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TRPM5 Negatively Regulates Calcium-Dependent Responses in Lipopolysaccharide-Stimulated B Lymphocytes

Taiki Sakaguchi1, Ryu Okumura2, Chisato Ono3

  • 1Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Suita, Japan; WPI Immunology Frontier Research Center, Osaka University, Suita, Japan; Department of Cardiovascular Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.

Cell Reports
|June 11, 2020
PubMed

Insights

The transient receptor potential melastatin 5 channel (TRPM5) regulates B cell responses to lipopolysaccharide (LPS). TRPM5 deficiency in mice enhances B cell proliferation and inflammatory cytokine production, worsening endotoxic shock.

Area of Science:

  • Immunology
  • Cell Biology
  • Calcium Signaling

Background:

  • B cells produce cytokines and immunoglobulins upon lipopolysaccharide (LPS) stimulation.
  • Calcium signaling regulates T cell cytokine production, but its role in LPS-stimulated B cells is less understood.
  • Calcium-activated monovalent cation channels (CAMs) control cytosolic calcium levels.

Purpose of the Study:

  • To investigate the role of the transient receptor potential melastatin 5 channel (TRPM5) in regulating B cell responses to LPS.
  • To determine TRPM5's impact on calcium signaling and inflammatory responses in LPS-stimulated B cells.

Main Methods:

  • Utilized Trpm5-deficient mice and wild-type littermates.
  • Stimulated B cells with LPS.
  • Measured cytosolic calcium concentration, cell proliferation, and cytokine production (interleukin-6, CXCL10).
  • Assessed endotoxic shock severity and mortality in mice.

Main Results:

  • Trpm5-deficient B cells showed increased cytosolic calcium concentration after LPS stimulation.
  • Enhanced B cell proliferation and elevated levels of interleukin-6 and CXCL10 were observed in Trpm5-deficient mice.
  • Trpm5-deficient mice exhibited exacerbated endotoxic shock with increased mortality.

Conclusions:

  • TRPM5 negatively modulates calcium signaling in LPS-stimulated splenic B cells.
  • TRPM5 plays a critical role in regulating B cell proliferation and inflammatory responses.
  • TRPM5 is important for controlling the severity of endotoxic shock.

Keywords:
B lymphocytesCa(2+) signalingIL-6TRPM5endotoxic shock

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