Maternal immune activation and autism - IL-6 - influenza vaccination

[Guest guest]

A juxtapositioning of several citations related to interleukin-6 and

brain development. No conclusive proof here, just speculationally

tantalizing tidbits possibly relevant to at least a small subgroup of

autistic children. Anecdotal insights would be appreciated.

Maternal immune activation and autism spectrum disorder: interleukin-6

signaling as a key mechanistic pathway.

<http://www.ncbi.nlm.nih.gov/pubmed/20924155>

-Athill EC, Tan J.

Neurosignals. 2010;18(2):113-28

http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20924155/?tool=pubmed

Activation of the maternal immune system induces endocrine changes in

the placenta via IL-6. <http://www.ncbi.nlm.nih.gov/pubmed/21195166>

Hsiao EY, PH.

Brain Behav Immun. 2011 May;25(4):604-15.

Maternal immune activation alters fetal brain development through

interleukin-6. <http://www.ncbi.nlm.nih.gov/pubmed/17913903>

SE, Li J, Garbett K, Mirnics K, PH.

J Neurosci. 2007 Oct 3;27(40):10695-702.

http://www.jneurosci.org/cgi/pmidlookup?view=long & pmid=17913903

Effect of influenza vaccine on markers of inflammation and lipid

profile. <http://www.ncbi.nlm.nih.gov/pubmed/15976761>

Tsai MY, Hanson NQ, Straka RJ, Hoke TR, Ordovas JM, Peacock JM, Arends

VL, Arnett DK.

J Lab Clin Med. 2005 Jun;145(6):323-7.

Despite wide use of the influenza vaccine, relatively little is known

about its effect on the measurement of inflammatory markers. Because

inflammatory markers such as C-reactive protein (CRP) are increasingly

being used in conjunction with lipids for the clinical assessment of

cardiovascular disease and in epidemiologic studies, we evaluated the

effect of influenza vaccination on markers of inflammation and plasma

lipid concentrations. We drew blood from 22 healthy individuals 1 to 6

hours before they were given an influenza vaccination and 1, 3, and 7

days after the vaccination. Plasma CRP, interleukin (IL)-6, monocyte

chemotactic protein 1, tumor necrosis factor alpha, IL-2 soluble

receptor alpha, and serum amyloid A were measured, and differences in

mean concentrations of absolute and normalized values on days 1, 3, and

7 were compared with mean baseline values. /*There was a significant

increase in mean IL-6 (P < .01 absolute values, P < .001 normalized

values) on day 1 after receiving the influenza vaccine*/. The mean

increases in normalized high sensitivity CRP values were significant on

day 1 (P < .01) and day 3 (P = .05), whereas the mean increase in

normalized serum amyloid A was significant only on day 1 (P < .05). No

significant changes were seen in mean concentrations of IL-2 soluble

receptor alpha, monocyte chemotactic protein-1, or tumor necrosis

factor-alpha. Of the lipids, significant decreases in mean

concentrations of normalized triglyceride values were seen on days 1 (P

< .05), 3 (P < .001), and 7 (P < .05) after vaccination. Our findings

show that the influenza vaccination causes transient changes in select

markers of inflammation and lipids. Consequently, clinical and

epidemiologic interpretation of the biomarkers affected should take into

account the possible effects of influenza vaccination.

See also:

Expression profiling of autism candidate genes during human brain

development implicates central immune signaling pathways.

<http://www.ncbi.nlm.nih.gov/pubmed/21935439>

Ziats MN, Rennert OM.

PLoS One. 2011;6(9):e24691.

http://dx.plos.org/10.1371/journal.pone.0024691

The Autism Spectrum Disorders (ASD) represent a clinically heterogeneous

set of conditions with strong hereditary components. Despite substantial

efforts to uncover the genetic basis of ASD, the genomic etiology

appears complex and a clear understanding of the molecular mechanisms

underlying Autism remains elusive. We hypothesized that focusing gene

interaction networks on ASD-implicated genes that are highly expressed

in the developing brain may reveal core mechanisms that are otherwise

obscured by the genomic heterogeneity of the disorder. Here we report an

in silico study of the gene expression profile from ASD-implicated genes

in the unaffected developing human brain. By implementing a biologically

relevant approach, we identified a subset of highly expressed

ASD-candidate genes from which interactome networks were derived.

Strikingly, immune signaling through NF?B, Tnf, and Jnk was central to

ASD networks at multiple levels of our analysis, and cell-type specific

expression suggested glia--in addition to neurons--deserve

consideration. */This work provides integrated genomic evidence that

ASD-implicated genes may converge on central cytokine signaling pathways/*.