Role of cytokines in hyperoxia mediated inflammation in the developing lung

Bustani, Porus; Kotecha, Sailesh

doi:10.2741/1113

Cited by 17 publications

(1 citation statement)

References 79 publications

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“…The lungs of preterm infants are often in the late-saccular to early-alveolar phase at birth and require respiratory support (249). Mechanical ventilation, continuous positive airway pressure (CPAP) or oxygen supplementation are necessary treatments, but cause inflammation, acute lung injury and lead to a neonatal CLD, also known as BPD (250)(251)(252)(253)(254). Lungs of infants with BPD are characterized by vascular and alveolar hypoplasia (255).…”

Section: Chronic Inflammation In Iugr-associated Cldmentioning

confidence: 99%

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

et al. 2021

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Lung development is not completed at birth, but expands beyond infancy, rendering the lung highly susceptible to injury. Exposure to various influences during a critical window of organ growth can interfere with the finely-tuned process of development and induce pathological processes with aberrant alveolarization and long-term structural and functional sequelae. This concept of developmental origins of chronic disease has been coined as perinatal programming. Some adverse perinatal factors, including prematurity along with respiratory support, are well-recognized to induce bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease that is characterized by arrest of alveolar and microvascular formation as well as lung matrix remodeling. While the pathogenesis of various experimental models focus on oxygen toxicity, mechanical ventilation and inflammation, the role of nutrition before and after birth remain poorly investigated. There is accumulating clinical and experimental evidence that intrauterine growth restriction (IUGR) as a consequence of limited nutritive supply due to placental insufficiency or maternal malnutrition is a major risk factor for BPD and impaired lung function later in life. In contrast, a surplus of nutrition with perinatal maternal obesity, accelerated postnatal weight gain and early childhood obesity is associated with wheezing and adverse clinical course of chronic lung diseases, such as asthma. While the link between perinatal nutrition and lung health has been described, the underlying mechanisms remain poorly understood. There are initial data showing that inflammatory and nutrient sensing processes are involved in programming of alveolarization, pulmonary angiogenesis, and composition of extracellular matrix. Here, we provide a comprehensive overview of the current knowledge regarding the impact of perinatal metabolism and nutrition on the lung and beyond the cardiopulmonary system as well as possible mechanisms determining the individual susceptibility to CLD early in life. We aim to emphasize the importance of unraveling the mechanisms of perinatal metabolic programming to develop novel preventive and therapeutic avenues.

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Section: Chronic Inflammation In Iugr-associated Cldmentioning

confidence: 99%

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

et al. 2021

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Maternal Alcohol Use and the Neonate

Gauthier¹,

Giliberti²,

Mohan³

et al. 2013

Alcohol Use Disorders and the Lung

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Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice

Zhang

Qing-xiang³

et al. 2013

Eur J Appl Physiol

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The aim of this work was to test the effect of treatment with hydrogen sulfide (H2S) on hyperoxia-induced acute lung injury in mice. Mice were exposed to room air or 95 % O2, and treated with NaHS (intraperitoneal injection of 0.1 ml/kg/day of 0.56 mol/l NaHS). Treatment with H2S partly restored the reduced H2S levels in plasma and lungs of mice exposed to hyperoxia. Treatment with H2S attenuated hyperoxia-induced acute lung injury marked by reduced ratio of lung weight to body weight, ratio of lung wet weight to dry weight, and cell numbers and protein content in bronchoalveolar lavage (BAL) and decreased apoptosis. Treatment with H2S markedly prolonged the survival of mice under oxygen exposure. Treatment with H2S abated hyperoxia-induced oxidative stress marked by reduced malondialdehyde and peroxynitrite formation, reduced NADPH oxidase activity, enhanced translocation of nuclear factor E2-related factor (Nrf2) into nucleus and increased activity of HO-1. Treatment with H2S decreased IL-1β, MCP-1, and MIP-2, and increased IL-10 expression in lungs of mice exposed to hyperoxia. Treatment with H2S decreased NFκB activity and iNOS expression in lungs, and reduced NOx content in BAL of mice exposed to hyperoxia. Treatment with H2S reduced lung permeability and suppressed VEGF release and VEGFR2 expression in lungs of mice under oxygen exposure. Treatment with exogenous H2S attenuated hyperoxia-induced acute lung injury through abating oxidative stress, suppressing inflammation, and reducing lung permeability in mice.

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Role of cytokines in hyperoxia mediated inflammation in the developing lung

Cited by 17 publications

References 79 publications

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

Maternal Alcohol Use and the Neonate

Treatment with exogenous hydrogen sulfide attenuates hyperoxia-induced acute lung injury in mice

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