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Defense Against Bacterial Pathogens01:31

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Related Experiment Video

Updated: Jul 1, 2025

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Bactericidal/permeability-increasing protein instructs dendritic cells to elicit Th22 cell response.

Sigrid Bülow1, Katharina U Ederer1, Jonas M Holzinger1

  • 1Institute of Clinical Microbiology and Hygiene, University Hospital Regensburg, 93053 Regensburg, Germany.

Cell Reports
|March 8, 2024
PubMed
Summary

Bactericidal/permeability-increasing protein (BPI) activates dendritic cells (DCs), promoting T helper 22 (Th22) cell differentiation. This BPI-DC-Th22 axis is crucial for maintaining intestinal homeostasis and protecting against colitis.

Keywords:
CP: ImmunologyDAMPT cellsTh22alarminbactericidal/permeability-increasing proteincolitisdendritic cellsinterleukin-2interleukin-22microbiota

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Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Neutrophil-derived bactericidal/permeability-increasing protein (BPI) exhibits known antimicrobial functions.
  • The role of BPI in modulating adaptive immune responses remains largely unexplored.

Purpose of the Study:

  • To investigate the function of BPI in dendritic cell (DC) activation and subsequent T cell differentiation.
  • To determine the role of the BPI-DC-Th22 axis in intestinal inflammation and homeostasis.

Main Methods:

  • Bone marrow-derived dendritic cells (BMDCs) were cultured and stimulated with BPI.
  • Cytokine production in response to BPI was analyzed using ELISA and flow cytometry.
  • T helper 22 (Th22) cell differentiation was assessed.
  • Dextran sodium sulfate (DSS)-induced colitis models in BPI-deficient and wild-type mice were employed.

Main Results:

  • BPI potently activates murine BMDCs, inducing the secretion of IL-2, IL-6, and TNF-α.
  • BPI stimulation of BMDCs promotes the differentiation of naive CD4+ T cells into Th22 cells, characterized by IL-22 production.
  • BPI-deficient mice exhibit exacerbated disease severity in DSS-induced colitis, correlating with impaired IL-22 induction.
  • Intestinal microbiota influences BPI-dependent IL-22 induction in CD4+ T cells from mesenteric lymph nodes.

Conclusions:

  • BPI serves as a potent activator of DCs, driving Th22 cell differentiation.
  • The BPI-mediated DC-Th22 cell pathway plays a significant role in maintaining intestinal homeostasis.
  • BPI is a key mediator in the immune response to gut microbiota and in protection against inflammatory conditions like colitis.