New data generated in mice by Andrew Gewirtz and colleagues at Emory University, Atlanta, has provided support for the hypothesis that defects in the innate immune system might underlie some cases of inflammatory bowel disease -- a group of disorders characterized by inflammation in the intestine.
In the study, mice lacking a protein known as TLR5 (which senses the bacterial protein flagellin and initiates a proinflammatory response) were found to spontaneously develop inflammation of the colon (colitis), whereas normal mice did not spontaneously develop this disease.
Just prior to the onset of spontaneous colitis increased numbers of bacteria were detected in the colon, as were very high levels of proinflammatory mediators. The latter observation was surprising given that TLR5-deficient mice lack an immune sensor of bacterial flagellin.
However, consistent with the authors idea that this increased proinflammatory response was induced by other sensors of bacterial products, mice lacking TLR4 and TLR5 did not develop colitis. These data indicate that a deficiency in an immune sensor of bacteria can lead to an increased inflammatory response in the intestine of mice.
Article: Deletion of TLR5 results in spontaneous colitis in mice, Journal of Clinical Investigation
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