Increased heme oxygenase-1 expression in premature infants with respiratory distress syndrome

Farkas, I; Maróti, Zoltán; Katona, Márta; Endreffy, E.; Peter, Markus; Mader, Krisztina; Túri, Sándor

doi:10.1007/s00431-008-0673-6

Cited by 11 publications

(9 citation statements)

References 25 publications

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“…The increase in oxidative stress that we observed following neonatal hyperoxia in mice is consistent with findings in humans. It has been shown that preterm infants who suffered from respiratory distress and required supplemental oxygen exhibited an eightfold increase in HO-1 expression within the blood 1-5 days after birth compared with term controls (25). Furthermore, this increase in oxidative stress persists; adolescent children born very preterm had greater expression of an oxidative stress marker (8-isoprostane) in exhaled breath condensate than term-matched controls, regardless of whether they developed BPD or not (27).…”

Section: Oxidative Stressmentioning

confidence: 99%

Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Bouch

O’Reilly

Harding

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Preterm infants often require supplemental oxygen due to lung immaturity, but hyperoxia can contribute to an increased risk of respiratory illness later in life. Our aim was to compare the effects of mild and moderate levels of neonatal hyperoxia on markers of pulmonary oxidative stress and inflammation and on lung architecture; both immediate and persistent effects were assessed. Neonatal mice (C57BL6/J) were raised in either room air (21% O2), mild (40% O2), or moderate (65% O2) hyperoxia from birth until postnatal day 7 (P7d). The mice were killed at either P7d (immediate effects) or lived in air until adulthood (P56d, persistent effects). We enumerated macrophages in lung tissue at P7d and immune cells in bronchoalveolar lavage fluid (BALF) at P56d. At P7d and P56d, we assessed pulmonary oxidative stress [heme oxygenase-1 (HO-1) and nitrotyrosine staining] and lung architecture. The data were interrogated for sex differences. At P7d, HO-1 gene expression was greater in the 65% O2 group than in the 21% O2 group. At P56d, the area of nitrotyrosine staining and number of immune cells were greater in the 40% O2 and 65% O2 groups relative to the 21% O2 group. Exposure to 65% O2, but not 40% O2, led to larger alveoli and lower tissue fraction in the short term and to persistently fewer bronchiolar-alveolar attachments. Exposure to 40% O2 or 65% O2 causes persistent increases in pulmonary oxidative stress and immune cells, suggesting chronic inflammation within the adult lung. Unlike 65% O2, 40% O2 does not affect lung architecture.

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Section: Oxidative Stressmentioning

confidence: 99%

Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Bouch

O’Reilly

Harding

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The measurement of oxidative biomarkers was performed in different timepoints (within 12 h after birth in our study versus 14 h to 21 d in various studies 20,38,41,42 ), which may also account for the different results as the levels of these markers may increase or decrease over time. 20 Ahola et al 43 showed that erythrocyte-glutathione concentration decreased during the first week of life whereas erythrocyte-cysteine concentration increased significantly from day 3 to day 7 in preterm infants with a birthweight of 500-1500 g. Farkas et al 16 found an eight-fold increase in haeme oxygenase-1 gene expression in the preterm infants with RDS on the fifth day as compared with the first day after birth. May et al 42 showed that end tidal carbon monoxide levels on day 14, but not on day 3, significantly predicted BPD development.…”

Section: Rdsmentioning

confidence: 99%

Total antioxidant capacity and total oxidant status after surfactant treatment in preterm infants with respiratory distress syndrome

et al. 2011

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Background: Oxidative damage is important in the pathogenesis of respiratory distress syndrome (RDS). However, data on the effect of surfactant therapy on oxidative stress in vivo are limited. We aimed to evaluate the oxidant/antioxidant status in preterm infants with RDS via measurement of total antioxidant capacity (TAC) and total oxidant status (TOS), to determine the effect of surfactant on oxidant/antioxidant balance and to assess the association between TAC, TOS and clinical outcomes of the patients. Methods: Sixty-nine infants with RDS were included. Blood samples for determining TAC and TOS were collected before and 48 h after surfactant treatment. TAC and TOS levels were analysed in serum. Patients were followed up until discharge or death. Results: Post-surfactant TAC levels were significantly higher than pre-surfactant TAC levels (P ¼ 0.029). TAC/TOS ratio significantly increased after surfactant treatment (P ¼ 0.018). Infants ,28 weeks of gestational age had lower levels of baseline TAC than those 28 weeks of gestational age (P ¼ 0.020), whereas TOS levels were similar. Baseline TAC/TOS ratio was lower in infants who died in the study period than those who survived (P ¼ 0.023). After controlling gestational age, baseline TAC levels were significantly and inversely correlated with the duration of total respiratory support (r ¼ 20.343; P ¼ 0.009) and hospitalization (r ¼ 20.341; P ¼ 0.009). TAC or TOS levels were not associated with the development of bronchopulmonary dysplasia or other complications as determined during the investigation period. Conclusions: Oxidant-antioxidant balance shifts in favour of the antioxidant system after surfactant treatment. Lower TAC/ TOS ratio in preterm infants may be associated with increased mortality.

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“…Indeed, increased expression of HO-1 protein has been found in the lungs of patients with acute respiratory distress syndrome (3), in monocytes of patients with systemic inflammatory response syndrome (4), and in the bone marrow macrophages of patients dying from severe sepsis or septic shock (5). In addition, HO-1 mRNA expression is increased in the blood cells of premature infants with respiratory distress syndrome and pediatric cancer patients with systemic inflammatory response syndrome (6,7). Upregulated HO-1 mRNA and protein levels have also been found in the livers of acute liver failure patients (8).…”

Section: Introductionmentioning

confidence: 97%

Heme Oxygenase 1 Polymorphisms and Plasma Concentrations in Critically Ill Patients

Saukkonen¹,

Lakkisto²,

Kaunisto

et al. 2010

Shock

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Heme oxygenase 1 (HO-1) is a cytoprotective enzyme upregulated by various critical illness-related stress stimuli. We investigated the association of HO-1 gene polymorphisms and plasma concentrations with the outcome of critically ill patients in a prospective cohort study of 231 critically ill patients admitted to tertiary care medical and medical-surgical intensive care units. Blood samples were collected on days 1, 2, and 3 to 4 in the intensive care unit. The HO-1 plasma concentration was measured in serial samples, and HO-1 single nucleotide polymorphisms, -413A/T and +99G/C, and HO-1 promoter GTn repeat length polymorphism were determined. The +99C and long GTn alleles were in perfect linkage disequilibrium, and the -413T/GT(L)/+99C haplotype had significant independent effect on first-day HO-1 plasma concentrations in linear regression analysis (P = 0.03) and associated with lower HO-1 plasma levels. Furthermore, -413T/GT(L)/+99C haplotype associated with a lower frequency of multiple-organ dysfunction compared with other haplotypes (P = 0.017). The HO-1 plasma concentrations of study patients were significantly higher than the values of healthy controls at all time points (P < 0.001), and the first-day plasma HO-1 levels were independently associated with the Sequential Organ Failure Assessment score (P = 0.001). In conclusion, the HO-1 -413T/GT(L)/+99C haplotype is associated with HO-1 plasma levels and the frequency of multiple-organ dysfunction in critically ill patients. The HO-1 plasma concentrations are significantly increased among critically ill patients and associated with the degree of organ dysfunction.

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Increased heme oxygenase-1 expression in premature infants with respiratory distress syndrome

Cited by 11 publications

References 25 publications

Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Neonatal exposure to mild hyperoxia causes persistent increases in oxidative stress and immune cells in the lungs of mice without altering lung structure

Total antioxidant capacity and total oxidant status after surfactant treatment in preterm infants with respiratory distress syndrome

Heme Oxygenase 1 Polymorphisms and Plasma Concentrations in Critically Ill Patients

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