Immune complex nephritis in <i>Schistosoma mansoni</i>‐ infected mice

Natali, Pier Giorgio; Cioli, Donato

doi:10.1002/eji.1830060511

Cited by 30 publications

(8 citation statements)

References 30 publications

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“…Glomerular deposits of immune complexes and ultrastructural glomerular lesions and Ig deposits have been described in infected mice, but the kidneys were often normal by light microscopy (Andrade & Susin 1974, Rousse & Romeiro 1974, Natali & Cioli 1976, Carneiro & Lopes 1986, Water et al 1988. Antigen and immune complex deposition were augmented by portocaval shunting (van Marck et al 1977) but were present even in unisexual infections (Lopes et al 1981).…”

Section: Extrahepatic Pathologymentioning

confidence: 99%

Experimental models of Schistosoma mansoni infection

Cheever

Lenzi²,

Lenzi³

et al. 2002

Mem. Inst. Oswaldo Cruz

121

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Section: Extrahepatic Pathologymentioning

confidence: 99%

Experimental models of Schistosoma mansoni infection

Cheever

Lenzi²,

Lenzi³

et al. 2002

Mem. Inst. Oswaldo Cruz

121

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“…The renal lesions of infected hamsters consisted of mesangial and endothelial hypercellularity (161). Glomeruli of heavily infected mice showed lesions consistent with nephritis (207), manifested by an increase in mesangial cells, electron-dense deposits, and local thickening of basement membranes (104). However, murine glomerulopathy, unlike human, does not progress to chronic renal failure.…”

Section: Introductionmentioning

confidence: 99%

Immunopathology of Schistosoma mansoni infection

1989

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Schistosomiasis mansoni is a chronic helminthic disease that affects about 100 million people in the tropics. The worms have a life span of 5 to 10 years, and they live in the mesenteric veins of the host. Lightly infected individuals are asymptomatic or manifest mild intestinal symptoms. Heavily infected individuals often develop severe morbidity with hepatosplenomegaly, sometimes with a fatal outcome. Morbidity is attributed to the strong humoral and T-cell-mediated host immune responses developed to a variety of parasite antigens and expressed as tissue inflammations. The immunopathology includes dermatitis, immune complex-mediated kidney disease, and, chiefly, T-cell-mediated granuloma formation and fibrosis around disseminated parasite eggs. This review describes the mechanisms of induction and expression of immunopathology in infected persons and experimental animals. Immunoregulatory mechanisms that modulate the enhanced immune responses and may ameliorate excessive morbidity are discussed.

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“…Demonstration of the presence of antigen in clinical material has been shown to be effective in the diagnosis of active microbial infection (Houba et al, 1970;Shahin et al, 1974;Natali and Cioli, 1976;Ngu and Blackett, 1977), and, recently, amoebic antigen in circulating immune complexes (CIC) has been detected in the sera of patients with amoebiasis by a solid phase radio-immunoassay (Pillai and Mohimen, 1982;Mohimen et al, 1989) or enzyme linked immunosorbent assay (Vinayak et al, 1986;Gandhi et al, 1988). However, the sensitivity and specificity of the detection of amoebic antigen and its level in differentiating present from past infection, or its relation to the severity of disease, has not been clearly understood.…”

Section: Introductionmentioning

confidence: 99%

Uses and limitations in the demonstration of specific circulating immune complexes in patients with amoebiasis

Vinayak¹,

Shandil²,

Bansal

et al. 1990

Journal of Medical Microbiology

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Summary.A micro-enzyme linked immuaosorbent assay (micro-ELISA) has been evaluated as a diagnostic test to detect amoebic antigen in polyethylene glycol (PEG) precipitated circulating immune complexes (CIC) in sera from patients with amoebiasis. The immune complexes were captured on rabbit anti-amoebic IgGcoated wells of microtitration plates and the complexed antigen was detected by enzyme linked antihuman immunoglobulins. A titre of > 160 for the immune complexes was considered to be of clinical significance. The immunoassay detected amoebic, antigen-specific CIC in 35 (94.5%) of 37 patients with confirmed amoebic liver abscess. Twenty (55.5%) of 36 clinically suspected cases of amoebic liver abscess had amoebic antigen-specific CIC and responded favourably to anti-amoebic chemotherapy. Only two (20%) of 10 cases of non-dysenteric symptomatic intestinal amoebic infection had amoebic antigen-specific CIC. One (10%) of 10 patients with non-amoebic intestinal disorders also had amoebic antigen in CIC. However, none of 15 cases of non-amoebic hepatic disorders that included hydatid disease, metastatic adenocarcinoma, hepatocellular carcinoma, cholecystitis and choledocal cyst, 13 cases of rheumatoid arthritis and 25 apparently healthy subjects had amoebic antigen in CIC. The levels of the amoebic antigen-specific CIC did not correlate (p>O-O5) with either the number of abscess(es) or lobe(s) of the liver involved. However, the levels of antigen-specific CIC were higher (p < 0.01) in patients with a liver size of more than 5 cm below the right costal margin. Antigen-specific CIC levels tended to decline or disappear during 3-6 months following completion of therapy. In spite of the limitations for diagnosing symptomatic intestinal amoebic disease, the demonstration of specific CIC is recommended as an immuno-diagnostic procedure for patients with suspected amoebic liver abscess.

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Immune complex nephritis in Schistosoma mansoni‐ infected mice

Cited by 30 publications

References 30 publications

Experimental models of Schistosoma mansoni infection

Experimental models of Schistosoma mansoni infection

Immunopathology of Schistosoma mansoni infection

Uses and limitations in the demonstration of specific circulating immune complexes in patients with amoebiasis

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