ArticlePLoS neglected tropical diseases2011
Differential expression of chemokine and matrix re-modelling genes is associated with contrasting schistosome-induced hepatopathology in murine models.
Article in PLoS neglected tropical diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Comprehensive Transcriptome Meta-analysis to Characterize Host Immune Responses in Helminth Infections.PLoS neglected tropical diseases · 2016Pooled it
- Pooled it
- Use of a cytochrome P450 humanized mouse model to refine schistosomiasis drug discovery.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Identification of Ferroptosis-Related Hub Genes Linked to Suppressed Sulfur Metabolism and Immune Remodeling inPathogens (Basel, Switzerland) · 2026Article
- Transcriptome analysis of peripheral blood of Schistosoma mansoni infected children from the Albert Nile region in Uganda reveals genes implicated in fibrosis pathology.PLoS neglected tropical diseases · 2023Article
- Modulation of the Host Immune Response by Schistosome Egg-Secreted Proteins Is a Critical Avenue of Host-Parasite Communication.Pathogens (Basel, Switzerland) · 2021Review
- Fasciola hepatica hijacks host macrophage miRNA machinery to modulate early innate immune responses.Scientific reports · 2021Article
- Live imaging of collagen deposition during experimental hepatic schistosomiasis and recovery: a view on a dynamic process.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Coalescing beneficial host and deleterious antiparasitic actions as an antischistosomal strategy.eLife · 2018Article
- Effect of praziquantel on the differential expression of mouse hepatic genes and parasite ATP binding cassette transporter gene family members during Schistosoma mansoni infection.PLoS neglected tropical diseases · 2017Article
- The NIH-NIAID Schistosomiasis Resource Center at the Biomedical Research Institute: Molecular Redux.PLoS neglected tropical diseases · 2016Review
- An ex vivo model for studying hepatic schistosomiasis and the effect of released protein from dying eggs.PLoS neglected tropical diseases · 2015Article
- Circulating miRNAs: Potential Novel Biomarkers for Hepatopathology Progression and Diagnosis of Schistosomiasis Japonica in Two Murine Models.PLoS neglected tropical diseases · 2015Article
- Cytokine and chemokine responses to helminth and protozoan parasites and to fungus and mite allergens in neonates, children, adults, and the elderly.Immunity & ageing : I & A · 2013Article
- Schistosomajaponicum Eggs Induce a Proinflammatory, Anti-Fibrogenic Phenotype in Hepatic Stellate Cells.PloS one · 2013Article
- Article
- MicroRNA-gene expression network in murine liver during Schistosoma japonicum infection.PloS one · 2013Article
Corrections and comments
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6 authors at 2 institutions in 1 country.
Funding
Abstract
The pathological outcomes of schistosomiasis are largely dependent on the molecular and cellular mechanisms of the host immune response. In this study, we investigated the contribution of variations in host gene expression to the contrasting hepatic pathology observed between two inbred mouse strains following Schistosoma japonicum infection. Whole genome microarray analysis was employed in conjunction with histological and immunohistochemical analysis to define and compare the hepatic gene expression profiles and cellular composition associated with the hepatopathology observed in S. japonicum-infected BALB/c and CBA mice. We show that the transcriptional profiles differ significantly between the two mouse strains with high statistical confidence. We identified specific genes correlating with the more severe pathology associated with CBA mice, as well as genes which may confer the milder degree of pathology associated with BALB/c mice. In BALB/c mice, neutrophil genes exhibited striking increases in expression, which coincided with the significantly greater accumulation of neutrophils at granulomatous regions seen in histological sections of hepatic tissue. In contrast, up-regulated expression of the eosinophil chemokine CCL24 in CBA mice paralleled the cellular influx of eosinophils to the hepatic granulomas. Additionally, there was greater down-regulation of genes involved in metabolic processes in CBA mice, reflecting the more pronounced hepatic damage in these mice. Profibrotic genes showed similar levels of expression in both mouse strains, as did genes associated with Th1 and Th2 responses. However, imbalances in expression of matrix metalloproteinases (e.g. MMP12, MMP13) and tissue inhibitors of metalloproteinases (TIMP1) may contribute to the contrasting pathology observed in the two strains. Overall, these results provide a more complete picture of the molecular and cellular mechanisms which govern the pathological outcome of hepatic schistosomiasis. This improved understanding of the immunopathogenesis in the murine model schistosomiasis provides the basis for a better appreciation of the complexities associated with chronic human schistosomiasis.
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