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      Relationship between production of acute-phase proteins and strength of inflammatory stimulation in rats

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          Abstract

          The relationship between intensity of inflammatory stimulation and production of α 2-macroglobulin ( α2M) and α 1-acid glycoprotein (AAG) in rats was investigated. Sprague-Dawley rats were injected with turpentine oil at doses of 0.05, 0.2 or 0.4 mL/rat. Serum levels of α2M, interleukin (IL)-6 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) were measured by enzyme-linked immunosorbent assay, and AAG was measured by single radial immunodiffusion. Peak serum levels of α2M and AAG in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. However, no significant differences were observed for peak serum levels of these acute-phase proteins between 0.2 and 0.4 mL/rat. Furthermore, peak serum levels of IL-6 and CINC-1 in rats injected at 0.05 mL/rat were significantly lower than those at 0.2 or 0.4 mL/rat. Thus, the production of these acute-phase proteins has upper limits, even under increased strength of inflammatory stimulation in rats injected with turpentine oil.

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          Human C-reactive protein: expression, structure, and function

          J Volanakis (2001)
          Molecular Immunology, 38(2-3), 189-197
          Article 0 comments Cited 182 times – based on 0 reviews     Review now
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            Alpha-1-acid glycoprotein.

            N Medjoubi-N, D Porquet, Jaeson T Fournier (2000)
            Alpha-1-acid glycoprotein (AGP) or orosomucoid (ORM) is a 41-43-kDa glycoprotein with a pI of 2.8-3.8. The peptide moiety is a single chain of 183 amino acids (human) or 187 amino acids (rat) with two and one disulfide bridges in humans and rats,respectively. The carbohydrate content represents 45% of the molecular weight attached in the form of five to six highly sialylated complex-type-N-linked glycans. AGP is one of the major acute phase proteins in humans, rats, mice and other species. As most acute phase proteins, its serum concentration increases in response to systemic tissue injury, inflammation or infection, and these changes in serum protein concentrations have been correlated with increases in hepatic synthesis. Expression of the AGP gene is controlled by a combination of the major regulatory mediators, i.e. glucocorticoids and a cytokine network involving mainly interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF alpha), interleukin-6 and IL-6 related cytokines. It is now well established that the acute phase response may take place in extra-hepatic cell types, and may be regulated by inflammatory mediators as observed in hepatocytes. The biological function of AGP remains unknown; however,a number of activities of possible physiological significance, such as various immunomodulating effects, have been described. AGP also has the ability to bind and to carry numerous basic and neutral lipophilic drugs from endogenous (steroid hormones) and exogenous origin; one to seven binding sites have been described. AGP can also bind acidic drugs such as phenobarbital. The immunomodulatory as well as the binding activities of AGP have been shown to be mostly dependent on carbohydrate composition. Finally, the use of AGP transgenic animals enabled to address in vivo, functionality of responsive elements and tissue specificity, as well as the effects of drugs that bind to AGP and will be an useful tool to determine the physiological role of AGP.
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              Defective inflammatory response in interleukin 6-deficient mice

              V. Poli, E. Fattori, G Fantuzzi … (1994)
              Systemic and localized inflammation elicit a number of host responses which include fever, cachexia, hypoglycemia, and major changes in the concentration of liver plasma proteins. Interleukin 6 (IL-6) is considered an important mediator of the inflammatory response, together with IL-1 and tumor necrosis factor alpha (TNF-alpha). The purpose of this study was to unequivocally determine the role of IL-6 in these phenomena making use of IL-6-deficient mice that we have recently generated by gene targeting. We report here that in the absence of IL- 6, mice are unable to mount a normal inflammatory response to localized tissue damage generated by turpentine injection. The induction of acute phase proteins is dramatically reduced, mice do not lose body weight and only suffer from mild anorexia and hypoglycemia. In contrast, when systemic inflammation is elicited through the injection of bacterial lipopolysaccharide (LPS), these parameters are altered to the same extent both in wild-type and IL-6-deficient mice, demonstrating that under these conditions IL-6 function is dispensable. Moreover, we show that LPS-treated IL-6-deficient mice produce three times more TNF-alpha than wild-type controls, suggesting that increased TNF-alpha production might be one of the compensatory mechanisms through which a normal response to LPS is achieved in the absence of IL-6. We also show that corticosterone is normally induced in IL-6-deficient mice, demonstrating that IL-6 is not required for the activation of the hypothalamic-pituitary-adrenal axis. Our results reinforce the idea that different patterns of cytokines are involved in systemic and localized tissue damage, and identify IL-6 as an essential mediator of the inflammatory response to localized inflammation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Lab Anim
                Journal ID (publisher-id): LA
                Journal ID (hwp): rsmla
                Title: Laboratory Animals
                Publisher: Royal Society of Medicine Press
                ISSN (Print): 0023-6772
                ISSN (Electronic): 1758-1117
                Publication date (Print): July 2011
                Volume: 45
                Issue: 3
                Pages: 215-218
                Affiliations
                simpleLaboratory of Immunology, School of Life and Environmental Science, Azabu University , 1-17-71 Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan
                Author notes
                Corresponding author: S Yamamoto. Email: yamamoto@ 123456azabu-u.ac.jp
                Article
                Publisher ID: LA-10-112
                DOI: 10.1258/la.2011.010112
                PMC ID: 3125702
                PubMed ID: 21669904
                SO-VID: 54a9b69b-035a-4a5c-b282-4b7119abd826
                Copyright © © Laboratory Animals Ltd
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date accepted : 24 April 2011
                Categories
                Subject: Original Articles

                ScienceOpen disciplines: Animal science & Zoology
                Keywords: rats,il-6,cinc-1,α2m,aag
                Data availability:
                ScienceOpen disciplines: Animal science & Zoology
                Keywords: rats, il-6, cinc-1, α2m, aag

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