Re: Activation of the maternal immune system induces endocrine changes in

[Guest guest]

If this same process occurs in humans,  how do they explain a twin pregnancy

that results in one neurotypical child and one with autism? 

 

Joyce

From: ElyseG <elyse-g@...>

Subject: Activation of the maternal immune system induces endocrine

changes in

Date: Wednesday, January 12, 2011, 12:39 AM

 

Brain Behav Immun. 2010 Dec 30.

Activation of the maternal immune system induces endocrine changes in the

placenta via IL-6.

Hsiao EY, PH.

California Institute of Technology, Pasadena, CA 91125, USA.

Abstract

Activation of the maternal immune system in rodent models sets in motion a

cascade of molecular pathways that ultimately result in autism- and

schizophrenia-related behaviors in offspring. The finding that interleukin-6

(IL-6) is a crucial mediator of these effects led us to examine the mechanism by

which this cytokine influences fetal development in vivo. Here we focus on the

placenta as the site of direct interaction between mother and fetus and as a

principal modulator of fetal development. We find that maternal immune

activation (MIA) with a viral mimic, synthetic double-stranded RNA (poly(I:C)),

increases IL-6 mRNA as well as maternally-derived IL-6 protein in the placenta.

Placentas from MIA mothers exhibit increases in CD69+ decidual macrophages,

granulocytes and uterine NK cells, indicating elevated early immune activation.

Maternally-derived IL-6 mediates activation of the JAK/STAT3 pathway

specifically in the spongiotrophoblast layer of the

placenta, which results in expression of acute phase genes. Importantly, this

parallels an IL-6-dependent disruption of the growth hormone-insulin-like growth

factor (GH-IGF) axis that is characterized by decreased GH, IGFI and IGFBP3

levels. In addition, we observe an IL-6-dependent induction in pro-lactin-like

protein-K (PLP-K) expression as well as MIA-related alterations in other

placental endocrine factors. Together, these IL-6-mediated effects of MIA on the

placenta represent an indirect mechanism by which MIA can alter fetal

development