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Article ; Online: Treating very preterm European infants with inhaled nitric oxide increased in-hospital mortality but did not affect neurodevelopment at 5 years of age.

Siljehav, Veronica / Gudmundsdottir, Anna / Tjerkaski, Jonathan / Aubert, Adrien M / Cuttini, Marina / Koopman, Corine / Maier, Rolf F / Zeitlin, Jennifer / Åden, Ulrika

Acta paediatrica (Oslo, Norway : 1992)

2023 Volume 113, Issue 3, Page(s) 461–470

Abstract: Aim: We examined the outcomes of using inhaled nitric oxide (iNO) to treat very preterm born (VPT) infants across Europe.: Methods: This was a sub-study of the Screening to Improve Health in Very Preterm Infants in Europe research. It focused on all ... ...

Abstract	Aim: We examined the outcomes of using inhaled nitric oxide (iNO) to treat very preterm born (VPT) infants across Europe. Methods: This was a sub-study of the Screening to Improve Health in Very Preterm Infants in Europe research. It focused on all infants born between 22 + 0 and 31 + 6 weeks/days of gestation from 2011 to 2012, in 19 regions in 11 European countries. We studied 7268 infants admitted to neonatal care and 5 years later, we followed up the outcomes of 103 who had received iNO treatment. They were compared with 3502 propensity score-matched controls of the same age who did not receive treatment. Results: All countries used iNO and 292/7268 (4.0%) infants received this treatment, ranging from 1.2% in the UK to 10.5% in France. There were also large regional variations within some countries. Infants treated with iNO faced higher in-hospital mortality than matched controls (odds ratio 2.03, 95% confidence interval 1.33-3.09). The 5-year follow-up analysis of 103 survivors showed no increased risk of neurodevelopmental impairment after iNO treatment. Conclusion: iNO was used for VPT patients in all 11 countries. In-hospital mortality was increased in infants treated with iNO, but long-term neurodevelopmental outcomes were not affected in 103 5-year-old survivors.
MeSH term(s)	Infant ; Infant, Newborn ; Humans ; Nitric Oxide ; Hospital Mortality ; Infant, Extremely Premature ; Respiratory Insufficiency ; Administration, Inhalation ; Infant, Premature, Diseases/therapy
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2023-12-23
Publishing country	Norway
Document type	Journal Article
ZDB-ID	203487-6
ISSN	1651-2227 ; 0365-1436 ; 0803-5253
ISSN (online)	1651-2227
ISSN	0365-1436 ; 0803-5253
DOI	10.1111/apa.17075
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Article: The cerebrospinal fluid proteome of preterm infants predicts neurodevelopmental outcome.

Leifsdottir, Kristin / Jost, Kerstin / Siljehav, Veronica / Thelin, Eric P / Lassarén, Philipp / Nilsson, Peter / Haraldsson, Ásgeir / Eksborg, Staffan / Herlenius, Eric

Frontiers in pediatrics

2022 Volume 10, Page(s) 921444

Abstract: Background: Survival rate increases for preterm infants, but long-term neurodevelopmental outcome predictors are lacking. Our primary aim was to determine whether a specific proteomic profile in cerebrospinal fluid (CSF) of preterm infants differs from ... ...

Abstract	Background: Survival rate increases for preterm infants, but long-term neurodevelopmental outcome predictors are lacking. Our primary aim was to determine whether a specific proteomic profile in cerebrospinal fluid (CSF) of preterm infants differs from that of term infants and to identify novel biomarkers of neurodevelopmental outcome in preterm infants. Methods: Twenty-seven preterm infants with median gestational age 27 w + 4 d and ten full-term infants were enrolled prospectively. Protein profiling of CSF were performed utilizing an antibody suspension bead array. The relative levels of 178 unique brain derived proteins and inflammatory mediators, selected from the Human Protein Atlas, were measured. Results: The CSF protein profile of preterm infants differed from that of term infants. Increased levels of brain specific proteins that are associated with neurodevelopment and neuroinflammatory pathways made up a distinct protein profile in the preterm infants. The most significant differences were seen in proteins involved in neurodevelopmental regulation and synaptic plasticity, as well as components of the innate immune system. Several proteins correlated with favorable outcome in preterm infants at 18-24 months corrected age. Among the proteins that provided strong predictors of outcome were vascular endothelial growth factor C, Neurocan core protein and seizure protein 6, all highly important in normal brain development. Conclusion: Our data suggest a vulnerability of the preterm brain to postnatal events and that alterations in protein levels may contribute to unfavorable neurodevelopmental outcome.
Language	English
Publishing date	2022-07-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2022.921444
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Article ; Online: Proteomic profiles in cerebrospinal fluid predicted death and disability in term infants with perinatal asphyxia: A pilot study.

Leifsdottir, Kristin / Thelin, Eric P / Lassarén, Philipp / Siljehav, Veronica / Nilsson, Peter / Eksborg, Staffan / Herlenius, Eric

Acta paediatrica (Oslo, Norway : 1992)

2022 Volume 111, Issue 5, Page(s) 961–970

Abstract: Aim: Perinatal asphyxia, resulting in hypoxic-ischaemic encephalopathy (HIE), has been associated with high mortality rates and severe lifelong neurodevelopmental disabilities. Our aim was to study the association between the proteomic profile in ... ...

Abstract	Aim: Perinatal asphyxia, resulting in hypoxic-ischaemic encephalopathy (HIE), has been associated with high mortality rates and severe lifelong neurodevelopmental disabilities. Our aim was to study the association between the proteomic profile in cerebrospinal fluid (CSF) and the degree of HIE and long-term outcomes. Methods: We prospectively enrolled 18-term born infants with HIE and 10-term born controls between 2000 and 2004 from the Karolinska University Hospital. An antibody suspension bead array and FlexMap3D analysis was used to characterise 178 unique brain-derived and inflammation associated proteins in their CSF. Results: Increased CSF concentrations of several brain-specific proteins were observed in the proteome of HIE patients compared with the controls. An upregulation of neuroinflammatory pathways was also noted and this was confirmed by pathway analysis. Principal component analysis revealed a gradient from favourable to unfavourable HIE grades and outcomes. The proteins that provided strong predictors were structural proteins, including myelin basic protein and alpha-II spectrin. The functional proteins included energy-related proteins like neuron-specific enolase and synaptic regulatory proteins. Increased CSF levels of 51 proteins correlated with adverse outcomes in infants with HIE. Conclusion: Brain-specific proteins and neuroinflammatory mediators in CSF may predict HIE degrees and outcomes after perinatal asphyxia.
MeSH term(s)	Asphyxia ; Asphyxia Neonatorum/complications ; Female ; Humans ; Hypoxia-Ischemia, Brain/complications ; Infant ; Infant, Newborn ; Pilot Projects ; Pregnancy ; Proteomics
Language	English
Publishing date	2022-02-17
Publishing country	Norway
Document type	Journal Article
ZDB-ID	203487-6
ISSN	1651-2227 ; 0365-1436 ; 0803-5253
ISSN (online)	1651-2227
ISSN	0365-1436 ; 0803-5253
DOI	10.1111/apa.16277
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Article ; Online: Il-1β and prostaglandin E2 attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice.

Siljehav, Veronica / Shvarev, Yuri / Herlenius, Eric

Journal of applied physiology (Bethesda, Md. : 1985)

2014 Volume 117, Issue 9, Page(s) 1027–1036

Abstract: Prostaglandin E2 (PGE2) serves as a critical mediator of hypoxia, infection, and apnea in term and preterm babies. We hypothesized that the prostaglandin E receptor type 3 (EP3R) is the receptor responsible for PGE2-induced apneas. Plethysmographic ... ...

Abstract	Prostaglandin E2 (PGE2) serves as a critical mediator of hypoxia, infection, and apnea in term and preterm babies. We hypothesized that the prostaglandin E receptor type 3 (EP3R) is the receptor responsible for PGE2-induced apneas. Plethysmographic recordings revealed that IL-1β (ip) attenuated the hypercapnic response in C57BL/6J wild-type (WT) but not in neonatal (P9) EP3R(-/-) mice (P < 0.05). The hypercapnic responses in brain stem spinal cord en bloc preparations also differed depending on EP3R expression whereby the response was attenuated in EP3R(-/-) preparations (P < 0.05). After severe hypoxic exposure in vivo, IL-1β prolonged time to autoresuscitation in WT but not in EP3R(-/-) mice. Moreover, during severe hypoxic stress EP3R(-/-) mice had an increased gasping duration (P < 0.01) as well as number of gasps (P < 0.01), irrespective of intraperitoneal treatment, compared with WT mice. Furthermore, EP3R(-/-) mice exhibited longer hyperpneic breathing efforts when exposed to severe hypoxia (P < 0.01). This was then followed by a longer period of secondary apnea before autoresuscitation occurred in EP3R(-/-) mice (P < 0.05). In vitro, EP3R(-/-) brain stem spinal cord preparations had a prolonged respiratory burst activity during severe hypoxia accompanied by a prolonged neuronal arrest during recovery in oxygenated medium (P < 0.05). In conclusion, PGE2 exerts its effects on respiration via EP3R activation that attenuates the respiratory response to hypercapnia as well as severe hypoxia. Modulation of the EP3R may serve as a potential therapeutic target for treatment of inflammatory and hypoxic-induced detrimental apneas and respiratory disorders in neonates.
MeSH term(s)	Animals ; Animals, Newborn ; Brain Stem/drug effects ; Brain Stem/metabolism ; Dinoprostone/pharmacology ; Female ; Hypercapnia/metabolism ; Hypoxia/metabolism ; Interleukin-1beta/pharmacology ; Male ; Mice ; Neurons/drug effects ; Neurons/metabolism ; Plethysmography ; Receptors, Prostaglandin E, EP3 Subtype/metabolism ; Respiration/drug effects ; Spinal Cord/drug effects ; Spinal Cord/metabolism
Chemical Substances	Interleukin-1beta ; Receptors, Prostaglandin E, EP3 Subtype ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2014-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.00542.2014
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Article ; Online: Prostaglandin E2 Mediates Cardiorespiratory Disturbances during Infection in Neonates.

Siljehav, Veronica / Hofstetter, Annika M / Leifsdottir, Kristin / Herlenius, Eric

The Journal of pediatrics

2015 Volume 167, Issue 6, Page(s) 1207–13.e3

Abstract: Objective: To determine whether infection, with associated eicosanoid release, is a main cause of respiratory disruption in neonates, by measuring levels of prostaglandin E2 (PGE2) and its metabolite (PGEM) in cerebrospinal fluid (CSF).: Study design!# ...

Abstract	Objective: To determine whether infection, with associated eicosanoid release, is a main cause of respiratory disruption in neonates, by measuring levels of prostaglandin E2 (PGE2) and its metabolite (PGEM) in cerebrospinal fluid (CSF). Study design: Of 59 eligible infants, 25 preterm infants (mean gestational age, 28 ± 0.5 weeks) and 22 full-term infants (mean gestational age, 40 ± 0.5 weeks) from a level 3 neonatal intensive care unit and the general maternity neonatal ward were enrolled prospectively. Infants with a condition that can cause secondary apnea were excluded. Cardiorespiratory disturbances, such as apnea, bradycardia, and desaturation (ABD) events, were quantified. All infants were subjected to standard laboratory analysis of blood and CSF concentrations of biomarkers, including PGE2 and PGEM, within 24 hours of lumbar puncture, which were correlated with ABD events and culture-verified infections. Results: PGEM levels were highest in infants with culture-verified sepsis and meningitis (P < .01). In infants without culture-verified bacterial infections, PGEM levels were higher in preterm infants compared with term infants (P < .05). The numbers of desaturation events and apnea events in neonates were positively associated with PGE2 levels in CSF (P < .05). Conclusion: PGE2 and PGEM are rapidly elevated in CSF during an infectious event and may explain cardiorespiratory disturbances, which are the major presenting symptoms of neonatal infections. PGE2 and PGEM are released during bacterial infections and could serve as biomarkers for sepsis and autonomic dysfunction in neonates.
MeSH term(s)	Apnea/etiology ; Apnea/metabolism ; Bacterial Infections/complications ; Bacterial Infections/metabolism ; Biomarkers/blood ; Biomarkers/cerebrospinal fluid ; Bradycardia/etiology ; Bradycardia/metabolism ; Dinoprostone/blood ; Dinoprostone/cerebrospinal fluid ; Dinoprostone/metabolism ; Female ; Humans ; Infant ; Infant, Newborn ; Infant, Premature ; Intensive Care Units, Neonatal ; Male ; Prospective Studies
Chemical Substances	Biomarkers ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3102-1
ISSN	1097-6833 ; 0022-3476
ISSN (online)	1097-6833
ISSN	0022-3476
DOI	10.1016/j.jpeds.2015.08.053
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Article ; Online: mPGES-1 and prostaglandin E2: vital role in inflammation, hypoxic response, and survival.

Siljehav, Veronica / Olsson Hofstetter, Annika / Jakobsson, Per-Johan / Herlenius, Eric

Pediatric research

2012 Volume 72, Issue 5, Page(s) 460–467

Abstract: Background: Apnea associated with infection and inflammation is a major medical concern in preterm infants. Prostaglandin E(2) (PGE(2)) serves as a critical mediator between infection and apnea. We hypothesize that alteration of the microsomal PGE ... ...

Abstract	Background: Apnea associated with infection and inflammation is a major medical concern in preterm infants. Prostaglandin E(2) (PGE(2)) serves as a critical mediator between infection and apnea. We hypothesize that alteration of the microsomal PGE synthase-1 (mPGES-1) PGE(2) pathway influences respiratory control and response to hypoxia. Methods: Nine-d-old wild-type (WT) mice, mPGES-1 heterozygote (mPGES-1(+/-)), and mPGES-1 knockout (mPGES-1(-/-)) mice were used. Respiration was investigated in mice using flow plethysmography after the mice received either interleukin-1β (IL-1β) (10 µg/kg) or saline. Mice were subjected to a period of normoxia, subsequent exposure to hyperoxia, and finally either moderate (5 min) or severe hypoxia (until 1 min after last gasp). Results: IL-1β worsened survival in WT mice but not in mice with reduced or no mPGES-1. Reduced expression of mPGES-1 prolonged gasping duration and increased the number of gasps during hypoxia. Response to intracerebroventricular PGE(2) was not dependent on mPGES-1 expression. Conclusion: Activation of mPGES-1 is involved in the rapid and vital response to severe hypoxia as well as inflammation. Attenuation of mPGES-1 appears to have no detrimental effects, yet prolongs autoresuscitation efforts and improves survival. Consequently, inhibition of the mPGES-1 pathway may serve as a potential therapeutic target for the treatment of apnea and respiratory disorders.
MeSH term(s)	Animals ; Apnea/enzymology ; Apnea/genetics ; Apnea/physiopathology ; Dinoprostone/administration & dosage ; Dinoprostone/metabolism ; Disease Models, Animal ; Female ; Hyperoxia/enzymology ; Hyperoxia/physiopathology ; Hypoxia/enzymology ; Hypoxia/genetics ; Hypoxia/physiopathology ; Inflammation/chemically induced ; Inflammation/enzymology ; Inflammation/genetics ; Inflammation/physiopathology ; Injections, Intraventricular ; Interleukin-1beta ; Intramolecular Oxidoreductases/deficiency ; Intramolecular Oxidoreductases/genetics ; Intramolecular Oxidoreductases/metabolism ; Male ; Mice ; Mice, Inbred DBA ; Mice, Knockout ; Plethysmography, Whole Body ; Prostaglandin-E Synthases ; Respiration ; Respiratory Center/enzymology ; Respiratory Center/physiopathology ; Severity of Illness Index ; Time Factors
Chemical Substances	Interleukin-1beta ; Intramolecular Oxidoreductases (EC 5.3.-) ; Prostaglandin-E Synthases (EC 5.3.99.3) ; Ptges protein, mouse (EC 5.3.99.3) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2012-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/pr.2012.119
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Article: The induced prostaglandin E₂ pathway is a key regulator of the respiratory response to infection and hypoxia in neonates

Hofstetter, Annika O / Saha, Sipra / Siljehav, Veronica / Jakobsson, Per-Johan / Herlenius, Eric

Proceedings of the National Academy of Sciences of the United States of America. 2007 June 5, v. 104, no. 23

2007

Abstract: Infection during the neonatal period commonly induces apnea episodes, and the proinflammatory cytokine IL-1β may serve as a critical mediator between these events. To determine the mechanism by which IL-1β depresses respiration, we examined a ... ...

Abstract	Infection during the neonatal period commonly induces apnea episodes, and the proinflammatory cytokine IL-1β may serve as a critical mediator between these events. To determine the mechanism by which IL-1β depresses respiration, we examined a prostaglandin E₂ (PGE₂)-dependent pathway in newborn mice and human neonates. IL-1β and transient anoxia rapidly induced brainstem-specific microsomal prostaglandin E synthase-1 (mPGES-1) activity in neonatal mice. Furthermore, IL-1β reduced respiratory frequency during hyperoxia and depressed hypoxic gasping and autoresuscitation in mPGES-1 wild-type mice, but not in mPGES-1 knockout mice. In wild-type mice, PGE₂ induced apnea and irregular breathing patterns in vivo and inhibited brainstem respiratory rhythm generation in vitro. Mice lacking the EP3 receptor (EP3R) for PGE₂ exhibited fewer apneas and sustained brainstem respiratory activity, demonstrating that PGE₂ exerts its respiratory effects via EP3R. In human neonates, the infectious marker C-reactive protein was correlated with elevated PGE₂ in the cerebrospinal fluid, and elevated central PGE₂ was associated with an increased apnea frequency. We conclude that IL-1β adversely affects breathing and its control by mPGES-1 activation and PGE₂ binding to brainstem EP3 receptors, resulting in increased apnea frequency and hypoxia-induced mortality.
Language	English
Dates of publication	2007-0605
Size	p. 9894-9899.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
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Article: The induced prostaglandin E2 pathway is a key regulator of the respiratory response to infection and hypoxia in neonates.

Hofstetter, Annika O / Saha, Sipra / Siljehav, Veronica / Jakobsson, Per-Johan / Herlenius, Eric

Proceedings of the National Academy of Sciences of the United States of America

2007 Volume 104, Issue 23, Page(s) 9894–9899

Abstract: Infection during the neonatal period commonly induces apnea episodes, and the proinflammatory cytokine IL-1beta may serve as a critical mediator between these events. To determine the mechanism by which IL-1beta depresses respiration, we examined a ... ...

Abstract	Infection during the neonatal period commonly induces apnea episodes, and the proinflammatory cytokine IL-1beta may serve as a critical mediator between these events. To determine the mechanism by which IL-1beta depresses respiration, we examined a prostaglandin E(2) (PGE(2))-dependent pathway in newborn mice and human neonates. IL-1beta and transient anoxia rapidly induced brainstem-specific microsomal prostaglandin E synthase-1 (mPGES-1) activity in neonatal mice. Furthermore, IL-1beta reduced respiratory frequency during hyperoxia and depressed hypoxic gasping and autoresuscitation in mPGES-1 wild-type mice, but not in mPGES-1 knockout mice. In wild-type mice, PGE(2) induced apnea and irregular breathing patterns in vivo and inhibited brainstem respiratory rhythm generation in vitro. Mice lacking the EP3 receptor (EP3R) for PGE(2) exhibited fewer apneas and sustained brainstem respiratory activity, demonstrating that PGE(2) exerts its respiratory effects via EP3R. In human neonates, the infectious marker C-reactive protein was correlated with elevated PGE(2) in the cerebrospinal fluid, and elevated central PGE(2) was associated with an increased apnea frequency. We conclude that IL-1beta adversely affects breathing and its control by mPGES-1 activation and PGE(2) binding to brainstem EP3 receptors, resulting in increased apnea frequency and hypoxia-induced mortality.
MeSH term(s)	Analysis of Variance ; Animals ; Animals, Newborn ; Brain Stem/metabolism ; C-Reactive Protein/cerebrospinal fluid ; Dinoprostone/metabolism ; Enzyme Induction/immunology ; Humans ; Hypoxia/immunology ; Hypoxia/metabolism ; Immunohistochemistry ; Infant, Newborn ; Infant, Newborn, Diseases/immunology ; Infant, Newborn, Diseases/metabolism ; Infections/immunology ; Infections/metabolism ; Interleukin-1beta/metabolism ; Intramolecular Oxidoreductases/genetics ; Intramolecular Oxidoreductases/metabolism ; Mice ; Mice, Inbred DBA ; Mice, Knockout ; Plethysmography ; Prostaglandin-E Synthases ; Respiratory Mechanics/immunology ; Signal Transduction/immunology
Chemical Substances	Interleukin-1beta ; C-Reactive Protein (9007-41-4) ; Intramolecular Oxidoreductases (EC 5.3.-) ; PTGES protein, human (EC 5.3.99.3) ; Prostaglandin-E Synthases (EC 5.3.99.3) ; Ptges protein, mouse (EC 5.3.99.3) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2007-05-29
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0611468104
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