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Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through

Ko Sato1,2, Ikumi Matsumoto3, Koya Suzuki4,5

  • 1Department of Intelligent Network for Infection Control, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan. ko-sato@med.tohoku.ac.jp.

Scientific Reports
|October 27, 2021
PubMed

Insights

Lung-specific claudin-18 (luCldn-18) is crucial for host defense against Cryptococcus deneoformans lung infections. Its deficiency impairs immune responses and alters the alveolar microenvironment, increasing susceptibility to fungal pathogens.

Area of Science:

  • Immunology
  • Mycology
  • Cell Biology

Background:

  • Cryptococcus deneoformans is an opportunistic fungal pathogen causing lung infections and meningoencephalitis.
  • Claudins (Cldns) form tight junctions in epithelial cells; Cldn-4 and Cldn-18 are expressed in airways, but their roles in respiratory infections are unclear.

Purpose of the Study:

  • To investigate the roles of Cldn-4 and lung-specific Cldn-18 (luCldn-18) in host defense against C. deneoformans pulmonary infection.

Main Methods:

  • Analysis of Cldn-4 and luCldn-18 deficient mice infected with C. deneoformans.
  • Measurement of cytokine production (e.g., IFN-γ), inflammatory cell infiltration (CD4+ T cells), K+ ion concentration, and pH in bronchoalveolar lavage fluids.
  • Assessment of fungal replication under varying pH conditions and in vivo.

Main Results:

  • luCldn-18 deficient mice showed increased susceptibility to pulmonary infection with impaired fungal clearance.
  • Decreased IFN-γ production and increased CD4+ T cell infiltration were observed in luCldn-18 deficient mice.
  • Deficiency in luCldn-18 led to elevated K+ ion concentrations, alveolar acidification, and enhanced fungal replication in acidic conditions.

Conclusions:

  • luCldn-18 plays a significant role in host defense against C. deneoformans lung infection.
  • luCldn-18 may influence cryptococcal infection outcomes by regulating the alveolar microenvironment's pH and ion balance.

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