Complex pattern of interaction between in utero hypoxia-ischemia and intra-amniotic inflammation disrupts brain development and motor function
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- 作者：Lauren L Jantzie (51) (52)
Christopher J Corbett (51)
Jacqueline Berglass (51)
Daniel J Firl (51)
Julian Flores (51)
Rebekah Mannix (51)
Shenandoah Robinson (51)
51. Departments of Neurology and Neurosurgery ; F.M. Kirby Center for Neurobiology ; Boston Children鈥檚 Hospital ; Harvard Medical School ; 300 Longwood Avenue ; Boston ; MA ; 02115 ; USA
52. Department of Pediatrics ; UNM ; Office of Pediatric Research ; MSC10 5590 ; 1 University of New Mexico ; Albuquerque ; NM ; 87131 ; USA - 关键词：Preterm ; Hypoxia ; ischemia ; Inflammation ; Lipopolysaccharide ; Erythropoietin ; Prematurity ; Myelin ; Neurofilament ; Gait ; Motor deficit
- 刊名：Journal of Neuroinflammation
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：11
- 期：1
- 全文大小：3,899 KB
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- 出版者：BioMed Central
- ISSN：1742-2094
文摘
Background Infants born preterm commonly suffer from a combination of hypoxia-ischemia (HI) and infectious perinatal inflammatory insults that lead to cerebral palsy, cognitive delay, behavioral issues and epilepsy. Using a novel rat model of combined late gestation HI and lipopolysaccharide (LPS)-induced inflammation, we tested our hypothesis that inflammation from HI and LPS differentially affects gliosis, white matter development and motor impairment during the first postnatal month. Methods Pregnant rats underwent laparotomy on embryonic day 18 and transient systemic HI (TSHI) and/or intra-amniotic LPS injection. Shams received laparotomy and anesthesia only. Pups were born at term. Immunohistochemistry with stereological estimates was performed to assess regional glial loads, and western blots were performed for protein expression. Erythropoietin ligand and receptor levels were quantified using quantitative PCR. Digigait analysis detected gait deficits. Statistical analysis was performed with one-way analysis of variance and post-hoc Bonferonni correction. Results Microglial and astroglial immunolabeling are elevated in TSHI + LPS fimbria at postnatal day 2 compared to sham (both P P P P P Conclusions Prenatal TSHI and TSHI + LPS lead to different patterns of injury with respect to myelination, axon integrity and gait deficits. Dual injury leads to acute alterations in glial response and cellular inflammation, while TSHI alone causes more prominent chronic white matter and axonal injury. Both injuries cause significant gait deficits. Further study will contribute to stratification of injury mechanisms in preterm infants, and guide the use of promising therapeutic interventions.