THE EFFECTS OF PERIODIC CHALLENGE ON THE RESPONSE OF α2-AP GLOBULIN AND OTHER ACUTE-PHASE REACTANTS OF RAT SERUM TO TISSUE INJURY

1967 ◽  
Vol 45 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Henry E. Weimer ◽  
Constance Humelbaugh

The effects of periodic challenge with turpentine on the concentration of the acute-phase reactants of serum were studied in young, adult, male Sprague–Dawley rats. The initial injection of the phlogogenic agent was followed by rapid and significant increases in the concentrations of plasma fibrinogen, total serum glycoprotein, serum complement, and the α2-AP globulin and seromucoid fractions. Variable response patterns were observed on subsequent challenges and in the intervals between. The conclusion was drawn that the acute-phase reactants of serum do not respond in a uniform manner to repeated challenge with a phlogogenic agent, and by inference their synthesis must be regulated by several different mechanisms.

1965 ◽  
Vol 43 (6) ◽  
pp. 925-935 ◽  
Author(s):  
Henry E. Weimer ◽  
James F. Godfrey

The effects of acute starvation, food restriction, and protein depletion on the response of serum proteins to turpentine-induced inflammation were investigated in adult, male, Sprague–Dawley rats. The animals were fed nutritionally inadequate diets until a 20% weight loss was attained, then they were challenged. Significant increases occurred in the concentrations of protein-bound hexose, protein-bound hexosamine, and protein-bound sialic acid, and in the fibrinogen, seromucoid, α2- and β-globulin fractions; a new protein, α2-AP (acute-phase) globulin, appeared in the serum concomitant with decreased levels of total protein, albumin, and γ-globulin after the injection of the phlogogenic agent. The same pattern of response to inflammation occurred, irrespective of whether the rats were fed the stock or experimental diets.The conclusion was drawn that the response of the acute-phase reactants of rat serum to tissue injury is of such magnitude that it is not suppressed by several types of severe nutritional stress. Possible factors involved in the response are discussed.


1967 ◽  
Vol 45 (12) ◽  
pp. 1937-1941 ◽  
Author(s):  
Henry E. Weimer ◽  
Constance Humelbaugh ◽  
Dorothy M. Roberts

The effects of growth of the Walker 256 carcinosarcoma on the α2-AP (acute phase) globulin, fibrinogen, seromucoid, and haptoglobin fractions of plasma were investigated in adult, male Sprague–Dawley rats in a longitudinal study. Early increases in α2-AP globulin and seromucoid levels were found to be related to the tissue injury associated with the implantation procedure. Significant elevations in the α2-AP globulin, fibrinogen, and seromucoid fractions coincided with the onset of progressive tumor growth. Serum haptoglobin concentrations exhibited a delayed rise. This was attributed to the in vivo formation of haptoglobin–hemoglobin complexes. It was suggested that the increases in all fractions reflected the release of humoral mediators from injured or necrotic cells wrhich stimulated increased synthesis of the fractions by the liver.


1991 ◽  
Vol 261 (3) ◽  
pp. C461-C466 ◽  
Author(s):  
S. J. Schwarzenberg ◽  
C. J. Potter ◽  
S. A. Berry

For evaluation of the ontogenetic regulation of the acute phase response, inflammation was induced in Fischer rat litters at different postnatal ages. Four homologous rat hepatic serine protease inhibitor (Spi 2.1, Spi 2.2, Spi 2.3, and alpha 1-antitrypsin) mRNAs were measured in livers 24 h after injection. Animals mounted both positive and negative acute phase responses at all ages, but responses were blunted in young animals, reaching adult levels by days 7-19. alpha 1-Antitrypsin mRNA had no response, and Spi 2.2 mRNA had 50% the rise seen in adults on days 3 and 7. Spi 2.1 and 2.3 mRNAs, negative acute phase reactants, showed attenuation of adult response to inflammation in infant animals of 33% (Spi 2.1) and 40% (Spi 2.3). In hypophysectomized animals, the responses of Spi 2.2, 2.3, and alpha 1-antitrypsin mRNAs after turpentine stimulation were similar to that of normal animals, whereas Spi 2.1 mRNA did not change. In conclusion, infant animals mount a blunted response to tissue injury; multiple factors may be involved in the development of the full adult response. Immaturity of the pituitary may play a role in the suppression of Spi 2.1 mRNA's response during inflammation in infant animals. These highly evolutionary related genes will be helpful in identifying specific factors regulating gene expression in inflammation and development.


Author(s):  
Syed Wali Peeran ◽  
Ahmed Elhassan ◽  
Tazeen Dawood ◽  
Karthikeyan Ramalingam ◽  
Syed Ali Peeran ◽  
...  

Acute phase reactants like C-reactive protein (CRP), and pentraxin 3 (PTX3) are increased with inflammation and tissue injury. PTX3 is an acute phase protein and a member of the long pentraxin family. CRP is synthesized in the liver but PTX3 is generated locally at the inflammatory site. It is a fluid-phase pattern-recognition molecule that regulates antimicrobial immunity and inflammation by interfering with selectin-dependent neutrophil recruitment and regulating the complement cascade. Hence, PTX3 could be used as a potential biomarker to identify inflammatory response in both acute and chronic diseases. In this review, we discuss the role of PTX3 in periodontal inflammation.


1992 ◽  
Vol 72 (1) ◽  
pp. 1-7 ◽  
Author(s):  
H. R. Colten

Proteins of the complement system are important effectors and modulators of inflammation. The complement cascade is triggered by microbes, tissue debris, and specific antibodies. Serum complement proteins are derived primarily from liver, but extrahepatic complement synthesis is important in homeostasis and in local host defenses. Tissue-specific regulation of expression of complement genes is governed by mechanisms similar to those that regulate other “acute phase reactants.” That is, tissue injury or infection elicit changes in expression of these acute phase proteins, which, although variable in kinetics, magnitude, and direction, are a consequence of an elaborate system of cell-to-cell communication. This communication is mediated via a complex network of cytokines, including the interferons, interleukins, several growth factors, and sex hormones. The cell biological and molecular biological details of these mechanisms are now under active investigation. An understanding in molecular terms of the balance between proinflammatory and counterregulatory forces on complement gene expression should provide new insight into the functions of complement and the design of novel therapies for disorders of inflammation.


1997 ◽  
Vol 322 (2) ◽  
pp. 663-669 ◽  
Author(s):  
Barbara KLUVE-BECKERMAN ◽  
Toshiyuki YAMADA ◽  
Joyce HARDWICK ◽  
Juris J. LIEPNIEKS ◽  
Merrill D. BENSON

Serum amyloid A (SAA) proteins SAA1 and SAA2 are prominent acute-phase reactants which circulate in association with the high-density-lipoprotein (HDL) fraction of plasma. Plasma levels of SAA1 and SAA2 increase dramatically, by as much as 1000-fold, within 24 h of tissue injury and then rapidly decrease with cessation of the inflammatory stimulus, suggesting that SAA clearance and/or catabolism is important to the re-establishment of homoeostasis. In this context, aberrant SAA catabolism has long been considered a potential factor in the pathogenesis of reactive amyloidosis. To initiate studies aimed at understanding the differential regulation of SAA metabolism, we have produced 35S-labelled murine SAA1 and SAA2 in Escherichia coli, bound them individually to HDL, and then compared the plasma-clearance characteristics of SAA1 and SAA2 under normal and acute-phase conditions. When bound to normal HDL, SAA2 [half-life (t½) = 30 min] was cleared significantly faster than SAA1 (t½ = 75 min). Clearance of SAA1 and SAA2 was significantly slower when each was bound to acute-phase HDL as opposed to normal HDL, when clearance rates were determined in acute-phase mice versus normal mice, and when normal HDL was remodelled to contain both recombinant isotypes rather than just one of the isotypes. Thus it appears that an increased amount of SAA on HDL, or possibly the combined presence of both isotypes on HDL, is associated with a prolongation in the plasma half-life of SAA.


Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1898
Author(s):  
Julian Hackler ◽  
Raban Arved Heller ◽  
Qian Sun ◽  
Marco Schwarzer ◽  
Joachim Diegmann ◽  
...  

The trace element copper (Cu) is part of our nutrition and essentially needed for several cuproenzymes that control redox status and support the immune system. In blood, the ferroxidase ceruloplasmin (CP) accounts for the majority of circulating Cu and serves as transport protein. Both Cu and CP behave as positive, whereas serum selenium (Se) and its transporter selenoprotein P (SELENOP) behave as negative acute phase reactants. In view that coronavirus disease (COVID-19) causes systemic inflammation, we hypothesized that biomarkers of Cu and Se status are regulated inversely, in relation to disease severity and mortality risk. Serum samples from COVID-19 patients were analysed for Cu by total reflection X-ray fluorescence and CP was quantified by a validated sandwich ELISA. The two Cu biomarkers correlated positively in serum from patients with COVID-19 (R = 0.42, p < 0.001). Surviving patients showed higher mean serum Cu and CP concentrations in comparison to non-survivors ([mean+/-SEM], Cu; 1475.9+/-22.7 vs. 1317.9+/-43.9 µg/L; p < 0.001, CP; 547.2.5 +/- 19.5 vs. 438.8+/-32.9 mg/L, p = 0.086). In contrast to expectations, total serum Cu and Se concentrations displayed a positive linear correlation in the patient samples analysed (R = 0.23, p = 0.003). Serum CP and SELENOP levels were not interrelated. Applying receiver operating characteristics (ROC) curve analysis, the combination of Cu and SELENOP with age outperformed other combinations of parameters for predicting risk of death, yielding an AUC of 95.0%. We conclude that the alterations in serum biomarkers of Cu and Se status in COVID-19 are not compatible with a simple acute phase response, and that serum Cu and SELENOP levels contribute to a good prediction of survival. Adjuvant supplementation in patients with diagnostically proven deficits in Cu or Se may positively influence disease course, as both increase in survivors and are of crucial importance for the immune response and antioxidative defence systems.


2014 ◽  
Vol 6 (2) ◽  
pp. 96-101 ◽  
Author(s):  
KV Vandana ◽  
KL Vandana

Abstract The acute phase refers to physiological and metabolic alterations that ensue immediately after onset of infection or tissue injury. A variety of changes in the organism act in concern to neutralize the inflammatory agent and faster healing of damaged tissues. In contrast with the specificity of cellular and humoral immunity, the acute phase changes are nonspecific and occur in response to many conditions. Periodontal disease is a chronic inflammatory process that occurs in response to a predominantly Gram-negative bacterial infection originating from dental plaque. Increased levels of acute-phase proteins have been noted with gingival inflammation, including during experimental gingivitis and periodontitis, reflecting the locally stressed environment. Here, an attempt is made to discuss the importance of acute phase reactants. How to cite this article Vandana KV, Vandana KL. Acute phase reactants - A review. CODS J Dent 2014;6;96-101


2004 ◽  
Vol 91 (05) ◽  
pp. 861-872 ◽  
Author(s):  
Tiny Hoekstra ◽  
Evert Schouten ◽  
Cees Kluft ◽  
Johanna Geleijnse

SummaryThe habitual level of PAI-1 is influenced by many factors, of which obesity and insulin resistance are the most important. It is possible to reduce plasma PAI-1 by changes in life style, e.g. weight reduction and physical activity. Data on potential interactions between environmental and metabolic variables on one hand, and the 4G/5G-polymorphism on the other hand, are still scarce. It becomes more and more clear that PAI-1 may possibly not be a major (causal) factor in cardiovascular disease, but its role in inflammation deserves further attention. In the presence of the 4G-allele not only the PAI-1 response was more pronounced, but also the response of other acute-phase reactants, which implies that the increases of these reactants are secondary to the increase in PAI-1. A myocardial infarction also provokes an acute phase response. It can thus be hypothesized that the 4G-allele might exacerbate tissue injury during the acute phase after a myocardial infarction, and thereby negatively affect the prognosis.


1985 ◽  
Vol 4 (1) ◽  
pp. 71-78 ◽  
Author(s):  
R. F. Dyck ◽  
M.I.C. Issa ◽  
S.L. Rogers ◽  
F. Murphy ◽  
G.G. Khachatourians

The effects of T-2 toxin on a murine model of the acute phase response were studied. Two murine acute phase reactants, serum amyloid P component and plasma fibronectin, were measured after subcutaneous and intraperitoneal administration of T-2 toxin in varying doses. No acute phase response was observed. Furthermore, T-2 toxin also blocked the acute phase reaction to subcutaneous AgNO3 in a dose-dependent fashion. These observations were not explained by damage to liver, the site of synthesis of acute phase proteins. Since the acute phase response is an immediate physiological reaction to tissue injury and may be a nonspecific participant in the repair phenomenon, its abrogation by T-2 toxin may contribute to the toxicity of this trichothecene mycotoxin.


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