M-ficolin concentrations in cord blood are related to circulating phagocytes and to early-onset sepsis

Schlapbach, Luregn J.; Kjær, Troels R.; Thiel, Steffen; Mattmann, Maika; Nelle, Mathias; Wagner, B. P.; Ammann, Roland A.; Aebi, Christoph; Jensenius, Jens C.

doi:10.1038/pr.2011.71

Cited by 15 publications

(12 citation statements)

References 29 publications

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“…In addition to its abundant presence within monocytes and granulocytes (13), M-ficolin is also located on the external surfaces of these cells, possibly via binding to sialic acids through the FBG domain (14), via interaction with the G-proteincoupled receptor GPCR43 (15), or through binding to leukosialin (CD43) (16). Upon stimulation of neutrophils, intracellular Mficolin is mobilized, resulting in the upregulation of surfacebound M-ficolin (17) and its release to the surroundings (18). Presumably, if the secreted M-ficolin then binds to nearby microorganisms, it can activate the complement system and thus initiate an antimicrobial reaction.…”

mentioning

confidence: 99%

M-Ficolin Binds Selectively to the Capsular Polysaccharides of Streptococcus pneumoniae Serotypes 19B and 19C and of a Streptococcus mitis Strain

et al. 2013

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confidence: 99%

M-Ficolin Binds Selectively to the Capsular Polysaccharides of Streptococcus pneumoniae Serotypes 19B and 19C and of a Streptococcus mitis Strain

et al. 2013

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“…[122][123][124] M-ficolin activates the complement system in a manner similar to MBL and its level is elevated in neonates with sepsis. 125…”

Section: Nod-like Receptors Retinoic Acid-inducible Protein I-like Rmentioning

confidence: 99%

Pathophysiology of Neonatal Sepsis

Wynn¹,

Wong²

2017

Fetal and Neonatal Physiology

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“…with Gram-negative and early-onset sepsis, and low H-ficolin levels have been associated with susceptibility to Gram-positive and late-onset sepsis (22,23). Low MBL levels in blood from neonates were related to an increased risk of neonatal sepsis and pneumonia (24,25).…”

Section: Lectin Pathway In Critically Ill Childrenmentioning

confidence: 99%

Lectin pathway of complement activation and relation with clinical complications in critically ill children

et al. 2013

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Background:Critically ill children are susceptible to nosocomial infections, which contribute to adverse outcomes. Deficiencies in the innate immunity lectin pathway of complement activation are implicated in a child's vulnerability to infections in conditions such as cancer, but the role during critical illness remains unclear. We hypothesized that low on-admission levels of the pathway proteins are, in part, genetically determined and associated with susceptibility to infectious complications and adverse outcomes. Methods: We studied protein levels of mannose-binding lectin (MBL), H-ficolin and M-ficolin, three MBL-associatedserine proteases (MASPs) and MBL-associated protein (MAp44), and relation with functional genetic polymorphisms, in 130 healthy children and upon intensive care unit (ICU) admission in 700 critically ill children of a randomized study on glycemic control. results: Levels of MASP-1, MASP-2, MASP-3, and MAp-44 were lower and the levels of M-ficolin were higher in ICU patients on admission than those in matched healthy controls. Only a low on-admission MASP-3 level was independently associated with risk of new ICU infections and prolonged ICU stay, after correcting for other risk factors. On-admission MASP-3 varied with age, illness severity, and genetic variation. conclusion: Low on-admission MASP-3 levels in critically ill children were independently associated with subsequent acquisition of infection and prolonged ICU stay. The biological explanation needs further investigation.

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M-ficolin concentrations in cord blood are related to circulating phagocytes and to early-onset sepsis

Cited by 15 publications

References 29 publications

M-Ficolin Binds Selectively to the Capsular Polysaccharides of Streptococcus pneumoniae Serotypes 19B and 19C and of a Streptococcus mitis Strain

M-Ficolin Binds Selectively to the Capsular Polysaccharides of Streptococcus pneumoniae Serotypes 19B and 19C and of a Streptococcus mitis Strain

Pathophysiology of Neonatal Sepsis

Lectin pathway of complement activation and relation with clinical complications in critically ill children

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