Acute inflammation, acute phase serum amyloid A and cholesterol metabolism in the mouse

Lindhorst, Elaine; Young, Dorothy C.; Bagshaw, William; Hyland, Meaghen; Kisilevsky, Robert

doi:10.1016/s0167-4838(96)00227-0

Cited by 102 publications

(88 citation statements)

References 53 publications

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“…On the basis of this result, 24 hr was selected as the time for analysis of SAA and SAP in subsequent experiments. Basal levels of SAA shown here are comparable to those reported by others (1-5 μg/ml) (Lindhorst et al 1997). …”

Section: Resultssupporting

confidence: 92%

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

Pruett

2006

Alcohol

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Binge ethanol (EtOH) consumption suppresses inflammatory responses and resistance to infection, but paradoxically it is associated with increased levels of acute phase proteins (which are indicators of inflammation) and an increased risk of inflammation mediated pathologies such as cardiovascular disease and cirrhosis of the liver. The latter effect may be mediated by increased translocation of bacteria leading to activation of toll-like receptor 4 (TLR4). In this study, the dose-response and time course of the effects of EtOH alone or EtOH in conjunction with a TLR 4 agonist (LPS) were evaluated in mice. Ethanol alone at a dosage of 6 g/kg induced an acute phase response (as indicated by ELISA for serum amyloid A and serum amyloid P) that was maximal 24 hr after dosing. Lower dosages of EtOH did not have this effect but did suppressed the acute phase response to LPS and the production of IL-6 up to 3 hr after dosing. EtOH at 6 g/kg did not induce an acute phase response in C3H/HeJ (TLR4 mutant) mice, indicating that this response is mediated through TLR4. These results provide a resolution for the apparently paradoxical pro-and anti-inflammatory actions of EtOH with regard to acute phase responses.

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Section: Resultssupporting

confidence: 92%

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

Pruett

2006

Alcohol

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“…60 As part of the systemic inflammatory response A-SAA displaces ApoA-1 from HDL to become the major HDL-associated apoprotein in inflammation. 61,62 In vitro studies have demonstrated that A-SAA-enriched HDL may be pro-atherogenic through a three-to fourfold higher affinity for macrophages and an increased affinity for uptake into vascular ECs when compared with unenriched HDL. 63 A-SAA has been implicated in a number of diseases characterized both by inflammation and increased cardiovascular mortality, including diabetes, the metabolic syndrome, malignancy, and primary cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

A Role for the High-Density Lipoprotein Receptor SR-B1 in Synovial Inflammation via Serum Amyloid-A

Mullan

McCormick

Connolly

et al. 2010

The American Journal of Pathology

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“…Although the precise function of amyloid A proteins is unknown, they are thought to play an important role in modulating the innate host defense against inflammatory agents and are involved in cholesterol transport and metabolism (19,(25)(26)(27). In humans, SAA3 has been postulated to be a pseudogene in some studies (28,29), although in another study the human SAA3 gene was expressed in mammary gland epithelial cells in response to either prolactin or LPS (30).…”

Section: Serum Amyloid A3 Induction In Preterm Lambsmentioning

confidence: 99%

Pulmonary and Systemic Induction of SAA3 After Ventilation and Endotoxin in Preterm Lambs

et al. 2005

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Serum amyloid A (SAA), an acute phase reactant (APR) protein, is induced in liver during systemic inflammation. Serum amyloid A3 (SAA3), an isoform of SAA, is induced in both liver and extra hepatic sites in response to proinflammatory stimuli such as cytokines. Previously, we showed a modest increase in plasma cytokine levels in a preterm lamb model of lung injury. The study objective was to determine the relative contributions of lung and liver to the acute phase response during postnatal lung injury. Preterm (130d) and near term (141d) newborn lambs (term ϭ 150d) were randomized to either no ventilation (controls), ventilation ϩ intratracheal (IT) endotoxin (endo) or ventilation ϩ IT saline. A group of near term lambs were exposed to ventilation ϩ IV endotoxin. In the lungs, ventilation alone increased SAA3 mRNA 3-and 13-fold while ventilation ϩ IT endotoxin increased SAA3 mRNA 64 and 366-fold above controls in preterm and near term lambs, respectively. In the liver, SAA3 mRNA was induced by ventilation alone (three-fold) and ventilation ϩ IT endotoxin (45-fold) above controls in both preterm and near term animals. Ventilation ϩ IV endotoxin caused the highest increase in SAA3 mRNA (212- The acute phase of the systemic inflammatory response is characterized by the hepatic synthesis and increased plasma concentrations of acute phase reactants (APR) such as heat shock proteins, C reactive protein (CRP), and the serum amyloids (1-3). The serum amyloid A family of proteins is one of the major APR whose plasma levels can increase up to 1000-fold in response to inflammation (4). Several isoforms of the SAA protein are conserved across species. The liver is the main source of SAA1 and SAA2 isoforms whereas SAA3 isoform expression is increased in liver as well as extra hepatic tissues (4 -7). We identified SAA3 as an endotoxin inducible gene in the fetal lung using subtraction hybridization of endotoxin versus saline exposed lung mRNA (8). No information is available regarding the biology of SAA3 in preterm newborn animals exposed to postnatal lung injury induced by mechanical ventilation, oxygen or endotoxin.Mechanical ventilation and pulmonary infections frequently cause lung injury in preterm infants. Mechanical ventilation contributes to neonatal morbidity and mortality (9,10) by causing lung inflammation with the induction of the proinflammatory cytokine cascade (11-13). Intratracheal endotoxin induces both lung inflammation and a systemic inflammatory response in preterm and term ventilated lambs (14). Whether there is induction of a lung acute phase reactant response in these models is not known. Furthermore, the occurrence of a systemic acute phase reactant response on lung exposure to pro-inflammatory stimuli is not well characterized. We hypothesized that SAA3 mRNA expression would increase in the preterm newborn lung postnatally exposed to proinflammatory stimuli. We, therefore, examined the effect of mechanical ventilation with or without endotoxin exposure on SAA3 mRNA induction in preterm and near term ...

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Acute inflammation, acute phase serum amyloid A and cholesterol metabolism in the mouse

Cited by 102 publications

References 53 publications

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

An explanation for the paradoxical induction and suppression of an acute phase response by ethanol

A Role for the High-Density Lipoprotein Receptor SR-B1 in Synovial Inflammation via Serum Amyloid-A

Pulmonary and Systemic Induction of SAA3 After Ventilation and Endotoxin in Preterm Lambs

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