Abstract: SA-PO646
Experimental Investigation of Exacerbation of IgA Nephropathy by Exposure to Fine Particulate Matter
Session Information
- Glomerular Diseases: IgA and Complement-Mediated GN
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1302 Glomerular Diseases: Immunology and Inflammation
Authors
- Park, Yohan, Konyang University Hospital, Daejeon, Korea (the Republic of)
- Yoon, Se-Hee, Konyang University Hospital, Daejeon, Korea (the Republic of)
- Yun, Sung-Ro, Konyang University Hospital, Daejeon, Korea (the Republic of)
- Hwang, Won Min, Konyang University Hospital, Daejeon, Korea (the Republic of)
Background
It is known that exposure to fine particulate matter, which has recently been highlighted as an environmental problem, occurs mainly through the respiratory tract, which increases various inflammatory reactions. This increase in mucosal inflammation is thought to cause aggravation of IgA nephropathy, but no studies have been reported on the relationship between IgA nephropathy and fine particulate matter so far.
Methods
The HIGA (high serum IgA) mouse model was used as a spontaneous IgA nephropathy animal model. Using a sealed fine particulate matter exposure cage system, the exposure group was exposed to fine particulate matter for 1 hour at a time, 3 times a week, for a total of 8 weeks. After 8 weeks of exposure to fine particulate matter, blood, urine, lung, and kidney tissues were obtained and analyzed.
Results
There was no significant difference in the total IgA concentration in the blood of the exposure group and the control group. However, in the lectin binding assay (Ricinus communis agglutinin I, Sambucus nigra agglutinin), the concentration of glycosylated IgA tended to be higher in the control group. In the lung tissue of the exposure group, interstitial thickening was evident and toll like receptor (TLR)-9 expression was significantly increased. In the kidney tissue of the exposure group, mesangial proliferation and mesangial expansion were increased, and the number of glomerular scleroses were higher in the exposure group compared to the control group. Mesangial IgA deposition in the exposure group was significantly increased compared to the control group in immunofluorescence assay.
Conclusion
It was observed that fine particulate matter increased TLR-9 expression in lung tissue, which increased hypoglycosylated IgA, resulting in renal glomerular damage and increased mesangial IgA deposition in HIGA mouse model. This suggests that chronic exposure to high concentrations of fine particulate matter in IgA nephropathy may exacerbate the disease severity.