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      Plasma proteomics reveals gestational age-specific responses to mechanical ventilation and identifies the mechanistic pathways that initiate preterm lung injury

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          Abstract

          The preterm lung is particularly vulnerable to ventilator-induced lung injury (VILI) as a result of mechanical ventilation. However the developmental and pathological cellular mechanisms influencing the changing patterns of VILI have not been comprehensively delineated, preventing the advancement of targeted lung protective therapies. This study aimed to use SWATH-MS to comprehensively map the plasma proteome alterations associated with the initiation of VILI following 60 minutes of standardized mechanical ventilation from birth in three distinctly different developmental lung states; the extremely preterm, preterm and term lung using the ventilated lamb model. Across these gestations, 34 proteins were differentially altered in matched plasma samples taken at birth and 60 minutes. Multivariate analysis of the plasma proteomes confirmed a gestation-specific response to mechanical ventilation with 79% of differentially-expressed proteins altered in a single gestation group only. Six cellular and molecular functions and two physiological functions were uniquely enriched in either the extremely preterm or preterm group. Correlation analysis supported gestation-specific protein-function associations within each group. In identifying the gestation-specific proteome and functional responses to ventilation we provide the founding evidence required for the potential development of individualized respiratory support approaches tailored to both the developmental and pathological state of the lung.

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          Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth.

          D. Roberts, S Dalziel (2006)
          Respiratory distress syndrome (RDS) is a serious complication of preterm birth and the primary cause of early neonatal mortality and disability. To assess the effects on fetal and neonatal morbidity and mortality, on maternal mortality and morbidity, and on the child in later life of administering corticosteroids to the mother before anticipated preterm birth. We searched the Cochrane Pregnancy and Childbirth Group Trials Register (30 October 2005). Randomised controlled comparisons of antenatal corticosteroid administration (betamethasone, dexamethasone, or hydrocortisone) with placebo or with no treatment given to women with a singleton or multiple pregnancy, expected to deliver preterm as a result of either spontaneous preterm labour, preterm prelabour rupture of the membranes or elective preterm delivery. Two review authors assessed trial quality and extracted data independently. Twenty-one studies (3885 women and 4269 infants) are included. Treatment with antenatal corticosteroids does not increase risk to the mother of death, chorioamnionitis or puerperal sepsis. Treatment with antenatal corticosteroids is associated with an overall reduction in neonatal death (relative risk (RR) 0.69, 95% confidence interval (CI) 0.58 to 0.81, 18 studies, 3956 infants), RDS (RR 0.66, 95% CI 0.59 to 0.73, 21 studies, 4038 infants), cerebroventricular haemorrhage (RR 0.54, 95% CI 0.43 to 0.69, 13 studies, 2872 infants), necrotising enterocolitis (RR 0.46, 95% CI 0.29 to 0.74, eight studies, 1675 infants), respiratory support, intensive care admissions (RR 0.80, 95% CI 0.65 to 0.99, two studies, 277 infants) and systemic infections in the first 48 hours of life (RR 0.56, 95% CI 0.38 to 0.85, five studies, 1319 infants). Antenatal corticosteroid use is effective in women with premature rupture of membranes and pregnancy related hypertension syndromes. The evidence from this new review supports the continued use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk of preterm birth. A single course of antenatal corticosteroids should be considered routine for preterm delivery with few exceptions. Further information is required concerning optimal dose to delivery interval, optimal corticosteroid to use, effects in multiple pregnancies, and to confirm the long-term effects into adulthood.
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            A repository of assays to quantify 10,000 human proteins by SWATH-MS.

            George Rosenberger, Ching Chiek Koh, Tiannan Guo … (2014)
            Mass spectrometry is the method of choice for deep and reliable exploration of the (human) proteome. Targeted mass spectrometry reliably detects and quantifies pre-determined sets of proteins in a complex biological matrix and is used in studies that rely on the quantitatively accurate and reproducible measurement of proteins across multiple samples. It requires the one-time, a priori generation of a specific measurement assay for each targeted protein. SWATH-MS is a mass spectrometric method that combines data-independent acquisition (DIA) and targeted data analysis and vastly extends the throughput of proteins that can be targeted in a sample compared to selected reaction monitoring (SRM). Here we present a compendium of highly specific assays covering more than 10,000 human proteins and enabling their targeted analysis in SWATH-MS datasets acquired from research or clinical specimens. This resource supports the confident detection and quantification of 50.9% of all human proteins annotated by UniProtKB/Swiss-Prot and is therefore expected to find wide application in basic and clinical research. Data are available via ProteomeXchange (PXD000953-954) and SWATHAtlas (SAL00016-35).
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              Manual ventilation with a few large breaths at birth compromises the therapeutic effect of subsequent surfactant replacement in immature lambs.

              Adam B. Robertson, Julia T. Vilstrup, Nicole Bjorklund … (1997)
              The reason why some infants with respiratory distress syndrome fail to respond to surfactant, or respond only transiently, is incompletely understood. We hypothesized that resuscitation with large breaths at birth might damage the lungs and blunt the effect of surfactant. Five pairs of lamb siblings were delivered by cesarean section at 127-128 d of gestation. One lamb in each pair was randomly selected to receive six manual inflations of 35-40 mL/kg ("bagging") before the start of mechanical ventilation, a volume roughly corresponding to the inspiratory capacity of lamb lungs after prophylactic surfactant supplementation. Both siblings were given rescue porcine surfactant, 200 mg/kg, at 30 min of age. Blood gases and deflation pressure-volume (P-V) curves of the respiratory system were recorded until the lambs were killed at 4 h. The P-V curves became steeper after surfactant in the control group, but no such effect was seen in those subjected to bagging. At 4 h, inspiratory capacity and maximal deflation compliance were almost three times higher (p < 0.01) in the controls than in the bagged lambs. The latter were also more difficult to ventilate and tended to have less well expanded alveoli and more widespread lung injury in histologic sections. We conclude that a few inflations with volumes that are probably harmless in other circumstances might, when forced into the surfactant-deficient lung immediately at birth, compromise the effect of subsequent surfactant rescue treatment. Our findings challenge current neonatal resuscitation practice of rapidly establishing a normal lung volume by vigorous manual ventilation.
              Article 0 comments Cited 95 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Prue M. Pereira-Fantini: prue.pereira@mcri.edu.au
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 22 August 2018
                Publication date PMC-release: 22 August 2018
                Publication date Collection: 2018
                Volume: 8
                Electronic Location Identifier: 12616
                Affiliations
                [1 ]ISNI 0000 0000 9442 535X, GRID grid.1058.c, Neonatal Research, , Murdoch Childrens Research Institute, ; Parkville, Australia
                [2 ]ISNI 0000 0001 2179 088X, GRID grid.1008.9, Department of Paediatrics, , University of Melbourne, ; Parkville, Australia
                [3 ]ISNI 0000 0001 2179 088X, GRID grid.1008.9, Department of Pathology, , University of Melbourne, ; Parkville, Australia
                [4 ]ISNI 0000 0001 2179 088X, GRID grid.1008.9, Centre for Systems Genomics, , University of Melbourne, ; Parkville, Australia
                [5 ]ISNI 0000 0001 0768 2743, GRID grid.7886.1, University College Dublin, ; Dublin, Ireland
                [6 ]ISNI 0000 0004 1937 0327, GRID grid.4643.5, Laboratorio di Tecnologie Biomediche, Dipartimento di Elettronica, Informazione e Ingegneria Biomedica-DEIB, , Politecnico di Milano University, ; Milano, Italy
                [7 ]ISNI 0000 0004 1936 826X, GRID grid.1009.8, Menzies Institute for Medical Research, , University of Tasmania, ; Hobart, Australia
                [8 ]ISNI 0000 0004 0386 2271, GRID grid.416259.d, The Royal Women’s Hospital, ; Parkville, Australia
                [9 ]ISNI 0000 0001 2179 088X, GRID grid.1008.9, Department of Obstetrics and Gynaecology, , University of Melbourne, ; Parkville, Australia
                [10 ]ISNI 0000 0000 9442 535X, GRID grid.1058.c, Haematology Research, , Murdoch Childrens Research Institute, ; Parkville, Australia
                [11 ]ISNI 0000 0004 0614 0346, GRID grid.416107.5, Department of Neonatology, , Royal Children’s Hospital, ; Parkville, Australia
                Author information
                http://orcid.org/0000-0002-3672-4591
                http://orcid.org/0000-0001-6742-7314
                http://orcid.org/0000-0003-1522-4691
                Article
                Publisher ID: 30868
                DOI: 10.1038/s41598-018-30868-x
                PMC ID: 6105628
                PubMed ID: 30135517
                SO-VID: 90f1413b-9a6d-4b71-a49d-f1b5b575dc2e
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 14 February 2018
                Date accepted : 2 August 2018
                Categories
                Subject: Article
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                issue-copyright-statement © The Author(s) 2018

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