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Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.ORCID-id: 0000-0002-6928-4473
Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
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2019 (engelsk)Inngår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 77, s. 141-149Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Maternal care is crucial for infants and profoundly affects their responses to different kinds of stressors. Here, we examined how maternal separation affects inflammatory gene expression and the corticosterone response to an acute immune challenge induced by lipopolysaccharide (LPS; 40 µg/kg ip) in mouse pups, 8–9 days old. Maternal separation initially attenuated LPS-induced hypothalamic pro-inflammatory gene expression, but later, at 3 h after immune challenge, robustly augmented such gene expression and increased serum corticosterone levels. Providing the pups with a warm and soft object prevented the separation-induced augmented hypothalamic-pituitary-adrenal (HPA)-axis response. It also prevented the potentiated induction of some, but not all, inflammatory genes to a similar extent as did the dam. Our results show that maternal separation potentiates the inflammatory response and the resulting HPA-axis activation, which may have detrimental effects if separation is prolonged or repeated.

sted, utgiver, år, opplag, sider
Elsevier, 2019. Vol. 77, s. 141-149
Emneord [en]
Lipopolysaccharide, Hypothalamus, Cytokines, Inflammation, Maternal separation, Corticosterone
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-154886DOI: 10.1016/j.bbi.2018.12.016PubMedID: 30590109Scopus ID: 2-s2.0-85059128986OAI: oai:DiVA.org:liu-154886DiVA, id: diva2:1293205
Tilgjengelig fra: 2019-03-04 Laget: 2019-03-04 Sist oppdatert: 2019-04-08bibliografisk kontrollert
Inngår i avhandling
1. Interactions between the brain and the immune system in pain and inflammation
Åpne denne publikasjonen i ny fane eller vindu >>Interactions between the brain and the immune system in pain and inflammation
2019 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Reciprocal interactions between the nervous and immune systems have gained a lot of attention in the last two decades, especially after demonstrating that cytokine immunotherapies can induce depression and after describing the inflammatory reflex. A lot of effort has been dedicated to understanding how the signals from the immune system reach the brain and vice versa, and on their role in health and disease. However, it is not well-known which of the brain circuits, receptors and signalling molecules give rise to behavioural and affective changes induced by inflammation, such as reduced food intake and induction of negative mood. Moreover, although it is well established that early life stress leads to an increased risk of developing inflammatory diseases in adulthood, the acute effects of stress on the inflammatory response in childhood are not well described. Using mouse models of systemic and local inflammation, I studied (1) how inflammatory pain elicits negative affect, (2) if CGRPα is necessary for parabrachial-amygdaloid pathway-mediated behaviours associated with pain and inflammation, and finally, (3) what are the effects of stress on the inflammatory process during early life. The results indicate that (1) the negative affect of inflammatory pain is triggered by inhibition of serotonergic neurons of the dorsal raphe nucleus, as a result of prostaglandin E2 binding to EP3 receptors; (2) CGRPα is dispensable for most pain- and inflammation-related protective behaviours; (3) acute stress potentiates the pro-inflammatory cytokine expression after an inflammatory challenge in mouse pups. The phenomena studied here can contribute to understanding how immune system activation induces changes in mood and behaviour common for inflammation and depression.

sted, utgiver, år, opplag, sider
Linköping: Linköping University Electronic Press, 2019
Serie
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1679
Emneord
inflammation, pain, EP3Rs, serotonin, CGRP, conditioned taste aversion, maternal separation, maternal buffering
HSV kategori
Identifikatorer
urn:nbn:se:liu:diva-156181 (URN)10.3384/diss.diva-156181 (DOI)978-91-7685-084-8 (ISBN)
Disputas
2019-05-10, Hasselquistsalen, Växthuset, Campus US, Linköping, 09:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2019-04-08 Laget: 2019-04-08 Sist oppdatert: 2019-04-11bibliografisk kontrollert

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