Linchuang shenzangbing zazhi (Oct 2023)
Exploratory study of serum IL-36 subfamily as biomarkers of disease progression in lupus nephritis
Abstract
Objective To explore whether or not serum interleukin (IL)-36 subfamily may serve as biomarkers for disease progression in lupus nephritis (LN). Methods From March 2017 to April 2020, 103 patients hospitalized with systemic lupus erythematosus (SLE) at Department of Nephrology, First Affiliated Hospital of Xi'an Jiaotong University were selected as research subjects. They were assigned into two groups of LN (n=30) and non-LN (n=73). In addition, 83 healthy volunteers without a history of kidney disease were recruited as healthy control group. Serum levels of IL-36α、IL-36β、IL-36γ、IL-36Ra and IL-17 were measured by enzyme-linked immunosorbent assay (ELISA). Results Compared with healthy control group, serum levels of IL-36α [13.12(9.01, 17.95)ng/L, 21.24(11.41, 26.37)ng/L vs 10.06 (6.80, 12.34)ng/L] and IL-17 [44.18(32.78, 66.95)ng/L, 49.73(33.26, 91.08)ng/L vs 33.14(20.67, 43.07)ng/L] rose in non-LN and LN groups and the increase was more significant in LN group than that in non-LN group (P<0.05). Serum level of IL-36β was also higher in LN group than that in healthy control and non-LN groups [25.67(11.52, 48.52)ng/L vs 8.60(4.59, 13.68)ng/L, 11.44(6.45, 26.91)ng/L] while the serum level of IL-36Ra [32.88(17.47, 51.69)ng/L vs 98.17(45.93, 161.80)ng/L, 49.11(26.40, 92.52)ng/L] was lower than that in healthy control and non-LN groups (P<0.05). In positive stepwise method, higher levels of IL-36α might elevate the risk of proteinuria in SLE patients (OR=1.346, 95%CI:1.134-1.596, P=0.001). And serum IL-36α in LN patients was significantly correlated positively with SLE disease activity index (SLEDAI), renal SLEDAI (rSLEDAI), SLICC/ACR injury index (SDI) and serum IL-17 (P<0.05) and negatively with levels of IL-36Ra and complement C3 (P<0.05). Glucocorticoid with or without immunosuppressant could lower serum level of IL-36 in SLE patients (P<0.05). Conclusions Independent of other confounding factors, IL-36α may be a biomarker associated with SLE proteinuria. And its mechanism of action may be associated with the regulation of Th17 cytokines.
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