Mitogen-Activated Protein Kinases (MAPKs) and Enteric Bacterial Pathogens: A Complex Interplay

Ipsita Nandi, Benjamin Aroeti*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Diverse extracellular and intracellular cues activate mammalian mitogen-activated protein kinases (MAPKs). Canonically, the activation starts at cell surface receptors and continues via intracellular MAPK components, acting in the host cell nucleus as activators of transcriptional programs to regulate various cellular activities, including proinflammatory responses against bacterial pathogens. For instance, binding host pattern recognition receptors (PRRs) on the surface of intestinal epithelial cells to bacterial pathogen external components trigger the MAPK/NF-κB signaling cascade, eliciting cytokine production. This results in an innate immune response that can eliminate the bacterial pathogen. However, enteric bacterial pathogens evolved sophisticated mechanisms that interfere with such a response by delivering virulent proteins, termed effectors, and toxins into the host cells. These proteins act in numerous ways to inactivate or activate critical components of the MAPK signaling cascades and innate immunity. The consequence of such activities could lead to successful bacterial colonization, dissemination, and pathogenicity. This article will review enteric bacterial pathogens’ strategies to modulate MAPKs and host responses. It will also discuss findings attempting to develop anti-microbial treatments by targeting MAPKs.

Original languageAmerican English
Article number11905
JournalInternational Journal of Molecular Sciences
Volume24
Issue number15
DOIs
StatePublished - Aug 2023

Bibliographical note

Publisher Copyright:
© 2023 by the authors.

Keywords

  • MAP kinases
  • MAPK inhibitors
  • anti-microbial treatments
  • cholera toxins
  • diarrheal diseases
  • enteric bacterial pathogens
  • host-pathogen interactions
  • inflammatory responses
  • type III secreted effectors

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