Fig 1: Immunoregulatory S100A8/A9 heterodimer induces the accumulation of MDSC in MS patients after glucocorticoid treatment. A, Serum S100A8/A9 heterodimer concentration in serum from MS patients (n = 15) before and after MPPT (MS patients before treatment vs MS patients after treatment, P = 0.0072). B, Levels of S100A8 mRNA were measured by qPCR (MS patients before treatment vs MS patients after treatment, P = 0.0298, n = 5). C, Levels of S100A9 mRNA were measured by qPCR (MS patients before treatment vs MS patients after treatment, P = 0.0814, n = 5). D, Correlation analysis between serum arginase activity and serum S100A8/A9 heterodimer concentration in MS (r 2 = 0.4563, P = 0.0225). E, Levels of Atf3 mRNA were measured by qPCR (MS patients before treatment vs MS patients after treatment, P = 0.7442, n = 5). F, Levels of Irf7 mRNA were measured by qPCR (MS patients before treatment vs MS patients after treatment, P = 0.2035, n = 5)
Fig 2: Comparison of serum markers between OSA patients and controls. (A) Preeclampsia-related markers; sFlt-1/PlGF ratio, sFlt-1, Endoglin, and PIGF. (B) Proinflammatory markers for OSA; IL-6, MRP8/14, and TNF-a.sFlt-1= soluble fms-like tyrosine kinase-1, PlGF = placental growth factor, OSA = obstructive sleep apnea, IL = interleukin, MRP = myeloid-related protein, TNF = tumor necrosis factor.
Fig 3: The correlations between serum/urinary S100A8/A9 and S100A12 and clinical parameters in 34 active MPO-AAV. A–G showed the correlations of serum S100A8/A9 and the level of MPO-ANCA (A), serum ferritin (B), CRP (C), D-Dimer (D), erythrocyte sedimentation rate (E), rheumatoid factor (F), serum albumin (G). H and I showed the correlations of serum S100A12 and the level of MPO-ANCA (H) and serum ferritin (I). J–N showed the correlations of urinary S100A8/A9 and MPO-ANCA (J), BVAS (K), serum creatinine (L), hematuria (M), and urinary NGAL (N). O Showed the correlation between urinary S100A12 and serum creatinine. BVAS: Birmingham vasculitis activity score. NGAL: neutrophil gelatinase-associated lipocalin
Fig 4: Levels of serum and urinary S100A8/A9 and S100A12 in MPO-AAV patients and normal controls. Comparison of concentrations of serum S100A8/A9 (A), serum S100A12 (B), urinary S100A8/A9 (C), and urinary S100A12 (D) between MPO-AAV patients in the active period or remission and NC. E The relationship between serum S100A8/A9 and serum S100A12 in active MPO-AAV. F The relationship between urinary S100A8/A9 and urinary S100A12 in active MPO-AAV. NC: normal controls. ns: not significant
Fig 5: S100A8/A9 and S100A12 played their pro-inflammatory effects through the p38 MAPK/NF-?B p65 pathway. The full-length blot of GAPDH in A was absent for the limited exposure space. A S100A8/A9 and S100A12 induced p38 MAPK phosphorylation and NF-?B p65 expression. B The phosphorylation ratios of p38 after neutrophils were stimulated with a combination of ANCA and S100A8/A9 or S100A12. C The activation of NF-?B p65 after neutrophils were stimulated with a combination of ANCA and S100A8/A9 or S100A12. D The phosphorylation of p38 MAPK and the activation of NF-?B p65 after the blockade of TLR4 and RAGE. E The phosphorylation ratio of p38 after blocking TLR4 and RAGE. F The expression of NF-?B p65 after blocking TLR4 and RAGE. *p < 0.05, **p < 0.01, ns: not significant
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