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Rod-shaped Bacteria in Proximal Small Intestine Tied to Celiac Disease in Children
http://www.celiac.com/articles/22005/1/Rod-shaped-Bacteria-in-Proximal-Small-Intestine-Tied-to-Celiac-Disease-in-Children/Page1.html
Jefferson Adams

Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.

He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.

 
By Jefferson Adams
Published on 02/8/2010
 
Research indicates that rod-shaped bacteria, of the species Clostridium, Prevotella, and Actinomyces, in the proximal small intestine may contribute to some cases of celiac disease in children.

Research indicates that rod-shaped bacteria, of the species Clostridium, Prevotella, and Actinomyces, in the proximal small intestine may contribute to some cases of celiac disease in children.

Recent data builds on previous research by the team from 1985 to 1996, which proved that rod-shaped bacteria were present in the proximal small intestine of Swedish children with celiac disease, but not in those without celiac disease.

For the current study, Sten Hammarström and colleagues from Umeå University in Sweden used an electron microscope to scan proximal small intestine biopsies from 45 children with celiac disease taken between 2004 and 2007, and 18 without the condition.

To identify the bacteria, they used 16S ribosomal DNA sequencing in DNA extracted from biopsies washed with solution containing an agent that enriches bacteria attached to the epithelial lining.

In healthy children with no celiac disease, Streptococcus and Neisseria bacteria are most common of the normal, mucosa-associated microbial flora of the proximal small intestine, along with a limited number of other genera, including Veillonella, Gemella, Actinomyces, Rothia, and Hemophilus.

Surprisingly, the researchers found that microbial flora of the proximal small intestine in biopsies from celiac disease patients differed only slightly from that of the control subjects. Only a single biopsy tested positive for rod-shaped bacteria.

This finding made the team to look more closely at the microbial flora of nine frozen celiac disease samples that showed the presence of rod-shaped bacteria. In these samples, microbial flora were substantially richer in Clostridium, Prevotella, and Actinomyces compared with biopsies lacking rod-shaped bacteria.

The researchers also note that all three types of bacteria could be found in two current celiac disease biopsies taken from children born during the celiac disease epidemic in Sweden in 1985–1996, when the earlier study was carried out. During this time, rates of celiac disease in children younger than 2 years of age increased four-fold.

“We hypothesize that the increased frequency of rod-shaped bacteria in the jejuna mucosa of celiac disease children at least partly was due to the changes in infant-feeding practice during that time,” write the researchers.

The changes resulted from new national feeding recommendations for infants to delay the introduction of gluten-containing foods from 4 to 6 months. This meant that many more children consumed their first gluten without the protective benefits of breastfeeding, the researchers write. The recommendation was later reversed.

The study by Hammarström and co-workers supports their conclusion that these rod-shaped bacteria may contribute to celiac disease in genetically susceptible individuals by uptaking and transforming gluten into large immunogenic peptides, which can then cross with the bacterium through the epithelium, or interfere with the barrier action of the epithelium to permit the passage of gluten into the under-laying tissue.

“Such bacteria could be seen as an adjuvant promoting T-cell activation,” they say. “Whether the identified bacteria have any of these properties remain to be elucidated.”



Am J Gastroenterol 2009; 104: 3058–3067