Abnormal Development - Maternal Inflammation: Difference between revisions

Revision as of 08:37, 17 February 2012

Historic Embryology - Viral
1941 Rubella Cataracts \| 1944 Rubella Defects

Some Recent Findings

Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.^[1] "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."

References

↑ <pubmed>21964917</pubmed>

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Articles

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Cite this page: Hill, M.A. (2026, February 27) Embryology Abnormal Development - Maternal Inflammation. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Maternal_Inflammation

What Links Here?

[1] <pubmed>21964917</pubmed>

[1]

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+:{{Template:Environmental}}
-==2011==
+:{{Bacterial Links}}
-===Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse===
+:{{Viral Links}}
-Brain. 2011 Nov;134(Pt 11):3236-48. Epub 2011 Sep 29.
+==Some Recent Findings==
+{|
+|-bgcolor="F5FAFF"
+|
+* '''Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.'''<ref><pubmed>21964917</pubmed></ref> "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."
-Stolp HB, Turnquist C, Dziegielewska KM, Saunders NR, Anthony DC, Molnár Z.
+|}
-Source
-Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK. helen.stolp@dpag.ox.ac.uk
-Abstract
-It has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inflammation in C57Bl/6 mice at embryonic Day 13.5 of pregnancy, as early as 8 h after challenge, caused a significant reduction in cell proliferation in the ventricular zone of the developing cerebral cortex, as revealed by quantification of anti-phospho-Histone H3 immunoreactivity and bromodeoxyuridine pulse labelling. The angle of mitotic cleavage, determined from analysis of haematoxylin and eosin staining, cyclin E1 gene expression and the pattern of β-catenin immunoreactivity were also altered by the challenge, which suggests a change from symmetric to asymmetric division in the radial progenitor cells. Modifications of cortical lamination and gene expression patterns were detected at post-natal Day 8 suggesting prolonged consequences of these alterations during embryonic development. Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour.
+==References==
-PMID 21964917
+<references/>
+===Reviews===
+===Articles===
+<pubmed></pubmed>
+===Search Pubmed===
+'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Maternal+Inflammation Maternal Inflammation]
+== External Links ==
+{{Template:Glossary}}
+{{Template:Footer}}
+[[Category:Abnormal Development]] [[Category:Environmental Abnormalities]]