Sunday, December 4, 2011

Intestinal bacteria


We've all heard that there are good and bad bacteria naturally in our bodies, but are they really that helpful in the intestine? What do they even do on the intestinal mucosal surface?

Vaishnava, et al. (2011) hypothesized spatial segregation and limited bacterial colonization of the small intestine mucosal surface between microbiota and host caused by the secreted antibacterial lectin RegIIIϒ. Spatial segregation is the space naturally produced between the small intestine's outer mucosal lining or surface and the microbiota (microscopic bacteria) living there. Intestinal microbiota is only developed after development in the womb and birth as the bacteria from the mother and the surrounding environment come into contact with the infant and work to colonize the previously sterile gastrointestinal tract. The majority of the bacteria that colonize the intestine and colon consist of E. coli and streptococci. These intestinal bacteria help with digestion of enzymes, stimulating cell growth and immune responses to pathogens, and inhibiting the growth of harmful microbiota.

This study used various hybridized probes selecting for 16S rRNA and four types of mice genetically altered to either express or lack
the antibacterial lectin RegIIIϒ. They wanted to determine which type of mouse would express spatial segregation between the intestinal mucosal lining and the colonizing (introduced and growing) microbiota and if lectin RegIIIϒ was responsible. If the lectin was responsible for the mutualistic relationship between the natural microbiota and the spatial segregation then the mice missing the RegIII expression would experience little if none at all separation in the space between where the microbiota grew and the intestinal surface did not exist. The space between the surface and the microbiota potentially helps with intestinal functions by is it important?

They determined the lectin was actually responsible for the observed spatial segregation between the small intestinal mucosal surface and the microbiota because it limites the number of other bacteria capable of colonizing the host surface. This supported the study's hypothesis. They also determined the lectin to be niche-specific antibacterial functions influenced the lectin's ability to limit adaptive immunity responses while restricting the number of surface-associated antibiotic-resistant Gram+ bacteria. This study resulted in a new focus for research to determine if Gram- bacteria are capable of maintaining the necessary spatial segregation like that of the RegIII
ϒ is because of similar antibacterial factors.

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