ArticleAmerican journal of translational research2019
Streptococcus may aggravate inflammatory damage in chronic nephritis via the chemotaxis of Th22 cells.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Construction of LncRNA-miRNA-mRNA regulatory network in IgA nephropathy mice model by RNA-sequencing and bioinformatics analysis.Genes & genomics · 2025Article
- Association of Neutrophil Percentage-to-Albumin Ratio with All-Cause and Cardiovascular Mortality in Maintenance Hemodialysis Patients: A Retrospective Study.Journal of inflammation research · 2025Article
- Effect of time-weighted average 25(OH)D on the occurrence of major adverse kidney events in IgA nephropathy-from a 10-year population-based cohort study.Frontiers in nutrition · 2025Article
- Exploration of the pathogenesis of nephrotic syndrome and traditional Chinese medicine intervention based on gut microbiota.Frontiers in immunology · 2024Review
- Characteristics of human oral microbiome and its non-invasive diagnostic value in chronic kidney disease.Bioscience reports · 2022Article
- Identification and validation of glomerulotubular crosstalk genes mediating IgA nephropathy by integrated bioinformatics.BMC nephrology · 2022Article
- Intestinal dysbiosis featuring abundance of Streptococcus associates with Henoch-Schönlein purpura nephritis (IgA vasculitis with nephritis) in adult.BMC nephrology · 2022Article
- Huangkui Capsule in Combination with Leflunomide Improves Immunoglobulin A Nephropathy by Inhibiting the TGF-β1/Smad3 Signaling Pathway.Clinics (Sao Paulo, Brazil) · 2021Article
- Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases.Frontiers in immunology · 2021Review
- T lymphocytes in IgA nephropathy.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInfection can induce and aggravate chronic kidney disease (CKD), and the chemotaxis of Th22 cells may aggravate CKD. However, the mechanism underlying group A Streptococcus (GAS) infections in CKD through the chemotaxis of Th22 cells remains unknown.
methodsThe experiment was divided into a normal control group, an IgAN model group, a GAS-treated normal group, a GAS-treated IgAN group and an anti-CCL intervention group. An IgA nephropathy model was established, and after the success of the IgA nephropathy model was confirmed,
resultsAn immunoglobulin A nephropathy model was successfully established. Streptococcus was successfully inoculated into the nasal cavity of the normal group and the IgA nephropathy infection control group. After intervention, pulmonary inflammatory cell infiltration was more obvious in the IgA nephropathy group than in the normal control group after Streptococcus infection. Th22 cells were detected more frequently in IgA nephropathy; after streptococcal infection, the percentage of Th22 cells in the IgAN group was higher than that in the normal group but decreased significantly when chemotaxis was blocked, the expression of CCL27, CCR10 and IL-22 declined simultaneously, and improvements in pathological changes were observed.
conclusionStreptococcus may cause the chemotaxis of Th22 cells to kidney tissue, leading to or aggravating nephritis injury.
Indexed as
Identifiers
31934290PMC6943466W3010088778What OpenQuestion holds
Registered trials
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