Acute LPS sensitization and continuous infusion exacerbates hypoxic brain injury in a piglet model of neonatal encephalopathy.

Autor:	Martinello KA; Institute for Women's Health, University College London, London, United Kingdom.; Robinson Research Institute, University of Adelaide, Adelaide, Australia., Meehan C; Institute for Women's Health, University College London, London, United Kingdom., Avdic-Belltheus A; Institute for Women's Health, University College London, London, United Kingdom., Lingam I; Institute for Women's Health, University College London, London, United Kingdom., Ragab S; Institute for Women's Health, University College London, London, United Kingdom., Hristova M; Institute for Women's Health, University College London, London, United Kingdom., Tann CJ; Institute for Women's Health, University College London, London, United Kingdom.; Maternal, Adolescent, Reproductive and Child Health Centre, Department of Infectious Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom., Peebles D; Institute for Women's Health, University College London, London, United Kingdom., Hagberg H; Centre of Perinatal Medicine & Health, Department of Clinical Sciences, Sahlgrenska Academy, Gothenburg University, Gothenburg, Sweden.; Centre for the Developing Brain, Department of Imaging Sciences and Biomedical Engineering, King's College London, King's Health Partners, St. Thomas' Hospital, London, United Kingdom., Wolfs TGAM; Department of Paediatrics, University of Maastricht, Maastricht, Netherlands., Klein N; Infection, Inflammation and Rheumatology, UCL Great Ormond Street Institute of Child Health, London, United Kingdom., Tachtsidis I; Medical Physics and Biomedical Engineering, University College London, London, United Kingdom., Golay X; Institute of Neurology, University College London, London, United Kingdom., Kramer BW; Department of Paediatrics, University of Maastricht, Maastricht, Netherlands., Fleiss B; Centre for the Developing Brain, Department of Imaging Sciences and Biomedical Engineering, King's College London, King's Health Partners, St. Thomas' Hospital, London, United Kingdom.; PROTECT, INSERM, Université Paris Diderot, Sorbonne Paris Cité, Paris, France., Gressens P; Centre for the Developing Brain, Department of Imaging Sciences and Biomedical Engineering, King's College London, King's Health Partners, St. Thomas' Hospital, London, United Kingdom.; PROTECT, INSERM, Université Paris Diderot, Sorbonne Paris Cité, Paris, France., Robertson NJ; Institute for Women's Health, University College London, London, United Kingdom. n.robertson@ucl.ac.uk.; Division of Neonatology, Sidra Medicine, Doha, Qatar. n.robertson@ucl.ac.uk.
Jazyk:	angličtina
Zdroj:	Scientific reports [Sci Rep] 2019 Jul 15; Vol. 9 (1), pp. 10184. Date of Electronic Publication: 2019 Jul 15.
DOI:	10.1038/s41598-019-46488-y
Abstrakt:	Co-existing infection/inflammation and birth asphyxia potentiate the risk of developing neonatal encephalopathy (NE) and adverse outcome. In a newborn piglet model we assessed the effect of E. coli lipopolysaccharide (LPS) infusion started 4 h prior to and continued for 48 h after hypoxia on brain cell death and systemic haematological changes compared to LPS and hypoxia alone. LPS sensitized hypoxia resulted in an increase in mortality and in brain cell death (TUNEL positive cells) throughout the whole brain, and in the internal capsule, periventricular white matter and sensorimotor cortex. LPS alone did not increase brain cell death at 48 h, despite evidence of neuroinflammation, including the greatest increases in microglial proliferation, reactive astrocytosis and cleavage of caspase-3. LPS exposure caused splenic hypertrophy and platelet count suppression. The combination of LPS and hypoxia resulted in the highest and most sustained systemic white cell count increase. These findings highlight the significant contribution of acute inflammation sensitization prior to an asphyxial insult on NE illness severity.
Databáze:	MEDLINE
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