Urinary bombesin-like peptide levels in infants and children with bronchopulmonary dysplasia and cystic fibrosis

Scher, Herschel; Miller, York E.; Aguayo, Samuel M.; Johnson, Karen; Miller, June E.; McCray, Paul B.

doi:10.1002/(sici)1099-0496(199811)26:5<326::aid-ppul4>3.0.co;2-s

Cited by 12 publications

(3 citation statements)

References 20 publications

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“…In addition, these cells can be viewed as ''sentinel cells,'' exposed to the external environment that monitors hypoxia/hypercapnia in the lung. These cells could potentially also serve as a premortem biological marker for SIDS, since bombesin/GRP and/or CGA, protein products synthesized by these cells, can be measured in the urine and serum, respectively [46,47]. Since PNEC/NEB cells can be cultured from postmortem tissues [48] and are amenable to laser capture microdissection, they can be used for detailed cellular studies and molecular profiling to test our hypothesis and to further define SIDS pathobiology [34].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Sudden Infant Death Syndrome: Potential Markers of Airway Chemoreceptor Dysfunction

et al. 2007

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Pulmonary neuroendocrine cells (PNEC), including neuroepithelial bodies (NEB), are amine- and peptide (for example, bombesin)-producing cells that function as hypoxia/hypercapnia-sensitive chemoreceptors that could be involved in the pathophysiology of sudden infant death syndrome (SIDS). We assessed morphometrically the frequency and size of PNEC/NEB in lungs of infants who died of SIDS (n = 21) and compared them to an equal number PNEC/NEB in lungs of age-matched control infants who died of accidental death or homicide, with all cases obtained from the San Diego SIDS/SUDC Research Project database. As a marker for PNEC/NEB we used an antibody against chromogranin A (CGA), and computer-assisted morphometric analysis was employed to determine the relative frequency of PNEC per airway epithelial area (% immunostained area, %IMS), the size of NEB, the number of nuclei/NEB, and the size of the NEB cells. The lungs of SIDS infants showed significantly greater %IMS of airway epithelium (2.72 +/- 0.28 [standard error of the mean, SEM] versus 1.88 +/- 0.24; P < 0.05) and larger NEB (1557 +/- 153 microm(2) versus 1151 +/- 106 microm(2); P < 0.05) compared to control infants. The size of NEB cells was also significantly increased in SIDS cases compared to the controls (180 +/- 6.39 microm(2) versus 157 +/- 8.0 microm(2); P < 0.05), indicating the presence of hypertrophy in addition to hyperplasia. Our findings support previous studies demonstrating hyperplasia of PNEC/NEB in lungs of infants who died of SIDS. These changes could be secondary to chronic hypoxia and/or could be attributable to maturational delay. Morphometric assessment and/or measurement of the secretory products of these cells (for example, CGA, bombesin) could provide a potential biological marker for SIDS.

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Section: Discussionmentioning

confidence: 99%

Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Sudden Infant Death Syndrome: Potential Markers of Airway Chemoreceptor Dysfunction

et al. 2007

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“… 140 , 150 Treatment with a neutralizing antibody to BLP corrected the thymic and lung pathology seen in preterm baboons treated with 100% oxygen. 140 BLP is also elevated in preterm human infants with BPD, 151 suggesting a mechanism linking lymphocyte dysregulation and BPD.…”

Section: Susceptibility Factors For Enhanced Inflammationmentioning

confidence: 99%

Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Pryhuber

2015

Clinics in Perinatology

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Synopsis Premature infants suffer significant respiratory morbidity during infancy with long-term negative consequences on health, quality of life, and health care costs. Enhanced susceptibility to a variety of infections and inflammation play a large role in early and prolonged lung disease following premature birth, though the mechanisms of susceptibility and immune dysregulation are active areas of research. This chapter will review aspects of host-pathogen interactions and immune responses that are altered by preterm birth and that impact chronic respiratory morbidity in these children.

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“…GRP is one of several biomarkers associated with ROS. Pulmonary neuroendocrine cell density and GRP concentrations are increasedfollowing oxygen therapy,20 smoking,18,32 ozone exposure,33 and chronic lung diseases such as cystic fibrosis 32,34. Oxidation of proteins, DNA, and lipids generate biomarkers that indicate ROS exposure.…”

mentioning

confidence: 99%

Urine gastrin‐releasing peptide in the first week correlates with bronchopulmonary dysplasia and post‐prematurity respiratory disease

Voynow

Fisher

Sunday

et al. 2020

Pediatric Pulmonology

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Rationale Bronchopulmonary dysplasia (BPD) is associated with post‐prematurity respiratory disease (PRD) in survivors of extreme preterm birth. Identifying early biomarkers that correlate with later development of BPD and PRD may provide insights for intervention. In a preterm baboon model, elevated gastrin‐releasing peptide (GRP) is associated with BPD, and GRP inhibition mitigates BPD occurrence. Objective We performed a prospective cohort study to investigate whether urine GRP levels obtained in the first postnatal week were associated with BPD, PRD, and other urinary biomarkers of oxidative stress. Methods Extremely low gestational age infants (23‐28 completed weeks) were enrolled in a US multicenter observational study, The Prematurity and Respiratory Outcomes Program (http://clinicaltrials.gov/ct2/show/NCT01435187). We used multivariable logistic regression to examine the association between urine GRP in the first postnatal week and multiple respiratory outcomes: BPD, defined as supplemental oxygen use at 36 + 0 weeks postmenstrual age, and post‐PRD, defined by positive quarterly surveys for increased medical utilization over the first year (PRD score). Results A total of 109 of 257 (42%) infants had BPD, and 120 of 217 (55%) had PRD. On adjusted analysis, GRP level more than 80 was associated with BPD (adjusted odds ratio [aOR], 1.83; 95% confidence interval [CI], 1.03‐3.25) and positive PRD score (aOR, 2.46; 95% CI, 1.35‐4.48). Urine GRP levels correlated with duration of NICU ventilatory and oxygen support and with biomarkers of oxidative stress: allantoin and 8‐hydroxydeoxyguanosine. Conclusions Urine GRP in the first postnatal week was associated with concurrent urine biomarkers of oxidative stress and with later diagnoses of BPD and PRD.

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Urinary bombesin-like peptide levels in infants and children with bronchopulmonary dysplasia and cystic fibrosis

Cited by 12 publications

References 20 publications

Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Sudden Infant Death Syndrome: Potential Markers of Airway Chemoreceptor Dysfunction

Pulmonary Neuroendocrine Cells and Neuroepithelial Bodies in Sudden Infant Death Syndrome: Potential Markers of Airway Chemoreceptor Dysfunction

Postnatal Infections and Immunology Affecting Chronic Lung Disease of Prematurity

Urine gastrin‐releasing peptide in the first week correlates with bronchopulmonary dysplasia and post‐prematurity respiratory disease

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