Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Pryhuber, Gloria S.

doi:10.1016/j.clp.2015.08.002

Cited by 28 publications

(29 citation statements)

References 170 publications

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“…43,44 In fact, very preterm infants who do not meet current definitions of BPD still have increased risks for poor pulmonary function, for susceptibility to viral illnesses and for morbidity throughout childhood. 45,46 We anticipate that individual studies currently underway as part of the PROP will result in definitions of respiratory disease of prematurity based on lung function, molecular underpinnings and long-term pulmonary outcomes. 47 …”

Section: Discussionmentioning

confidence: 99%

Increasing F2-isoprostanes in the first month after birth predicts poor respiratory and neurodevelopmental outcomes in very preterm infants

Matthews¹,

Aschner

Stark

et al. 2016

J Perinatol

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OBJECTIVE This study examined the association between increased early oxidative stress, measured by F2-isoprostanes (IsoPs), and respiratory morbidity at term equivalent age and neurological impairment at 12 months of corrected age (CA). STUDY DESIGN Plasma samples were collected from 136 premature infants on days 14 and 28 after birth. All participants were infants born at ≤28 weeks of gestational age enrolled into the Prematurity and Respiratory Outcomes Program (PROP) study. Respiratory morbidity was determined at 40 weeks of postmenstrual age (PMA) by the Respiratory Severity Index (RSI), a composite measure of oxygen and pressure support. Neurodevelopmental assessment was performed using the Developmental Assessment of Young Children (DAYC) at 12 months of CA. Multivariable logistic regression models estimated associations between IsoP change, RSI and DAYC scores. Mediation analysis was performed to determine the relationship between IsoPs and later outcomes. RESULTS Developmental data were available for 121 patients (90% of enrolled) at 12 months. For each 50-unit increase in IsoPs, regression modeling predicted decreases in cognitive, communication and motor scores of − 1.9, − 1.2 and − 2.4 points, respectively (P<0.001). IsoP increase was also associated with increased RSI at 40 weeks of PMA (odds ratio = 1.23; P = 0.01). RSI mediated 25% of the IsoP effect on DAYC motor scores (P = 0.02) and had no significant impact on cognitive or communication scores. CONCLUSIONS In the first month after birth, increases in plasma IsoPs identify preterm infants at risk for respiratory morbidity at term equivalent age and worse developmental outcomes at 12 months of CA. Poor neurodevelopment is largely independent of respiratory morbidity.

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Section: Discussionmentioning

confidence: 99%

Increasing F2-isoprostanes in the first month after birth predicts poor respiratory and neurodevelopmental outcomes in very preterm infants

Matthews¹,

Aschner

Stark

et al. 2016

J Perinatol

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“…Chorioamnionitis, postnatal infection, oxygen therapy, and mechanical ventilation can induce inflammation in the newborn lung (38). These proinflammatory insults may increase chronic respiratory morbidity (38), but the long-term consequences of early pulmonary inflammation on lung structure and function have been incompletely characterized.…”

Section: Introductionmentioning

confidence: 99%

“…The mammalian lung undergoes five distinct developmental stages: the embryonic [3-7 gestational weeks (GW) in humans and embryonic day (E) 9.5-14 in mice], pseudoglandular (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) GW in humans and E14 -16.5 in mice), canalicular (16 -26 GW in humans and E16.5-17.5 in mice), saccular [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38] in humans and E17.5-postnatal day (PN) 5 in mice], and alveolar stages (from 36 GW to early childhood in humans and PN5-30 in mice) (34).…”

Section: Introductionmentioning

confidence: 99%

Pulmonary IL-1β expression in early life causes permanent changes in lung structure and function in adulthood

Hogmalm

Bry

2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chorioamnionitis, mechanical ventilation, oxygen therapy, and postnatal infection promote inflammation in the newborn lung. The long-term consequences of pulmonary inflammation during infancy have not been well characterized. The aim of this study was to examine the impact of inflammation during the late saccular to alveolar stages of lung development on lung structure and function in adulthood. To induce IL-1β expression in the pulmonary epithelium of mice with a tetracycline-inducible human IL-1β transgene, doxycycline was administered via intraperitoneal injections to bitransgenic pups and their littermate controls on postnatal days (PN) 0, 0.5, and 1. Lung structure, inflammation, and airway reactivity were studied in adulthood. IL-1β production in early life resulted in increased numbers of macrophages and neutrophils on PN21, but inflammation subsided by PN42. Permanent changes in alveolar structure, i.e., larger alveoli and thicker alveolar walls, were present from PN21 to PN84. Lack of alveolar septation thus persisted after IL-1β production and inflammation had ceased. Early IL-1β production caused goblet cell hyperplasia, enhanced calcium-activated chloride channel 3 (CLCA3) protein expression, and increased airway reactivity in response to methacholine on PN42. Lymphoid follicles were present adjacent to small airways in the lungs of adult bitransgenic mice, and levels of the B cell chemoattractant CXC-motif ligand (CXCL) 13 were elevated in the lungs of bitransgenic mice compared with controls. In conclusion, IL-1β-induced pulmonary inflammation in early life causes a chronic lung disease in adulthood.

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“…56–59 In preterm infants, respiratory viral LRI in the first years are later associated with long-term pulmonary consequences and diminished lung function. 60–63 …”

Section: Premature Infants and Respiratory Virusesmentioning

confidence: 99%

“…66 In a report of postmortem autopsies of NICU infants who died of respiratory illness, none had HMPV or RSV. 63 However, there are few published prospective studies of viral ARI in the NICU. Moreover, the absence of documented HMPV in the available data may simply be due to the recent discovery of HMPV and use of viral culture in many studies, since sensitive detection of HMPV requires RT-PCR (reverse transcription polymerase chain reaction).…”

Section: Respiratory Viruses In the Neonatal Intensive Care Unitmentioning

confidence: 99%

Human metapneumovirus in the preterm neonate: current perspectives

Maitre

Williams

2016

RRN

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Premature birth (<37 weeks gestation) occurs in ~11% of all births in the US. These infants are at risk of chronic lung disease and respiratory conditions, including bronchopulmonary dysplasia. Respiratory viruses are important causes of acute respiratory illness (ARI) in preterm infants, leading to rehospitalization, increased health care burden, and long-term morbidity. Human metapneumovirus (HMPV) is a paramyxovirus discovered in 2001 that is related to respiratory syncytial virus. Epidemiologic studies show that HMPV is a leading cause of ARI in children and adults worldwide. Prematurity is a major risk factor for severe HMPV disease, requiring hospitalization. Moreover, limited data suggest that HMPV infection during infancy is associated with asthma and recurrent wheezing, which are common long-term pulmonary complication of prematurity. HMPV causes nosocomial outbreaks of ARI in hospitals and long-term care facilities, although there are few studies of the prevalence of HMPV in neonatal intensive care unit populations. HMPV is a common and important virus in premature infants, and caregivers for preterm infants should consider this virus in patients with acute respiratory symptoms.

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Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Cited by 28 publications

References 170 publications

Increasing F2-isoprostanes in the first month after birth predicts poor respiratory and neurodevelopmental outcomes in very preterm infants

Increasing F2-isoprostanes in the first month after birth predicts poor respiratory and neurodevelopmental outcomes in very preterm infants

Pulmonary IL-1β expression in early life causes permanent changes in lung structure and function in adulthood

Human metapneumovirus in the preterm neonate: current perspectives

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