scholarly journals Relationship between gastro-intestinal complaints and endotoxaemia, cytokine release and the acute-phase reaction during and after a long-distance triathlon in highly trained men

Clinical Science â—½  
10.1042/cs0980047 â—½  
1999 â—½  
Vol 98 (1) â—½  
pp. 47-55 â—½  
Author(s):  
A. E. JEUKENDRUP â—½  
K. VET-JOOP â—½  
A. STURK â—½  
J. H. J. C. STEGEN â—½  
J. SENDEN â—½  
...  
Keyword(s):  
Creatine Kinase â—½  
Muscle Damage â—½  
Acute Phase â—½  
Endurance Exercise â—½  
Acute Phase Response â—½  
Fold Increase â—½  
C Reactive Protein â—½  
Long Distance â—½  
Reactive Protein â—½  
Ultra Endurance

The aim of the present study was to establish whether gastro-intestinal (GI) complaints observed during and after ultra-endurance exercise are related to gut ischaemia-associated leakage of endotoxins [lipopolysaccharide (LPS)] into the circulation and associated cytokine production. Therefore we collected blood samples from 29 athletes before, immediately after, and 1, 2 and 16 h after a long-distance triathlon for measurement of LPS, tumour necrosis factor-α and interleukin-6 (IL-6). As the cytokine response would trigger an acute-phase response, characteristic variables of these responses were also measured, along with creatine kinase (CK) to obtain an indicator of muscle damage. There was a high incidence (93% of all participants) of GI symptoms; 45% reported severe complaints and 7% of the participants abandoned the race because of severe GI distress. Mild endotoxaemia (5–15 pg/ml) was evident in 68% of the athletes immediately after the race, as also indicated by a reduction in IgG anti-LPS levels. In addition, we observed production of IL-6 (27–fold increase immediately after the race), leading to an acute-phase response (20-fold increase in C-reactive protein and 12% decrease in pre-albumin 16 h after the race). The extent of endotoxaemia was not correlated with the GI complaints or the IL-6 response, but did show a correlation with the elevation in C-reactive protein (rs 0.389; P = 0.037). Creatine kinase levels were increased significantly immediately post-race, and increased further in the follow-up period. Creatine kinase levels did not correlate with those of either IL-6 or C-reactive protein. It is therefore concluded that LPS does enter the circulation after ultra-endurance exercise and may, together with muscle damage, be responsible for the increased cytokine response and hence GI complaints in these athletes.

scholarly journals Secretion of C-reactive protein becomes more efficient during the course of the acute phase response.

1985 â—½  
Vol 260 (7) â—½  
pp. 4169-4173 â—½  
Author(s):  
S S Macintyre â—½  
I Kushner â—½  
D Samols
Keyword(s):  
Acute Phase â—½  
Acute Phase Response â—½  
Phase Response â—½  
C Reactive Protein â—½  
Reactive Protein

Acute phase response after myocardial infarction: Correlation between serum levels of cytokines and C-reactive protein

10.1007/bf01649312 â—½  
1990 â—½  
Vol 68 (21) â—½  
pp. 1083-1083 â—½  
Author(s):  
H. Tilg â—½  
J. Mair â—½  
M. Herold â—½  
W. E. Aulitzky â—½  
P. Lechleitner â—½  
...  
Keyword(s):  
Myocardial Infarction â—½  
Acute Phase â—½  
Acute Phase Response â—½  
Serum Levels â—½  
Phase Response â—½  
C Reactive Protein â—½  
Reactive Protein

The acute phase response and C-reactive protein

2020 â—½  
pp. 2199-2207
Author(s):  
Mark B. Pepys
Keyword(s):  
Acute Phase â—½  
Acute Phase Response â—½  
Serum Amyloid A â—½  
Acute Phase Proteins â—½  
Phase Response â—½  
Serum Amyloid â—½  
C Reactive Protein â—½  
Reactive Protein â—½  
Amyloid A â—½  
Serum Amyloid A Protein

The acute phase response—trauma, tissue necrosis, infection, inflammation, and malignant neoplasia induce a complex series of nonspecific systemic, physiological, and metabolic responses including fever, leucocytosis, catabolism of muscle proteins, greatly increased de novo synthesis and secretion of a number of ‘acute phase’ plasma proteins, and decreased synthesis of albumin, transthyretin, and high- and low-density lipoproteins. The altered plasma protein concentration profile is called the acute phase response. Acute phase proteins—these are mostly synthesized by hepatocytes, in which transcription is controlled by cytokines including interleukin 1, interleukin 6, and tumour necrosis factor. The circulating concentrations of complement proteins and clotting factors increase by up to 50 to 100%; some of the proteinase inhibitors and α‎1-acid glycoprotein can increase three- to fivefold; but C-reactive protein (CRP) and serum amyloid A protein (an apolipoprotein of high-density lipoprotein particles) are unique in that their concentrations can change by more than 1000-fold. C-reactive protein—this consists of five identical, nonglycosylated, noncovalently associated polypeptide subunits. It binds to autologous and extrinsic materials which contain phosphocholine, including bacteria and their products. Ligand-bound CRP activates the classical complement pathway and triggers the inflammatory and opsonizing activities of the complement system, thereby contributing to innate host resistance to pneumococci and probably to recognition and safe ‘scavenging’ of cellular debris. Clinical features—(1) determination of CRP in serum or plasma is the most useful marker of the acute phase response in most inflammatory and tissue damaging conditions. (2) Acute phase proteins may be harmful in some circumstances. Sustained increased production of serum amyloid A protein can lead to the deposition of AA-type, reactive systemic amyloid.

scholarly journals P168 Adjusting serum ferritin concentrations to remove the effects of acute-phase response in patients with IBD and iron deficiency: is using C-reactive protein sufficient?

2019 â—½  
Vol 13 (Supplement_1) â—½  
pp. S173-S173
Author(s):  
K Farrag â—½  
V Ademaj-Kospiri â—½  
I Mavrommataki â—½  
A Aksan â—½  
E Leventi â—½  
...  
Keyword(s):  
Iron Deficiency â—½  
Acute Phase â—½  
Serum Ferritin â—½  
Acute Phase Response â—½  
Phase Response â—½  
C Reactive Protein â—½  
Reactive Protein

Biology of C-Reactive Protein and the Acute Phase Response

Hospital Practice â—½  
1982 â—½  
Vol 17 (6) â—½  
pp. 67-81 â—½  
Author(s):  
Henry Gewurz
Keyword(s):  
Acute Phase â—½  
Acute Phase Response â—½  
Phase Response â—½  
C Reactive Protein â—½  
Reactive Protein

scholarly journals Studies of translatable mRNA for rabbit C-reactive protein

Biochemical Journal â—½  
10.1042/bj2270759 â—½  
1985 â—½  
Vol 227 (3) â—½  
pp. 759-765 â—½  
Author(s):  
D Samols â—½  
S S MacIntyre â—½  
I Kushner
Keyword(s):  
Acute Phase â—½  
Acute Phase Response â—½  
Phase Response â—½  
Translation Product â—½  
C Reactive Protein â—½  
Reactive Protein â—½  
Primary Translation Product â—½  
Free Translation â—½  
Translatable Mrna

C-reactive protein (CRP) mRNA was assayed by cell-free translation of poly(A)-containing liver RNA isolated both from rabbits stimulated to undergo the acute-phase response and from unstimulated control rabbits. No CRP-related translation products were identified until the denaturant methylmercury hydroxide (CH3HgOH) was added to the RNA before cell-free translation. In the presence of the denaturant, a 24000-Da translation product was synthesized which was immunochemically identifiable as the CRP primary translation product. It is likely that rabbit CRP mRNA can form a stable intramolecular duplex which interferes with its translatability in vitro. The 24000-Da CH3HgOH-facilitated cell-free translation product was not detected in poly(A)-containing liver RNA from unstimulated animals, indicating that the concentration of translatable CRP mRNA was dramatically induced during the acute-phase response. On the basis of absorption experiments, the 24000-Da CRP primary translation product was immunochemically more closely related to denatured CRP than to native CRP.

scholarly journals C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

1999 â—½  
Vol 190 (12) â—½  
pp. 1733-1740 â—½  
Author(s):  
M. Griselli â—½  
J. Herbert â—½  
W.L. Hutchinson â—½  
K.M. Taylor â—½  
M. Sohail â—½  
...  
Keyword(s):  
Myocardial Infarction â—½  
Infarct Size â—½  
Acute Phase â—½  
Acute Phase Response â—½  
Myocardial Injury â—½  
Peak Plasma â—½  
C Reactive Protein â—½  
Reactive Protein â—½  
Coronary Ligation

Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ∼40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease.

Strenuous exercise: analogous to the acute-phase response?

Clinical Science â—½  
10.1042/cs0810677 â—½  
1991 â—½  
Vol 81 (5) â—½  
pp. 677-683 â—½  
Author(s):  
Lindsay M. Weight â—½  
Donald Alexander â—½  
Peter Jacobs
Keyword(s):  
Acute Phase â—½  
Total Protein â—½  
Protein Level â—½  
Acute Phase Response â—½  
Interleukin 1 â—½  
Phase Response â—½  
Strenuous Exercise â—½  
Iron Level â—½  
C Reactive Protein â—½  
Reactive Protein

1. It has been suggested that the physiological consequences of strenuous exercise are analogous to those of the acute-phase response. 2. In 70 male and 20 female competitive distance runners, a marked, but transient, neutrophil leucocytosis occurred immediately after these athletes completed a standard (42 km) marathon race. Concomitant significant increases were noted in the plasma cortisol levels, creatine kinase activity, C-reactive protein level, total protein level and albumin level (P <0.01). 3. The plasma fibrinogen, C-reactive protein and total protein concentrations were markedly increased both 24 h and 48 h after exercise (P <0.01). The serum haptoglobin level was significantly decreased after exercise (P <0.01), and increased 48 h later (P <0.05). There was no change in the serum iron level, total iron-binding capacity, per cent saturation of transferrin and serum ferritin level. 4. A significant increase in interleukin-1-type activity was demonstrated immediately and 24 h after exercise (P <0.01). 5. It is concluded that the metabolic sequelae of sustained exercise are similar, but not analogous, to the acute-phase response, and interleukin-1 probably plays a significant role in linking the haematological and immunological changes observed after sustained strenuous exercise.

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