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Crohn's disease

Suppression of p21Rac1 signalling contributes to skip-lesion phenotype in Crohn's disease

Nature Reviews Gastroenterology & Hepatology volume 11, page 332 (2014)Cite this article

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“Differences in immune signalling might underlie the dichotomy observed in the intestine of patients with Crohn's disease, in which apparently healthy mucosa alternates with ulcerated intestinal lesions in so called skip-lesions,” hypothesizes Maikel Peppelenbosch, author of a recent study published in Science Translational Medicine. Kinome profiles of uninflamed tissue from patients with IBD showed a striking suppression of p21Rac1-dependent signalling versus inflamed tissue from patients with IBD and healthy individuals as controls. Reduced signalling owing to the deregulation of proteins affecting p21Rac1 GTP hydrolysis and loading was associated with improved innate immune function.

This theory was borne out when the investigators inhibited p21Rac1 GTP loading with NSC23766 in monocytes derived from areas of patient tissue affected by Crohn's disease. After treatment, monocytes demonstrated levels of phagocytosis on a par with cells from healthy controls. In addition, monocytes isolated from areas of inflammation, which have hyperactive p21Rac1 signalling, displayed reduced rates of phagocytosis.

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References

  1. Parikh, K. et al. Suppression of p21Rac signaling and increased innate immunity mediate remission in Crohn's disease. Sci. Transl. Med. 6, 233ra53 (2014)

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Authors
  1. Gillian Patman
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Patman, G. Suppression of p21Rac1 signalling contributes to skip-lesion phenotype in Crohn's disease. Nat Rev Gastroenterol Hepatol 11, 332 (2014). https://doi.org/10.1038/nrgastro.2014.72

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