination. Thus, the extent to which the immune system of these patient populations remain operational versus compromised warrants further investigation. We examined (1) the immune response of end-stage renal disease patients undergoing hemodialysis (HD) when stimulated with the SARS-CoV-2 mRNA vaccine, as well as (2) associations between the immune transcriptome with gut microbiome in sarcoidosis patients. Given the complexity of the immune system, we employed omics technologies and approaches that would span the gene, protein, and metabolite levels. To assess the functional component of the HD immune response to vaccine stimulation, anti-spike IgG and neutralizing antibody titers were measured at time points before and after vaccination and revealed antibody responses on par with healthy control subjects. However, RNA-seq and differential gene expression analysis of the immune transcriptome revealed that the innate immune response in HD, while intact, was delayed compared to controls. Network analysis of differential gene module co-expression and transcription factor-gene interactions further implicated weakened transcriptional regulation of dendritic cell activation pathways. To characterize the gut microbiome in sarcoidosis, taxonomic and functional profiles were constructed from metagenomic shotgun sequencing of stool, differential abundance analysis of microbial species, and functional annotation of the taxonomic profile, yielding 12 microbial species and 79 metabolic pathways that were significantly differentially abundant in sarcoidosis. KEGG enrichment analysis of these pathways revealed overall decreased activity in pathways related to microbial energy metabolism and HIF-1 signaling. Since these pathways are important for intestinal epithelial cells to maintain hypoxia in the gut environment, their widespread loss indicates this hypoxic homeostasis is disrupted in sarcoidosis. Moreover, previous studies reported HIF-1 overexpression in sarcoidosis macrophages and granulomas, further implicating its involvement in sarcoidosis pathogenesis. Our work demonstrates the power of omics approaches in unraveling multilayered insights into immune dysregulation in chronic inflammatory states that may inform clinical interventions for managing these diseases."]},{"key":"dc:title","label":"Title","values":["Host Immune-Microbial Interactions in Inflammatory States"]}]}],"canonical_facts":{"dc:creator":["Jessica Lee (733479)"],"dc:date":["2026-05-01T00:00:00Z"],"dc:description":["Chronic inflammation is a seemingly paradoxical state characterized by both persistent immune activation and immune suppression. Patients afflicted with chronic inflammatory diseases such as end-stage renal disease and sarcoidosis face increased susceptibility to infection as well as mixed responses to vaccination. Thus, the extent to which the immune system of these patient populations remain operational versus compromised warrants further investigation. We examined (1) the immune response of end-stage renal disease patients undergoing hemodialysis (HD) when stimulated with the SARS-CoV-2 mRNA vaccine, as well as (2) associations between the immune transcriptome with gut microbiome in sarcoidosis patients. Given the complexity of the immune system, we employed omics technologies and approaches that would span the gene, protein, and metabolite levels. To assess the functional component of the HD immune response to vaccine stimulation, anti-spike IgG and neutralizing antibody titers were measured at time points before and after vaccination and revealed antibody responses on par with healthy control subjects. However, RNA-seq and differential gene expression analysis of the immune transcriptome revealed that the innate immune response in HD, while intact, was delayed compared to controls. Network analysis of differential gene module co-expression and transcription factor-gene interactions further implicated weakened transcriptional regulation of dendritic cell activation pathways. To characterize the gut microbiome in sarcoidosis, taxonomic and functional profiles were constructed from metagenomic shotgun sequencing of stool, differential abundance analysis of microbial species, and functional annotation of the taxonomic profile, yielding 12 microbial species and 79 metabolic pathways that were significantly differentially abundant in sarcoidosis. KEGG enrichment analysis of these pathways revealed overall decreased activity in pathways related to microbial energy metabolism and HIF-1 signaling. Since these pathways are important for intestinal epithelial cells to maintain hypoxia in the gut environment, their widespread loss indicates this hypoxic homeostasis is disrupted in sarcoidosis. Moreover, previous studies reported HIF-1 overexpression in sarcoidosis macrophages and granulomas, further implicating its involvement in sarcoidosis pathogenesis. Our work demonstrates the power of omics approaches in unraveling multilayered insights into immune dysregulation in chronic inflammatory states that may inform clinical interventions for managing these diseases."],"dc:identifier":["10.25417/uic.32994116.v1"],"dc:relation":["https://figshare.com/articles/thesis/Host_Immune-Microbial_Interactions_in_Inflammatory_States/32994116"],"dc:rights":["In Copyright"],"dc:subject":["Biology, Microbiology","Health Sciences, Immunology"],"dc:title":["Host Immune-Microbial Interactions in Inflammatory States"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T21:33:42Z"}