more on antibiotic otitis Re: You AhR what you eat: linking diet, intestinal immune function, microbiota

[Guest guest]

Here is another excerpt, this from the paragraph following the

previously posted tidbit from Li et al.

We show that AhR deficiency or the reduced intake of dietary

AhR ligands contributes to increased immunopathology in a

model of DSS-induced colitis, causing injury to colonic epithelial

cells with enhanced immunopathology due to bacterial dissemination

(Wirtz et al., 2007). Although reduced control of the

microbial load or composition in mice deficient in critical microorganism

control mechanisms results in increased susceptibility

to DSS-induced injury and reduced epithelial proliferation

(Rakoff-Nahoum et al., 2004; Vijay-Kumar et al., 2007), mice

treated with broad-spectrum antibiotics or bred under germfree

conditions are similarly susceptible to DSS-induced colitis

(Maslowski et al., 2009; Rakoff-Nahoum et al., 2004). This indicates

that both elements of the microbiota and detection mechanisms

are required for maintaining a healthy epithelial barrier

(Mazmanian et al., 2008). Although IELs were important in reducing

excessive DSS-induced colitis, the kinetics of initial

accelerated weight loss after adoptive transfer of control IELs

(Figure 5D) could indicate that other cell types may play an additional

role. In line with this, we show that in the absence of IELs,

approximately 50% of AhR transcripts can still be detected in the

small intestine of mice fed an AhR ligand-low diet compared with

controls (Figure 4A). It is possible that AhR, although not essential

for the survival, development, or migration of other cell types,

is important for their function, for example, for the induced production

of IL-22 in Th17 cells or in populations of innate lymphoid

cells (Cua and Tato, 2010; Veldhoen et al., 2008) that may influence

recovery from DSS.

- - - -

Numerous anecdotes from parents of autistic children delineate

excessively recurrent otitis media during the child's first two years

and, correspondingly, numerous rounds of antibiotics. These

retrospective tellings generally include a description of the child's

regression into autism, often accompanied by the development of

persistent gastrointestinal pathology. ~//

Here is an excerpt from Li et al, highlight added:

An altered bacterial composition, but not load, in the absence

of AhR activity was not confined to the small intestine, where the

IEL populations are reduced, but was also observed in the colon.

This results in an accumulation of lymphocytes that show a

predominant type 1 profile characterized by the production of

IFN-g. This is in line with other murine models of colitis that report

a deleterious role of the intestinal microbiota, especially during

the transfer of T cells, and are dominated by a type 1 profile

(Cong et al., 1998). */The direct importance of the microbiota in

the activation of T cells was illustrated when AhR-deficient

mice were treated with a broad-spectrum antibiotic, reducing

both the number of T cells and their activation status/*. Our data

are in also line with observations made in mice genetically engineered

to lack TCRgd lymphocytes, contributing over half of the

intestinal IELs, which are more susceptible to certain bacterial,

protozoal, and viral infections and show increased morbidity

(King et al., 1999; Mombaerts et al., 1993; et al., 2000;

et al., 1996; Selin et al., 2001), and they are in agreement

with increased morbidity of AhR-deficient mice and their increased

susceptibility to colitis and rectal prolapse (Fernandez-

Salguero et al., 1997; Kimura et al., 2009).

>

> You AhR what you eat: linking diet and immunity.

> <http://www.ncbi.nlm.nih.gov/pubmed/22036556>

> Hooper LV.

> Cell. 2011 Oct 28;147(3):489-91.

>

> The aryl hydrocarbon receptor (AhR) is responsible for the toxic

> effects of environmental pollutants such as dioxin, but little is

> known about its normal physiological functions. Li et al. (2011) now

> show that specific dietary compounds present in cruciferous vegetables

> act through the AhR to promote intestinal immune function, revealing

> AhR as a critical link between diet and immunity.

>

>

> Comment on

>

> Exogenous stimuli maintain intraepithelial lymphocytes via aryl

> hydrocarbon receptor activation.

> <http://www.ncbi.nlm.nih.gov/pubmed/21999944>

> Li Y, Innocentin S, Withers DR, NA, Gallagher AR, Grigorieva

> EF, Wilhelm C, Veldhoen M.

> Cell. 2011 Oct 28;147(3):629-40. Epub 2011 Oct 13.

>

>

> PS: Everyone benefits when parents share informative anecdotes. This

> post may be forwarded hither and yon.

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