2012
DOI: 10.1016/s0016-5085(12)62645-6
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Mo1791 MyD88 Has a Key Role for OLFM4, a Novel Anti-Inflammatory Mediator in H. pylori Infection

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“…Experiments in a MyD88 and OLFM4 double-knockout mouse model have demonstrated that the H. pylori colonization level in the model is similar to that in wild-type mice[ 25 ]. Even though the immune and inflammatory responses are enhanced compared with those in wild-type mice, infiltration of inflammatory cells in the gastric mucosa of double-knockout mice is lower than that in OLFM4 knockout mice[ 25 ]. Additionally, knocking out OLFM4 significantly up-regulates the MyD88 expression.…”
Section: Olfm4 In H Pylori Infectionmentioning
confidence: 99%
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“…Experiments in a MyD88 and OLFM4 double-knockout mouse model have demonstrated that the H. pylori colonization level in the model is similar to that in wild-type mice[ 25 ]. Even though the immune and inflammatory responses are enhanced compared with those in wild-type mice, infiltration of inflammatory cells in the gastric mucosa of double-knockout mice is lower than that in OLFM4 knockout mice[ 25 ]. Additionally, knocking out OLFM4 significantly up-regulates the MyD88 expression.…”
Section: Olfm4 In H Pylori Infectionmentioning
confidence: 99%
“…Additionally, knocking out OLFM4 significantly up-regulates the MyD88 expression. It has been shown that deletion of OLFM4 indirectly increases the MyD88 expression by enhancing NOD2 expression, whereas the deficiency of MyD88 leads to a loss of the feedback inhibition of the NF-κB pathway and of the resulting response[ 25 , 26 ].…”
Section: Olfm4 In H Pylori Infectionmentioning
confidence: 99%