Temporal Expression of Chemokines Dictates the Hepatic Inflammatory Infiltrate in a Murine Model of Schistosomiasis.
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE14367
PROVIDER: PRJNA111407 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Schistosomiasis continues to be an important cause of parasitic morbidity and mortality world-wide. Determining the molecular mechanisms regulating the development of granulomas and fibrosis will be essential for understanding how schistosome antigens interact with the host environment. We report here the first whole genome microarray analysis of the murine liver during the progression of Schistosoma japonicum egg-induced granuloma formation and hepatic fibrosis. Our results reveal a distinct temporal relationship between the expression of chemokine subsets and the recruitment of cells to the infected liver. Genes up-regulated earlier in the response included T- and B-cell chemoattractants, reflecting the early recruitment of these cells illustrated by flow cytometry. The later phases of the response corresponded with peak recruitment of eosinophils, neutrophils, macrophages and myofibroblasts/hepatic stellate cells (HSCs) and the expression of chemokines with activity for these cells including CCL11 (eotaxin 1), members of the Monocyte-chemoattractant protein family (CCL7, CCL8, CCL12) and the Hepatic Stellate Cell/Fibrocyte chemoattractant CXCL1. Peak expression of macrophage chemoattractants (CCL6, CXCL14) and markers of alternatively-activated macrophages (e.g. Retnla) during this later phase provides further evidence of a role for these cells in schistosome-induced pathology. Additionally, we demonstrate that CCL7 immunolocalises to the fibrotic zone of granulomas. Furthermore, striking up-regulation of neutrophil markers and the localisation of neutrophils and the neutrophil chemokine S100A8 to fibrotic areas suggests the involvement of neutrophils in S. japonicum¬-induced hepatic fibrosis. These results further our understanding of the immunopathogenic and, especially, chemokine signalling pathways that regulate the development of S. japonicum-induced granulomas and fibrosis and may provide correlative insight into the pathogenesis of other chronic inflammatory diseases of the liver where fibrosis is a common feature. Keywords: Time course, disease state analysis
2009-01-10 | GSE14367 | GEO
Project description: Not available
| S-EPMC2817718 | biostudies-literature
Project description:Immunoprofiling of prostate cancer infiltrate
| PRJNA644438 | ENA
Project description:We have performed a genome wide transcriptional survey of liver biopsies obtained from patients in Hunan China, who have chronic schistosomiasis with and without past viral hepatitis history, compared to patients with no liver disease history or indicators. These results present a comprehensive transcriptional profile of chronic schistosomiasis japonica patients and demonstrate similarities and differences with other hepatic diseases. These unique features of gene expression, in conjunction with previous reports of the cellular composition of granuloma formation and recovery, present an improved understanding of the molecular immunopathology and general physiological status underlying hepatic schistosomiasis. The gene expression profile of the human liver was examined for chronic patients with Schistosoma japonicum infections. Microarray analysis was performed on cRNA synthesised from total RNA derived from the liver biopsy tissue from huan China. Three groups were examined based on infections status [C] were without history or indicators of schistosomiasis or viral heapatitis controls ; [S] with a history or active for schistosomiasis but no indicators of viral heapatitis; and [S]
2014-09-13 | E-GEOD-61376 | biostudies-arrayexpress
Project description:We have performed a genome wide transcriptional survey of liver biopsies obtained from patients in Hunan China, who have chronic schistosomiasis with and without past viral hepatitis history, compared to patients with no liver disease history or indicators. These results present a comprehensive transcriptional profile of chronic schistosomiasis japonica patients and demonstrate similarities and differences with other hepatic diseases. These unique features of gene expression, in conjunction with previous reports of the cellular composition of granuloma formation and recovery, present an improved understanding of the molecular immunopathology and general physiological status underlying hepatic schistosomiasis.
2014-09-13 | GSE61376 | GEO
Project description:Increased expression of chemokines in UNC1999-treated tumor tissues were successfully checked out through chemokines profiles screening of a total 25 different mouse chemokines using control and UNC1999-treated tumor tissues.
2022-08-25 | GSE211880 | GEO
Project description:Nucleosome conformation dictates the histone code
| PRJNA632919 | ENA
Project description:Nuclear chromosome location dictates segregation error frequency
| PRJEB52892 | ENA
Project description:Chemokines are chemotactic cytokines that control the migratory patterns and positioning of immune cells. Many chemokines have been associated with systemic autoimmune diseases that have chronic IFN signature. We now describe that a series of chemokines, including CXCL4, CXCL10, CXCL12 and CCL5, can superinduce type I IFN (IFN-I) by TLR9-activated plasmacytoid DCs (pDCs), independently of their respective known chemokine receptors. Mechanistically, we show that chemokines such as CXCL4 mediate transcriptional and epigenetic changes in pDCs, mostly targeted to the IFN-I pathways. We also describe that chemokines physically interact with DNA to form nanoparticles which promote clathrin-mediated cellular uptake and delivery of DNA in the early endosomes of pDCs. Using two mouse models of skin inflammation, we observed the presence of CXCL4 associated with DNA in vivo. These data thus reveal a non-canonical role for chemokines to modulate TLR signaling, and extend our understanding on the mechanism associated with the chronic expression of IFN-I by pDCs in autoimmune diseases.
2022-05-24 | GSE202333 | GEO
Project description:Background and aims: There are considerable evidences demonstrating that angiogenesis and chronic inflammation are mutually dependent. However, although cirrhosis progression is characterized with a chronic hepatic inflammatory process, this connection is not sufficiently explored as a therapeutic strategy. Therefore, this study was aimed to assess the potential benefits of targeting angiogenesis in cirrhotic livers to modulate inflammation and fibrosis. For this purpose, we evaluate the therapeutic utility of angiogenesis inhibitors. Methods: The in vivo effects of angiogenesis inhibitors were monitored in liver of cirrhotic rats by measuring angiogenesis, inflammatory infiltrate, fibrosis, a-smooth muscle actin (a-SMA) accumulation, differential gene expression (by microarrays), and portal pressure. Results: Cirrhosis progression was associated with a significant enhancement of vascular density and expression of vascular endothelial growth factor-A (VEGF-A), angiopoietin-1, angiopoietin-2 and placental growth factor (PlGF) in cirrhotic livers. The newly formed hepatic vasculature expressed vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Interestingly, the expression of these adhesion molecules correlated well with local inflammatory infiltrate. Livers of cirrhotic rats treated with angiogenesis inhibitors presented a significant decrease in hepatic vascular density, inflammatory infiltrate, a-SMA abundance, collagen expression and portal pressure. Conclusion: Angiogenesis inhibitors may offer a potential novel therapy for cirrhosis due to its multiple mechanisms of action against angiogenesis, inflammation and fibrosis in cirrhotic livers. Keywords: angiogenesis, cirrhosis, liver, Affymetrix, fibrosis
2007-10-18 | GSE6929 | GEO