High-fat diet activates splenic NOD1 and enhances neutrophil recruitment and neutrophil extracellular traps release in the spleen of ApoE-deficient mice.
Nod1(+/+) mice with chronic H. pylori infection exhibited significantly increased gastric IL-33 and splenic IL-13 responses but decreased IFN-gamma responses when compared with Nod1(-/-) animals. Collectively our data identify NOD1 as an important regulator of mucosal IL-33 responses in H. pylori infection. We suggest that NOD1 may play a role in protection against excessive inflammation.
this paper shows that deletion of NOD1 aggravated bone resorption induced by Gram-negative bacteria accompanied by an increase in the numbers of osteoclasts
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