Simple, reliable and sensitive enzyme immunoassays have been developed for the quantification of the mouse acute-phase SAP and C3 proteins. The ELISA systems were validated using sera from mice injected with S. dysenteriae endotoxin, and detected 500 pg protein/ml. The assays use 96-well microtitre plates permitting rapid processing of a large number of samples.
"In mice bearing PDT-treated tumors, the levels of serum C3 first show a temporal decline at 1 h after therapy (suggesting its consumption above the rate of production and release into circulation) followed later by a pronounced rise persisting between 24 and 72 h after PDT (caused presumably by the release of C3 from the liver). The latter is a classical manifestation of acute phase reaction in mice , with C3 involved as acute phase reactant in the regulation of systemic host response triggered by tumor-localized PDT treatment . As already indicated by our preliminary findings  and the in vitro studies , PDT-induced activation of the complement cascade proceeds primarily through the alternative pathway while the classical activation pathway appears not to be significantly involved (Fig. 1(b)). "
[Show abstract][Hide abstract] ABSTRACT: Following treatment of Lewis lung carcinomas (LLC) by Photofrin-mediated photodynamic therapy (PDT), tumor tissues and sera of host mice were collected for the analysis of complement activity. Elevated tumor C3 levels were detected between 1 and 24 h after PDT, while serum C3 levels increased significantly at 24 h post therapy. Increased alternative complement pathway activity in the serum was evident between 1 and 3 days post PDT. Blocking C3a- or C5a-receptors in the host mice decreased the efficacy of PDT in producing LLC tumor cures, supporting the importance of complement action in PDT-mediated tumor destruction.
Cancer Letters 08/2005; 225(2):215-23. DOI:10.1016/j.canlet.2004.11.059 · 5.62 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. Here, we report experiments with IL-6 gene-disrupted mice (IL-60/0). We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. We studied the response to TNF in three different models: (i) murine TNF administration; (ii) TNF in galactosamine (GalN)-sensitized mice; (iii) TNF in Bacillus Calmette-Guérin-sensitized mice. We observed no significant difference between the two types of mice in any of the three models. Furthermore, IL-60/0 mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. We also observed that, in response to turpentine, TNF or IL-1, IL-60/0 mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. In IL-60/0 mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system.
European Journal of Immunology 09/1994; 24(9):2237 - 2242. DOI:10.1002/eji.1830240945 · 4.03 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Complement has been shown to lyse protoscoleces of Echinococcus granulosus, but products from this parasite are able to consume complement, and this has been proposed as an evasion mechanism. The murine secondary hydatidosis model, with intraperitoneal inoculation, is used in this work to assess the occurrence in vivo of complement consumption by the parasite as well as the role of complement during the establishment of infection. Although the measurement of systemic levels of C3 activation, total C3, and hemolytic complement in challenged mice yielded no evidence of complement consumption, the relevance of local consumption at the site of infection cannot be ruled out. The role of complement during establishment of infection was assessed by comparing parasite burdens in normal and complement-depleted mice. Complement depletion by treatment with cobra venom factor caused a 79% reduction in cyst numbers (P < 0.05). Possible explanations of this unexpected result are discussed. The results presented suggest that lysis or opsonization by host complement are not effective against the establishing parasite in this model. They also indicate the significance of complement activation by the parasite needs to be studied at a local level.
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