The protective role of Foxp3 in crescentic GN was associated with a markedly suppressed expression of proinflammatory interleukin-1 beta (IL-1β), tumour necrosis factor-alpha (TNF-α) and monocyte chemoattractant protein 1 (MCP-1), and diminished infiltration of the kidneys by CD3<sup>+</sup> T cells and F4/80<sup>+</sup> macrophages.
TLR3 expression correlated positively with HCV viral load, interleukin-1β, serum creatinine and inversely with creatinine clearance in patients with HCV-positive glomerulonephritis.
We previously demonstrated that angiotensin II (AII) combined with Habu snake venom (HV) induces glomerulonephritis (GN) in rats, with lesions being restricted to the glomeruli 2 days after the administration of both reagents, but the mechanisms inducing GN are unclear.
Angiotensin II (Ang II) has been shown to be implicated in the development of renal fibrosis in several forms of chronic glomerulonephritides, but the precise mechanisms of its effects remain unclear.
To address whether these two diseases have a common genetic background, the polymorphism of the variable number tandem repeat (VNTR) of IL-1 receptor antagonist (IL-1ra) gene has been analyzed using PCR in patients diagnosed with HSPN (N = 43) and IgAN (N = 97), together with normal controls (N = 98) and patients with acute post-infectious glomerulonephritis (APGN), under the concept that IL-1 might play an important role in mediating pathogenesis of vasculitis and glomerulonephritis.
In segmental sclerosing lesions in FSGS and in IgA-GN with marked glomerular proliferation and/or sclerosis, a reduced expression of the PP-44 antigen and a diminished ability of podocytes to produce IL-1/IL-1 related peptides are noted.
Then, we made an anti-glomerular basement membrane (GBM) GN rat model and compared the AM expression and production in each glomeruli obtained from the control or m-PSL-treated anti-GBM GN rats.
These results suggest that mycophenolate mofetil suppresses the renal damage in rats with autoimmune glomerulonephritis and renal adrenomedullin may participate in the pathophysiology of autoimmune glomerulonephritis.
Considering the antiproliferative and proapoptotic effects of AM, its action on mesangial cells may be related to the amelioration of glomerulonephritis.
We previously reported that the gene expression of six CC chemokines-MCP-1, MCP-3, MIP-1alpha, MIP-1beta, RANTES, and TCA3-was enhanced in a rat model of crescentic glomerulonephritis, the most severe form of glomerulonephritis.