Hyperoxia in the Pathogenesis of Bronchopulmonary Dysplasia

Harijith, Anantha; Bhandari, Vineet

doi:10.1007/978-3-319-28486-6_1

Cited by 7 publications

(6 citation statements)

References 142 publications

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“…Hyperoxia-induced injury to the developing lung, impaired alveolarization, and dysregulated vascularization are critical factors in the pathogenesis of bronchopulmonary dysplasia (BPD) (1,2); however, mechanisms for hyperoxia (HYP)-induced development of BPD are not fully known. After hyperoxia-induced acute lung injury (HALI) or mechanical ventilation during premature birth, damage-associated molecular patterns are released from necrotic cells and recognized by pattern recognition receptors that include Toll-like receptors and nucleotidebinding oligomerization domain-like receptors (3)(4)(5).…”

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confidence: 99%

TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice

Syed

Shah

Das

et al. 2019

Am J Respir Cell Mol Biol

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Hyperoxia-induced injury to the developing lung, impaired alveolarization, and dysregulated vascularization are critical factors in the pathogenesis of bronchopulmonary dysplasia (BPD); however, mechanisms for hyperoxia-induced development of BPD are not fully known. In this study, we show that TREM-1 (triggering receptor expressed on myeloid cells 1) is upregulated in hyperoxiaexposed neonatal murine lungs as well as in tracheal aspirates and lungs of human neonates with respiratory distress syndrome and BPD as an adaptive response to survival in hyperoxia. Inhibition of TREM-1 function using an siRNA approach or deletion of the Trem1 gene in mice showed enhanced lung inflammation, alveolar damage, and mortality of hyperoxia-exposed neonatal mice. The treatment of hyperoxia-exposed neonatal mice with agonistic TREM-1 antibody decreased lung inflammation, improved alveolarization, and was associated with diminished necroptosis-regulating protein RIPK3 (receptor-interacting protein kinase 3). Mechanistically, we show that TREM-1 activation alleviates lung inflammation and improves alveolarization through downregulating RIPK3-mediated necroptosis and NLRP3 (nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3) inflammasome activation in hyperoxia-exposed neonatal mice. These data show that activating TREM-1, enhancing angiopoietin 1 signaling, or blocking the RIPK3-mediated necroptosis pathway may be used in new therapeutic interventions to control adverse effects of hyperoxia in the development of BPD.

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confidence: 99%

TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice

Syed

Shah

Das

et al. 2019

Am J Respir Cell Mol Biol

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“…BPD is a disease of genetic-environmental interactions; among the latter contributors, hyperoxia per se (depending upon dose and duration of exposure) is sufficient to initiate and result in persistent inflammation on the path to BPD. 1,23 In addition, ante (chorioamnionitis) and postnatal Neutrophils are modestly increased while macrophages are robustly increased in the BPD group as compared with room air (RA) controls. After treatment with AVR-25, there is no change in the neutrophil population in both the RA and in the BPD group.…”

Section: Resultsmentioning

confidence: 99%

Chitin Analog AVR-25 Prevents Experimental Bronchopulmonary Dysplasia

Das

Acharya

Shah

et al. 2020

J Pediatr Intensive Care

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Infants born extremely preterm are at a high risk of developing bronchopulmonary dysplasia (BPD) which is characterized by large, simplified alveoli, increased inflammation, disrupted and dysregulated vasculogenesis, decreased cell proliferation, and increased cell death in the lungs. Due to lack of specific drug treatments to combat this condition, BPD and its long-term complications have taken a significant toll of healthcare resources. AVR-25, a novel immune modulator experimental compound, was able to partially recover the pulmonary phenotype in the hyperoxia-induced experimental mouse model of BPD. We anticipate that AVR-25 will have therapeutic potential for managing human BPD.

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“…As exposure to hyperoxia is a critical factor in the pathogenesis of BPD 16 , it is important to try and reduce the exposure to high concentrations of supplemental O 2 as early as possible given the immature anti-oxidant defenses of the preterm newborn 17 . Pulse oximetry has been used to assess “normal” oxygen saturation (SpO 2 ) values after birth in preterm infants, and the median time to achieve SpO 2 of >80% and >90% was 7.3 and 8.1 minutes, respectively 18 .…”

Section: How To Decrease Bronchopulmonary Dysplasia Todaymentioning

confidence: 99%

“…In 2010, while the American Heart Association (AHA), the European Resuscitation Council (ERC), and the International Liaison Committee on Resuscitation (ILCOR) issued recommendations that have clearly stated that room air should be used to initiate resuscitation in term infants 15 , recommendations for preterm infants are still not definitive. As exposure to hyperoxia is a critical factor in the pathogenesis of BPD 16 , it is important to try and reduce the exposure to high concentrations of supplemental O 2 as early as possible given the immature anti-oxidant defenses of the preterm newborn 17 . Pulse oximetry has been used to assess “normal” oxygen saturation (SpO 2 ) values after birth in preterm infants, and the median time to achieve SpO 2 of >80% and >90% was 7.3 and 8.1 minutes, respectively 18 .…”

Section: How To Decrease Bronchopulmonary Dysplasia Todaymentioning

confidence: 99%

How to decrease bronchopulmonary dysplasia in your neonatal intensive care unit today and “tomorrow”

Nelin

Bhandari

2017

F1000Res

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Bronchopulmonary dysplasia, or BPD, is the most common chronic lung disease in infants. Genetic predisposition and developmental vulnerability secondary to antenatal and postnatal infections, compounded with exposure to hyperoxia and invasive mechanical ventilation to an immature lung, result in persistent inflammation, culminating in the characteristic pulmonary phenotype of BPD of impaired alveolarization and dysregulated vascularization. In this article, we highlight specific areas in current management, and speculate on therapeutic strategies that are on the horizon, that we believe will make an impact in decreasing the incidence of BPD in your neonatal intensive care units.

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Hyperoxia in the Pathogenesis of Bronchopulmonary Dysplasia

Cited by 7 publications

References 142 publications

TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice

TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice

Chitin Analog AVR-25 Prevents Experimental Bronchopulmonary Dysplasia

How to decrease bronchopulmonary dysplasia in your neonatal intensive care unit today and “tomorrow”

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