Tyrosine kinases, drugs, and Shigella flexneri dissemination

Abstract

Shigella flexneri is an enteropathogenic bacterium responsible for approximately 100 million cases of severe dysentery each year. S. flexneri colonization of the human colonic epithelium is supported by direct spread from cell to cell, which relies on actin-based motility. We have recently uncovered that, in intestinal epithelial cells, S. flexneri actin-based motility is regulated by the Bruton’s tyrosine kinase (Btk). Consequently, treatment with Ibrutinib, a specific Btk inhibitor currently used in the treatment of B-cell malignancies, effectively impaired S. flexneri spread from cell to cell. Thus, therapeutic intervention capitalizing on drugs interfering with host factors supporting the infection process may represent an effective alternative to treatments with antimicrobial compounds.

Keywords: :

• dissemination
• spread from cell to cell
• actin-based motility
• Shigella flexneri
• N-WASP
• phosphorylation
• Btk
• tyrosine kinase
• Ibrutinib

This article refers to:

10.4161/gmic.26523

Disclosure of Potential Conflicts of Interest

No potential conflict of interest was disclosed.