Hyaluronan turnover in relation to infection and sepsis

Berg, Sören

doi:10.1046/j.1365-2796.1997.00177.x

Cited by 24 publications

(21 citation statements)

References 27 publications

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“…The magnitude of increase in both analytes was similar across the 3 patient groups and has previously been reported for HA during standard Interferon treatment 22, 23 . Hyaluronic acid is known to be cleared by liver sinusoids and the enhanced hepatic blood flow as a result of ribavirin induced anemia could have led to increased levels during treatment as has been noted in septic patients with a hyperdynamic circulation 27 . Alternatively, interferon treatment could reduce endothelial cell uptake of HA in the liver 22 .…”

Section: Discussionmentioning

confidence: 99%

Serum Fibrosis Marker Levels Decrease After Successful Antiviral Treatment in Chronic Hepatitis C Patients With Advanced Fibrosis

Fontana

Bonkovsky

Naishadham

et al. 2009

Clinical Gastroenterology and Hepatology

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Section: Discussionmentioning

confidence: 99%

Serum Fibrosis Marker Levels Decrease After Successful Antiviral Treatment in Chronic Hepatitis C Patients With Advanced Fibrosis

Fontana

Bonkovsky

Naishadham

et al. 2009

Clinical Gastroenterology and Hepatology

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“…5) in patients with respiratory failure may not only reflect ongoing glycocalyx degradation but also could indicate an impairment of glycosaminoglycan clearance. Although hepatic or renal dysfunction may delay clearance of circulating glycosaminoglycans (32)(33)(34), the relative homogeneity of indices of renal function (blood urea nitrogen, creatinine) and hepatic function (bilirubin, international normalized ratio) across groups (Table 1) suggests that the observed glycosaminoglycan signatures are not the primary consequence of aberrant liver or kidney clearance. Our data, however, cannot exclude subtle abnormalities in renal and/or hepatic function that are not captured by these common indices of organ function.…”

Section: Discussionmentioning

confidence: 99%

The Circulating Glycosaminoglycan Signature of Respiratory Failure in Critically Ill Adults

Schmidt

et al. 2014

Journal of Biological Chemistry

129

137

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Background: Endothelial glycocalyx degradation contributes to the pathogenesis of critical illness. Results: Mechanically ventilated subjects exhibited plasma glycocalyx breakdown signatures (glycosaminoglycan fragments) characteristic of direct versus indirect etiologies of respiratory failure. Conclusion: Circulating glycosaminoglycans provide insight into respiratory failure pathophysiology. Significance: This is the first study to characterize circulating glycosaminoglycans during critical illness, offering insight into the mechanisms underlying respiratory failure.

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“…Numerous physiological changes such as injury, shock (47,48), heat (49), and cold (7), increase HA concentration locally and systematically. HA fragment sizes are altered in these conditions, and altered sizes of HA show different effects on host cells.…”

Section: Discussionmentioning

confidence: 99%

NLRP3/Cryopyrin Is Necessary for Interleukin-1β (IL-1β) Release in Response to Hyaluronan, an Endogenous Trigger of Inflammation in Response to Injury

Yamasaki¹,

Muto²,

Taylor³

et al. 2009

Journal of Biological Chemistry

255

191

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Inflammation under sterile conditions is a key event in autoimmunity and following trauma. Hyaluronan, a glycosaminoglycan released from the extracellular matrix after injury, acts as an endogenous signal of trauma and can trigger chemokine release in injured tissue. Here, we investigated whether NLRP3/ cryopyrin, a component of the inflammasome, participates in the inflammatory response to injury or the cytokine response to hyaluronan. Mice with a targeted deletion in cryopyrin showed a normal increase in Cxcl2 in response to sterile injuries but had decreased inflammation and release of interleukin-1␤ (IL-1␤). Similarly, the addition of hyaluronan to macrophages derived from cryopyrin-deficient mice increased release of Cxcl2 but did not increase IL-1␤ release. To define the mechanism of hyaluronan-mediated activation of cryopyrin, elements of the hyaluronan recognition process were studied in detail. IL-1␤ release was inhibited in peritoneal macrophages derived from CD44-deficient mice, in an MH-S macrophage cell line treated with antibodies to CD44, or by inhibitors of lysosome function. The requirement for CD44 binding and hyaluronan internalization could be bypassed by intracellular administration of hyaluronan oligosaccharides (10 -18-mer) in lipopolysaccharide-primed macrophages. Therefore, the action of CD44 and subsequent hyaluronan catabolism trigger the intracellular cryopyrin 3 IL-1␤ pathway. These findings support the hypothesis that hyaluronan works through IL-1␤ and the cryopyrin system to signal sterile inflammation.Inflammation, as defined by changes in vascular permeability and leukocyte recruitment, is an essential step for the control of microbial invasion. Specific microbial products trigger this process through a diverse array of innate immune pattern recognition receptors. However, an inflammatory response independent of infection is also an important process for maintenance of biological homeostasis. For example, normal wound healing requires a controlled inflammatory response to enable the recruitment of monocytes and the release of growth factors required for repair. This response can occur in the absence of microbial stimuli. Furthermore, inflammation and the release of proinflammatory mediators is also associated with many diseases such as rheumatoid arthritis and Crohn disease (1). These diseases are not well understood in terms of their triggers but rather are described by the subsequent release of proinflammatory mediators. Identification of the triggers of sterile inflammation represents an important goal with immediate diagnostic and therapeutic significance.Recent work has begun to elucidate pathways of inflammation that occur in the absence of microbial stimuli. Stress signals such as heat-shock proteins, intracellular components of necrotic cells not normally seen by immune cells, and components of the extracellular matrix have all been implicated as endogenous triggers of injury (2-4). Among this group is the glycosaminoglycan hyaluronan (HA), 6 an important structural compo...

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Hyaluronan turnover in relation to infection and sepsis

Cited by 24 publications

References 27 publications

Serum Fibrosis Marker Levels Decrease After Successful Antiviral Treatment in Chronic Hepatitis C Patients With Advanced Fibrosis

Serum Fibrosis Marker Levels Decrease After Successful Antiviral Treatment in Chronic Hepatitis C Patients With Advanced Fibrosis

The Circulating Glycosaminoglycan Signature of Respiratory Failure in Critically Ill Adults

NLRP3/Cryopyrin Is Necessary for Interleukin-1β (IL-1β) Release in Response to Hyaluronan, an Endogenous Trigger of Inflammation in Response to Injury

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