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http://www.jneuroinflammation.com/content/5/1/52

<http://www.jneuroinflammation.com/content/5/1/52>

*1: *J Neuroinflammation. <javascript:

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Neuroinflammation.');> 2008 Nov 21;5(1):52. [Epub ahead of print]Click

here to read

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Impact of innate immunity in a subset of children with autism

spectrum disorders: a case control study.

*Jyonouchi H*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Jyonouchi\

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*Geng L*

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*Cushing-Ruby A*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cushing-R\

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*Quraishi H*

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Quraishi%\

20H%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

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ABSTRACT: BACKGROUND: Among patients with autism spectrum disorders

(ASD) evaluated in our clinic, there appears to be a subset that can

be clinically distinguished from other ASD children because of

frequent infections (usually viral) accompanied by worsening

behavioural symptoms and/or loss/decrease in acquired skills. This

study assessed whether these clinical features of this ASD subset

are associated with atopy, asthma, food allergy (FA), primary

immunodeficiency (PID), or innate immune responses important in

viral infections. METHODS: This study included the ASD children

described above (ASD test, N=26) and the following controls: ASD

controls (N=107), non-ASD controls with FA (N=24), non-ASD controls

with chronic rhinosinusitis/recurrent otitis media (CRS/ROM; N=38),

and normal controls (N=43). We assessed prevalence of atopy, asthma,

FA, CRS/ROM, and PID. Innate immune responses were assessed by

measuring production of proinflammatory and counter-regulatory

cytokines by peripheral blood mononuclear cells (PBMCs) in response

to agonists of Toll-like receptors (TLRs), with or without

pre-treatment of lipopolysaccharide (LPS), a TLR4 agonist. RESULTS:

Non-IgE mediated FA was equally prevalent in both ASD test and ASD

control groups, occurring at higher frequency than in the non-ASD

controls. Allergic rhinitis, atopic/non-atopic asthma, and atopic

dermatitis were equally prevalent among the study groups except for

the CRS/ROM group in which non-atopic asthma was more prevalent

(52.6%). CRS/ROM and specific polysaccharide antibody deficiency

(SPAD) were more prevalent in the ASD test group than in the ASD

control, FA, and normal control groups: 23.1% vs. <5% for CRS/ROS

and 19.2% vs. <1% for SPAD. However, CRS/ROM patients had the

highest prevalence of SPAD (34.2%). When compared to ASD and normal

case controls, PBMCs from 19 non-SPAD, ASD test group children

produced: 1) less IL-1beta with a TLR7/8 agonist, less IL-10 with a

TLR2/6 agonist, and more IL-23 with a TLR4 agonist without LPS

pre-treatment, and 2) less IL-1beta with TLR4/7/8 agonists with LPS

pre-treatment. These are cytokines associated with the neuro-immune

network. CONCLUSIONS: Clinical features of the ASD test group were

not associated with atopy, asthma, FA, or PID in our study but may

be associated with altered TLR responses mediating neuro-immune

interactions.

PMID: 19025588

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