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Systemic Inflammatory Activation of Astrocytes in Postnatal Development
Author(s) -
Alves Michele Joana,
Blackbourn Jessica,
Melo e Silva Talita,
Alzate Diego,
Jones Mikayla,
Otero Jose,
Czeiler Catherine
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.802.49
Subject(s) - astrocyte , neuroinflammation , microglia , inflammation , immune system , neuroscience , biology , neuroprotection , hypoxia (environmental) , central nervous system , immunology , chemistry , oxygen , organic chemistry
Systemic inflammation during the postnatal period triggers neuroinflammation which can have a multitude of deleterious effects on the newborn, including increased susceptibility to hypoxia. Astrocytes in the brainstem are capable of sensing oxygen levels and modulating the respiratory response accordingly. Astrocytes are also crucial players in neuroinflammation by regulating immune responses in the central nervous system. Upon activation, astrocytes promote the release of cytokines, which trigger immune cell infiltration and contribute to the exacerbation of existing inflammation. Paradoxically, astrocytes can also exert neuroprotective effects during activation. Therefore, it is important to understand the mechanism whereby astrocytes become activated and the factors affecting astrocyte behavior during inflammation. One of the hallmarks of astrocyte activation is a change in morphology and an increase in migratory behavior. It is unclear how this global change in morphology and migratory behavior affects the astrocyte's ability to sense and react to changing oxygen levels. In this study, we investigate the effects of systemic inflammation on the morphological/migratory pattern and oxygen sensing capacity of astrocyte populations derived from the hindbrain of 5‐day‐old mice. Results of this study increase our current understanding of astrocyte functional and morphological responses to an inflammatory milieu. Support or Funding Information This work was supported by NIH grant R01HL132355. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .