Serial blood cytokine and chemokine mRNA and microRNA over 48 h are insult specific in a piglet model of inflammation-sensitized hypoxia-ischaemia.


Journal

Pediatric research
ISSN: 1530-0447
Titre abrégé: Pediatr Res
Pays: United States
ID NLM: 0100714

Informations de publication

Date de publication:
02 2021
Historique:
received: 02 12 2019
accepted: 09 04 2020
revised: 06 04 2020
pubmed: 11 6 2020
medline: 11 1 2022
entrez: 11 6 2020
Statut: ppublish

Résumé

Exposure to inflammation exacerbates injury in neonatal encephalopathy (NE). We hypothesized that brain biomarker mRNA, cytokine mRNA and microRNA differentiate inflammation (E. coli LPS), hypoxia (Hypoxia), and inflammation-sensitized hypoxia (LPS+Hypoxia) in an NE piglet model. Sixteen piglets were randomized: (i) LPS 2 μg/kg bolus; 1 μg/kg infusion (LPS; n = 5), (ii) Saline with hypoxia (Hypoxia; n = 6), (iii) LPS commencing 4 h pre-hypoxia (LPS+Hypoxia; n = 5). Total RNA was acquired at baseline, 4 h after LPS and 1, 3, 6, 12, 24, 48 h post-insult (animals euthanized at 48 h). Quantitative PCR was performed for cytokines (IL1A, IL6, CXCL8, IL10, TNFA) and brain biomarkers (ENO2, UCHL1, S100B, GFAP, CRP, BDNF, MAPT). MicroRNA was detected using GeneChip (Affymetrix) microarrays. Fold changes from baseline were compared between groups and correlated with cell death (TUNEL) at 48 h. Within 6 h post-insult, we observed increased IL1A, CXCL8, CCL2 and ENO2 mRNA in LPS+Hypoxia and LPS compared to Hypoxia. IL10 mRNA differentiated all groups. Four microRNAs differentiated LPS+Hypoxia and Hypoxia: hsa-miR-23a, 27a, 31-5p, 193-5p. Cell death correlated with TNFA (R = 0.69; p < 0.01) at 1-3 h and ENO2 (R = -0.69; p = 0.01) at 48 h. mRNA and miRNA differentiated hypoxia from inflammation-sensitized hypoxia within 6 h in a piglet model. This information may inform human studies to enable triage for tailored neuroprotection in NE. Early stratification of infants with neonatal encephalopathy is key to providing tailored neuroprotection. IL1A, CXCL8, IL10, CCL2 and NSE mRNA are promising biomarkers of inflammation-sensitized hypoxia. IL10 mRNA levels differentiated all three pathological states; fold changes from baseline was the highest in LPS+Hypoxia animals, followed by LPS and Hypoxia at 6 h. miR-23, -27, -31-5p and -193-5p were significantly upregulated within 6 h of a hypoxia insult. Functional analysis highlighted the diverse roles of miRNA in cellular processes.

Sections du résumé

BACKGROUND
Exposure to inflammation exacerbates injury in neonatal encephalopathy (NE). We hypothesized that brain biomarker mRNA, cytokine mRNA and microRNA differentiate inflammation (E. coli LPS), hypoxia (Hypoxia), and inflammation-sensitized hypoxia (LPS+Hypoxia) in an NE piglet model.
METHODS
Sixteen piglets were randomized: (i) LPS 2 μg/kg bolus; 1 μg/kg infusion (LPS; n = 5), (ii) Saline with hypoxia (Hypoxia; n = 6), (iii) LPS commencing 4 h pre-hypoxia (LPS+Hypoxia; n = 5). Total RNA was acquired at baseline, 4 h after LPS and 1, 3, 6, 12, 24, 48 h post-insult (animals euthanized at 48 h). Quantitative PCR was performed for cytokines (IL1A, IL6, CXCL8, IL10, TNFA) and brain biomarkers (ENO2, UCHL1, S100B, GFAP, CRP, BDNF, MAPT). MicroRNA was detected using GeneChip (Affymetrix) microarrays. Fold changes from baseline were compared between groups and correlated with cell death (TUNEL) at 48 h.
RESULTS
Within 6 h post-insult, we observed increased IL1A, CXCL8, CCL2 and ENO2 mRNA in LPS+Hypoxia and LPS compared to Hypoxia. IL10 mRNA differentiated all groups. Four microRNAs differentiated LPS+Hypoxia and Hypoxia: hsa-miR-23a, 27a, 31-5p, 193-5p. Cell death correlated with TNFA (R = 0.69; p < 0.01) at 1-3 h and ENO2 (R = -0.69; p = 0.01) at 48 h.
CONCLUSIONS
mRNA and miRNA differentiated hypoxia from inflammation-sensitized hypoxia within 6 h in a piglet model. This information may inform human studies to enable triage for tailored neuroprotection in NE.
IMPACT
Early stratification of infants with neonatal encephalopathy is key to providing tailored neuroprotection. IL1A, CXCL8, IL10, CCL2 and NSE mRNA are promising biomarkers of inflammation-sensitized hypoxia. IL10 mRNA levels differentiated all three pathological states; fold changes from baseline was the highest in LPS+Hypoxia animals, followed by LPS and Hypoxia at 6 h. miR-23, -27, -31-5p and -193-5p were significantly upregulated within 6 h of a hypoxia insult. Functional analysis highlighted the diverse roles of miRNA in cellular processes.

Identifiants

pubmed: 32521540
doi: 10.1038/s41390-020-0986-3
pii: 10.1038/s41390-020-0986-3
doi:

Substances chimiques

Biomarkers 0
Chemokines 0
Cytokines 0
Lipopolysaccharides 0
MicroRNAs 0
Nerve Tissue Proteins 0
RNA, Messenger 0
Tumor Necrosis Factor-alpha 0
Phosphopyruvate Hydratase EC 4.2.1.11

Types de publication

Comparative Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

464-475

Subventions

Organisme : Medical Research Council
ID : MR/M006743/1
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

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Auteurs

Ingran Lingam (I)

Neonatology, Institute for Women's Health, University College London, London, UK.

Adnan Avdic-Belltheus (A)

Neonatology, Institute for Women's Health, University College London, London, UK.

Christopher Meehan (C)

Neonatology, Institute for Women's Health, University College London, London, UK.

Kathryn Martinello (K)

Neonatology, Institute for Women's Health, University College London, London, UK.
Robinson Research Institute, University of Adelaide, Adelaide, SA, Australia.

Sara Ragab (S)

Neonatology, Institute for Women's Health, University College London, London, UK.

Donald Peebles (D)

Maternal Fetal Medicine, Institute for Women's Health, University College London, London, UK.

Melinda Barkhuizen (M)

Department of Pediatrics, University of Maastricht, Maastricht, The Netherlands.

Cally J Tann (CJ)

Neonatology, Institute for Women's Health, University College London, London, UK.
Maternal Adolescent, Reproductive and Child Health (MARCH) Centre, Department of Infectious Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, UK.

Ilias Tachtsidis (I)

Medical Physics and Biomedical Engineering, University College London, London, UK.

Tim G A M Wolfs (TGAM)

Department of Pediatrics, University of Maastricht, Maastricht, The Netherlands.

Henrik Hagberg (H)

Centre of Perinatal Medicine & Health, Department of Clinical Sciences, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.

Nigel Klein (N)

Paediatric Infectious Diseases & Immunology, Institute of Child Health, University College London, London, UK.

Bobbi Fleiss (B)

Centre for the Developing Brain, Kings College London, London, UK.

Pierre Gressens (P)

Centre for the Developing Brain, Kings College London, London, UK.
PROTECT, INSERM, Université Paris Diderot, Sorbonne Paris Cité, 75019, Paris, France.

Xavier Golay (X)

Department of Brain Repair & Rehabilitation, Institute of Neurology, University College London, London, UK.

Boris W Kramer (BW)

Maternal Fetal Medicine, Institute for Women's Health, University College London, London, UK.

Nicola J Robertson (NJ)

Neonatology, Institute for Women's Health, University College London, London, UK. n.robertson@ucl.ac.uk.

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