Exploration of Acute Phase Proteins and Inflammatory Cytokines in Early Stage Diagnosis of Acute Mountain Sickness

2018 ◽  
Vol 19 (2) ◽  
pp. 170-177 ◽  
Author(s):  
Chi Wang ◽  
Hui Jiang ◽  
Jinyan Duan ◽  
Jingwen Chen ◽  
Qi Wang ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Acute Phase ◽  
Acute Phase Proteins ◽  
Early Stage ◽  
Acute Mountain Sickness ◽  
Mountain Sickness

scholarly journals Adipokines: inflammation and the pleiotropic role of white adipose tissue

2004 ◽  
Vol 92 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Paul Trayhurn ◽  
I. Stuart Wood
Keyword(s):  
Adipose Tissue ◽  
Growth Factor ◽  
Inflammatory Cytokines ◽  
Acute Phase ◽  
White Adipose Tissue ◽  
Acute Phase Proteins ◽  
Endocrine Function ◽  
Low Grade ◽  
Circulating Levels

White adipose tissue is now recognised to be a multifunctional organ; in addition to the central role of lipid storage, it has a major endocrine function secreting several hormones, notably leptin and adiponectin, and a diverse range of other protein factors. These various protein signals have been given the collective name ‘adipocytokines’ or ‘adipokines’. However, since most are neither ‘cytokines’ nor ‘cytokine-like’, it is recommended that the term ‘adipokine’ be universally adopted to describe a protein that is secreted from (and synthesised by) adipocytes. It is suggested that the term is restricted to proteins secreted from adipocytes, excluding signals released only by the other cell types (such as macrophages) in adipose tissue. Theadipokinome(which together with lipid moieties released, such as fatty acids and prostaglandins, constitute thesecretomeof fat cells) includes proteins involved in lipid metabolism, insulin sensitivity, the alternative complement system, vascular haemostasis, blood pressure regulation and angiogenesis, as well as the regulation of energy balance. In addition, there is a growing list of adipokines involved in inflammation (TNFα, IL-1β, IL-6, IL-8, IL-10, transforming growth factor-β, nerve growth factor) and the acute-phase response (plasminogen activator inhibitor-1, haptoglobin, serum amyloid A). Production of these proteins by adipose tissue is increased in obesity, and raised circulating levels of several acute-phase proteins and inflammatory cytokines has led to the view that the obese are characterised by a state of chronic low-grade inflammation, and that this links causally to insulin resistance and the metabolic syndrome. It is, however, unclear as to the extent to which adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and whether there is a generalised or local state of inflammation. The parsimonious view is that the increased production of inflammatory cytokines and acute-phase proteins by adipose tissue in obesity relates primarily to localised events within the expanding fat depots. It is suggested that these events reflect hypoxia in parts of the growing adipose tissue mass in advance of angiogenesis, and involve the key controller of the cellular response to hypoxia, the transcription factor hypoxia inducible factor-1.

Some mechanisms regulating nutrient utilisation in livestock during immune activation: an overview

2004 ◽  
Vol 44 (5) ◽  
pp. 453 ◽  
Author(s):  
I. G. Colditz
Keyword(s):  
Fatty Acid ◽  
Inflammatory Cytokines ◽  
Acute Phase ◽  
Immune Activation ◽  
Acute Phase Proteins ◽  
Tissue Injury ◽  
Acid Synthesis ◽  
Acid Uptake ◽  
Nutrient Utilisation ◽  
Pro Inflammatory Cytokines

The pro-inflammatory cytokines, IL-1, IL-6, TNFα and IFN α/β, produced during immune activation and tissue injury, override control of nutrient utilisation by the hypothalamic-somatotropic axis. The many effects of these cytokines include induction of fever and sickness behaviour, reduced fatty acid uptake by adipose tissue, reduced protein synthesis and enhanced protein breakdown in skeletal muscle, and gluconeogenesis, increased fatty acid synthesis and synthesis of acute phase proteins in the liver. Resistance to the effects of insulin, GH and IGF-1 is induced in adipose tissues, liver and muscle, at least in part through induction by pro-inflammatory cytokines of SOCS proteins which inhibit signal transduction and activation of gene transcription via the JAK/STAT pathway. These homeorhetic changes mobilise nutrients to fuel host defence responses. While an understanding of the mechanisms contributing to the catabolic state have arisen largely from studies of sepsis, trauma and acute challenge with biological mediators of the acute phase response, recent evidence in livestock suggests that graded production of pro-inflammatory cytokines during challenge with pathogens or subclinical infection can induce an incremental reduction in nutrient accretion in products of commercial value from livestock. This relationship highlights the value of good hygiene and reduced stress to improved feed utilisation for growth.

Metabolic effects of host defence responses during gastrointestinal parasitism in sheep

2003 ◽  
Vol 43 (12) ◽  
pp. 1437 ◽  
Author(s):  
I. G. Colditz
Keyword(s):  
Inflammatory Cytokines ◽  
Acute Phase ◽  
De Novo ◽  
Acute Phase Proteins ◽  
Gastrointestinal Nematode ◽  
Host Defence ◽  
Metabolic Effects ◽  
Future Research ◽  
Nutrient Utilisation ◽  
Pro Inflammatory Cytokines

Following stimulation of the immune system, tissue trauma, or exposure to some stressors, there can be activation of the acute phase response (APR). This is a primitive defence reaction that helps protect the host against noxious insults. Part of the response involvess a change in priorities for nutrient utilisation, when the pro-inflammatory cytokines IL-1α/β, TNFα, IL-6 and IFNα/β override the normal hypothalamic-somatotropic control of nutrient utilisation. The pro-inflammatory cytokines reduce protein synthesis and increase protein catabolism in muscle, induce synthesis of acute phase proteins in liver, and decrease de novo fatty acid synthesis and increase lipolysis in adipose tissue. In the central nervous system there is induction of fever, which increases metabolic rate, and induction of sickness behaviour. There are few reports in the literature of studies on the APR during gastrointestinal nematode (GIN) infection in sheep. However, IL-6 message is present in mucosa during Trichostrongylus colubriformis infection and mast cells in many species contain preformed TNFα. The changes in appetite, growth and nitrogen metabolism seen during GIN parasitism in sheep are in accord with the systemic effects of the APR. This review reports studies on activation of the APR in mastitis and fly strike, and the effects of APR on wool growth in high and low tensile strength genotypes and during Haemonchus contortus infection. The modified capacity of tissues to take up amino acids during pro-inflammatory cytokine perturbation of nutrient utilisation may limit the capacity for dietary supplementation to remedy the cost of host defence. Genetic variation may occur in production of pro-inflammatory cytokines or in tissue sensitivity to pro-inflammatory cytokines during GIN infection and may provide a basis for selection for resilience. Some questions for future research are identified.

Lymphocyte Phenotype Alterations, Pro-Inflammatory Cytokines and Acute Phase Proteins Following Repeated Bouts of Mountainous Hill-Running

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S412-S413
Author(s):  
Richard J. Simpson ◽  
Keith Guy ◽  
Greg P. Whyte ◽  
Natalie Middleton ◽  
James R. Black ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Acute Phase ◽  
Acute Phase Proteins ◽  
Lymphocyte Phenotype ◽  
Pro Inflammatory Cytokines

scholarly journals Administration of the Mitochondrial Permeability Transition Pore Inhibitor, TRO40303, prior to Primary Percutaneous Coronary Intervention, Does Not Affect the Levels of Pro-Inflammatory Cytokines or Acute-Phase Proteins

Cardiology ◽  
2017 ◽  
Vol 138 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Noreen Butt ◽  
Lena K. Bache-Mathiesen ◽  
Jan Erik Nordrehaug ◽  
Vegard Tuseth ◽  
Peter Scott Munk ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Acute Phase ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Acute Phase Proteins ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Coronary Intervention ◽  
Percutaneous Coronary ◽  
Pro Inflammatory Cytokines

Objectives: In the MITOCARE study, reperfusion injury was not prevented after administration of the mitochondrial permeability transition pore (mPTP) opening inhibitor, TRO40303, in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). The effects of TRO40303 on pro-inflammatory cytokines and acute-phase proteins were assessed. Methods: STEMI patients (n = 163, mean age 62 years) with chest pain within 6 h before admission for pPCI were randomized to intravenous bolus of TRO40303 (n = 83) or placebo (n = 80) prior to reperfusion. We tested whether the groups differed in levels of IL-1β, IL-6, IL-10, TNF, and high-sensitive C-reactive protein at various time points (0, 12, and 72 h) after PCI. Further, potential differences between groups in the change of biomarker levels between 0 and 72 h, 0 and 12 h, and 12 and 72 h were tested. Results: There were no statistically significant differences between the two groups, neither in levels of pro-inflammatory cytokines nor in levels of acute-phase proteins, and there were no statistically significant differences in the change of biomarker levels between the groups considering the time intervals from 0 to 72 h, from 0 to 12 h, and from 12 to 72 h. Conclusion: The administration of the mPTP, TRO40303, prior to reperfusion does not alter the pharmacokinetics of pro-inflammatory cytokines or acute-phase proteins during the first 72 h after PCI.

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