St Andrews Research Repository

St Andrews University Home
View Item 
  •   St Andrews Research Repository
  • University of St Andrews Research
  • University of St Andrews Research
  • University of St Andrews Research
  • View Item
  •   St Andrews Research Repository
  • University of St Andrews Research
  • University of St Andrews Research
  • University of St Andrews Research
  • View Item
  •   St Andrews Research Repository
  • University of St Andrews Research
  • University of St Andrews Research
  • University of St Andrews Research
  • View Item
  • Login
JavaScript is disabled for your browser. Some features of this site may not work without it.

Early-life adversity programs long-term cytokine and microglia expression within the HPA axis in female Japanese quail

Thumbnail
View/Open
Walker_2019_JEB_Early_life_FinalPubVersion.pdf (735.6Kb)
Date
27/02/2019
Author
Walker, David J.
Zimmer, Cédric
Larriva Hormigos, Maria
Healy, Susan D.
Spencer, Karen A.
Keywords
Cytokines
Developmental programming
Glucocorticoids
Neuroinflammation
Anti-inflammatory
Neuroimmune
QH301 Biology
RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
DAS
Metadata
Show full item record
Abstract
Stress exposure during prenatal and postnatal development can have persistent and often dysfunctional effects on several physiological systems, including immune function, affecting the ability to combat infection. The neuroimmune response is inextricably linked to the action of the hypothalamic–pituitary–adrenal (HPA) axis. Cytokines released from neuroimmune cells, including microglia, activate the HPA axis, while glucocorticoids in turn regulate cytokine release from microglia. Because of the close links between these two physiological systems, coupled with potential for persistent changes to HPA axis activity following developmental stress, components of the neuroimmune system could be targets for developmental programming. However, little is known of any programming effects of developmental stress on neuroimmune function. We investigated whether developmental stress exposure via elevated prenatal corticosterone (CORT) or postnatal unpredictable food availability had long-term effects on pro- (IL-1β) and anti-inflammatory (IL-10) cytokine and microglia-dependent gene (CSF1R) expression within HPA axis tissues in a precocial bird, the Japanese quail (Coturnix japonica). Following postnatal stress, we observed increased IL-1β expression in the pituitary gland, reduced IL-10 expression in the amygdala and hypothalamus, and reduced CSF1R expression within the hypothalamus and pituitary gland. Postnatal stress disrupted the ratio of IL-1β:IL-10 expression within the hippocampus and hypothalamus. Prenatal stress only increased IL-1β expression in the pituitary gland. We found no evidence for interactive or cumulative effects across life stages on basal cytokine and glia expression in adulthood. We show that postnatal stress may have a larger impact than elevated prenatal CORT on basal immunity in HPA-axis-specific brain regions, with changes in cytokine homeostasis and microglia abundance. These results provide evidence for postnatal programming of a pro-inflammatory neuroimmune phenotype at the expense of reduced microglia, which could have implications for central nervous system health and subsequent neuroimmune responses.
Citation
Walker , D J , Zimmer , C , Larriva Hormigos , M , Healy , S D & Spencer , K A 2019 , ' Early-life adversity programs long-term cytokine and microglia expression within the HPA axis in female Japanese quail ' , Journal of Experimental Biology , vol. 222 , jeb187039 . https://doi.org/10.1242/jeb.187039
Publication
Journal of Experimental Biology
Status
Peer reviewed
DOI
https://doi.org/10.1242/jeb.187039
ISSN
0022-0949
Type
Journal article
Rights
Copyright © 2019 The Authors. Published by The Company of Biologists Ltd. http://www.biologists.com/user-licence-1-1/ This work is made available online in accordance with the publisher’s policies. This is the final published version of the work, which was originally published at: https://doi.org/10.1242/jeb.187039
Description
This work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC grant no. BB/L002264/1 to K.A.S., C.Z. and S.D.H.), a David Phillips Research Fellowship (K.A.S.) and an EASTBIO BBSRC Doctoral Training Programme studentship (grant no. BB/J01446X/1 to D.J.W., supervisors K.A.S., S.D.H.). Data are available from Mendeley (Walker, 2019): http://dx.doi.org/10.17632/ 6r7d2pg2zk.1
Collections
  • University of St Andrews Research
URI
http://hdl.handle.net/10023/19542

Items in the St Andrews Research Repository are protected by copyright, with all rights reserved, unless otherwise indicated.

Advanced Search

Browse

All of RepositoryCommunities & CollectionsBy Issue DateNamesTitlesSubjectsClassificationTypeFunderThis CollectionBy Issue DateNamesTitlesSubjectsClassificationTypeFunder

My Account

Login

Open Access

To find out how you can benefit from open access to research, see our library web pages and Open Access blog. For open access help contact: openaccess@st-andrews.ac.uk.

Accessibility

Read our Accessibility statement.

How to submit research papers

The full text of research papers can be submitted to the repository via Pure, the University's research information system. For help see our guide: How to deposit in Pure.

Electronic thesis deposit

Help with deposit.

Repository help

For repository help contact: Digital-Repository@st-andrews.ac.uk.

Give Feedback

Cookie policy

This site may use cookies. Please see Terms and Conditions.

Usage statistics

COUNTER-compliant statistics on downloads from the repository are available from the IRUS-UK Service. Contact us for information.

© University of St Andrews Library

University of St Andrews is a charity registered in Scotland, No SC013532.

  • Facebook
  • Twitter