Plasmodium berghei malaria: effect of acute phase serum on immunity generated in rats by infection and by vaccination

1987 ◽  
Vol 74 (2) ◽  
pp. 116-122 ◽  
Author(s):  
J. D. Alder ◽  
B. Brooks-Alder ◽  
J. P. Kreier
Keyword(s):  
Acute Phase ◽  
Plasmodium Berghei ◽  
Acute Phase Serum

scholarly journals Rabbit and rat C-reactive proteins bind apolipoprotein B-containing lipoproteins.

1984 ◽  
Vol 159 (2) ◽  
pp. 604-616 ◽  
Author(s):  
I F Rowe ◽  
A K Soutar ◽  
I M Trayner ◽  
M L Baltz ◽  
F C de Beer ◽  
...  
Keyword(s):  
Acute Phase ◽  
Apolipoprotein B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Free Form ◽  
Low Density ◽  
Serum Samples ◽  
Acute Phase Serum

Immobilized rabbit and rat C-reactive protein (CRP) were found to selectively bind apolipoprotein B (apoB)-containing lipoproteins (low density lipoprotein, LDL and very low density lipoprotein, VLDL) from whole serum in a manner similar to that previously reported with human CRP. In acute phase human serum the CRP is in a free form, not complexed with lipoprotein or any other macromolecular ligand, and in acute phase serum from most rabbits fed on a normal diet the rabbit CRP was also free. However, in acute phase serum or heparinized plasma from hypercholesterolemic rabbits part or all of the CRP was found by gel filtration and immunoelectrophoretic techniques to be complexed with beta-VLDL, an abnormal apoB-containing plasma lipoprotein present in these animals. The presence of extent in different serum samples of CRP complexed with lipoprotein correlated closely with the serum apoB concentration. The formation of complexes between native, unaggregated rabbit CRP in solution and apoB-containing lipoproteins was readily demonstrable experimentally both with the isolated proteins and in whole serum. In all cases these interactions were calcium-dependent and inhibitable by free phosphoryl choline. The present findings extend earlier work in man and the rabbit and indicate that among the C-reactive proteins from different species, which are structurally highly conserved, the capacity for selective binding to apoB-containing plasma lipoproteins is also a constant feature. These interactions may therefore be related to the in vivo function of CRP in all species and this function may in turn be relevant to pathological conditions, such as atherosclerosis, in which lipoproteins are important.

scholarly journals Investigation of the solubility and the potentials for purification of serum amyloid A (SAA) from equine acute phase serum – a pilot study

2013 ◽  
Vol 6 (1) ◽  
Author(s):  
Michelle B Christensen ◽  
Jens Christian Sørensen ◽  
Stine Jacobsen ◽  
Mads Kjelgaard-Hansen
Keyword(s):  
Pilot Study ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Acute Phase Serum

In search of the “LINK”: Acute Phase Serum Amyloid A

2011 ◽  
Vol 216 (2) ◽  
pp. 266-268
Author(s):  
Sidika Karakas ◽  
Rami Mortada ◽  
Clinical Fellow
Keyword(s):  
Acute Phase ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Acute Phase Serum

scholarly journals Posttransfusion purpura associated with an autoantibody directed against a previously undefined platelet antigen

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1458-1463
Author(s):  
RB Stricker ◽  
BH Lewis ◽  
L Corash ◽  
MA Shuman
Keyword(s):  
Acute Phase ◽  
Platelet Destruction ◽  
Autoantibody Production ◽  
Antiplatelet Antibodies ◽  
Platelet Protein ◽  
Gp 120 ◽  
Platelet Antigen ◽  
Immunoblot Technique ◽  
Posttransfusion Purpura ◽  
Acute Phase Serum

Although alloantibody against the PLA1 platelet antigen is usually found in patients with posttransfusion purpura (PTP), the mechanism of destruction of the patient's own PLA1-negative platelets is unexplained. We used a sensitive immunoblot technique to detect antiplatelet antibodies in a patient with classic PTP. The patient's acute-phase serum contained antibodies against three proteins present in control (PLA1-positive) platelets: an antibody that bound to a previously unrecognized platelet protein of mol wt 120,000 [glycoprotein (GP) 120], antibodies that bound to PLA1 (mol wt 90,000), and an epitope of GP IIb (mol wt 140,000). The antibodies against PLA1 and GP IIb did not react with the patient's own PLA1-negative platelets, control PLA1-negative platelets, or thrombasthenic platelets. In contrast, the antibody against GP 120 recognized this protein in all three platelet preparations, but not in Bernard-Soulier or Leka (Baka)-negative platelets. Antibody against GP 120 was not detected in the patient's recovery serum, although the antibodies against PLA1 and GP IIb persisted. F(ab)2 prepared from the patient's acute-phase serum also bound to GP 120. These results suggest that in PTP, transient autoantibody production may be responsible for autologous (PLA1-negative) platelet destruction. In addition, alloantibodies against more than one platelet alloantigen may be found in this disease. The nature of the GP 120 autoantigen and the GP IIb- related alloantigen defined by our patient's serum remains to be determined.

Age-Dependent Evaluation of Immunoglobulin G Response after Chikungunya Virus Infection

2021 ◽  
Author(s):  
Harshad P. Patil ◽  
Mrunal Gosavi ◽  
Akhilesh C. Mishra ◽  
Vidya A. Arankalle
Keyword(s):  
Acute Phase ◽  
Chikungunya Virus ◽  
Indirect Elisa ◽  
Neutralizing Antibody ◽  
Antibody Prevalence ◽  
Exposure Age ◽  
Age Dependent ◽  
Antibody Titers ◽  
Binding Antibody ◽  
Acute Phase Serum

Current chikungunya antibody prevalence and titers are likely to differ based on exposure rates before the 2006 reemergence. For vaccine usage, such data are of immense importance. This study addresses age-stratified IgG titers and its subtypes in Pune, India, endemic for the disease. One hundred seventy serum pools (791 individuals with prior chikungunya exposure, age stratified) from exposed and 15 samples from acute disease phase were screened. Inactivated chikungunya virus (CHIKV)–based indirect ELISA was used to determine anti–CHIKV-IgG and its subtypes. Neutralizing antibody titers (plaque reduction neutralization test [PRNT]) were compared with binding antibody titers (ELISA). Anti–CHIKV-IgG titers along with IgG1 and IgG4 increased till the age-group of 11–15 years and remained comparable thereafter till > 65 years. IgG1 was the predominant IgG subtype detected in all the pools, whereas IgG4 was present in 151/170 pools. Strong correlation of IgG1 was obtained with CHIKV–PRNT50 titers. None of the sample had anti–CHIKV-IgG2, whereas five pools had IgG3 antibody. In the acute-phase serum sample, IgG1 was present in all the samples, whereas IgG4 was present in 8/15 samples. IgG4 was predominant in four samples. During acute phase and at different times postinfection, IgG1 circulated in high titers followed by IgG4. Higher antibody titers in adults reflect reexposures. The data will prove useful in assessing immune response to CHIKV vaccine.

scholarly journals Posttransfusion purpura associated with an autoantibody directed against a previously undefined platelet antigen

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1458-1463 ◽  
Author(s):  
RB Stricker ◽  
BH Lewis ◽  
L Corash ◽  
MA Shuman
Keyword(s):  
Acute Phase ◽  
Platelet Destruction ◽  
Autoantibody Production ◽  
Antiplatelet Antibodies ◽  
Platelet Protein ◽  
Gp 120 ◽  
Platelet Antigen ◽  
Immunoblot Technique ◽  
Posttransfusion Purpura ◽  
Acute Phase Serum

Abstract Although alloantibody against the PLA1 platelet antigen is usually found in patients with posttransfusion purpura (PTP), the mechanism of destruction of the patient's own PLA1-negative platelets is unexplained. We used a sensitive immunoblot technique to detect antiplatelet antibodies in a patient with classic PTP. The patient's acute-phase serum contained antibodies against three proteins present in control (PLA1-positive) platelets: an antibody that bound to a previously unrecognized platelet protein of mol wt 120,000 [glycoprotein (GP) 120], antibodies that bound to PLA1 (mol wt 90,000), and an epitope of GP IIb (mol wt 140,000). The antibodies against PLA1 and GP IIb did not react with the patient's own PLA1-negative platelets, control PLA1-negative platelets, or thrombasthenic platelets. In contrast, the antibody against GP 120 recognized this protein in all three platelet preparations, but not in Bernard-Soulier or Leka (Baka)-negative platelets. Antibody against GP 120 was not detected in the patient's recovery serum, although the antibodies against PLA1 and GP IIb persisted. F(ab)2 prepared from the patient's acute-phase serum also bound to GP 120. These results suggest that in PTP, transient autoantibody production may be responsible for autologous (PLA1-negative) platelet destruction. In addition, alloantibodies against more than one platelet alloantigen may be found in this disease. The nature of the GP 120 autoantigen and the GP IIb- related alloantigen defined by our patient's serum remains to be determined.

Characterization of the acute phase serum protein response in pigs

1994 ◽  
Vol 15 (1) ◽  
pp. 672-676 ◽  
Author(s):  
Fermín Lampreave ◽  
Nieves González-Ramón ◽  
Silvio Martínez-Ayensa ◽  
Miguel-Angel Hernández ◽  
Hans-Kristian Lorenzo ◽  
...  
Keyword(s):  
Serum Protein ◽  
Acute Phase ◽  
Protein Response ◽  
Acute Phase Serum
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