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Updated: Apr 25, 2026

Assessing Anti-fungal Activity of Isolated Alveolar Macrophages by Confocal Microscopy
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The Tyrosine Kinase Receptor EphA2 in Alveolar Macrophages Provides a Protective Role in Host Defense Against

Theodore J Kottom1, Madeline Pellegrino1, Conrad Achilonu1

  • 1Department of Pulmonary and Critical Care Medicine, Thoracic Diseases Research Unit, Mayo Clinic College of Medicine, 221 First Street SW, Rochester, Minnesota 55905, USA.

The Journal of Infectious Diseases
|April 24, 2026
PubMed
Abstract

Insights

EphA2 signaling is crucial for alveolar macrophages to fight Pneumocystis pneumonia (PCP) by promoting inflammation. Targeting EphA2 may help manage inflammation during severe PCP while maintaining host defense.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Alveolar macrophages (AMs) are key in host defense against Pneumocystis, balancing pathogen clearance and lung inflammation.
  • EphA2 receptor binds fungal β-glucans and regulates host-pathogen interactions, but its role in AMs during Pneumocystis pneumonia (PCP) is unclear.

Purpose of the Study:

  • To investigate the role of EphA2 in alveolar macrophage inflammatory responses to Pneumocystis.
  • To determine the impact of EphA2 signaling on host defense and inflammation during Pneumocystis pneumonia (PCP).

Main Methods:

  • Evaluated AM inflammatory responses to Pneumocystis β-glucans with and without EphA2.
  • Utilized a CD4-depleted mouse model of PCP, comparing wild-type and EphA2-deficient mice.
  • Assessed lung cytokine levels and organism burden; inhibited EphA2 signaling pharmacologically.

Main Results:

  • EphA2 deficiency reduced AM pro-inflammatory cytokine responses to Pneumocystis β-glucans.
  • EphA2-deficient mice showed decreased lung inflammation but increased organism burden in a PCP model.
  • Pharmacological EphA2 inhibition suppressed lung inflammation during antimicrobial therapy.

Conclusions:

  • EphA2 signaling is critical for AM-mediated host defense against Pneumocystis, promoting essential inflammatory responses for organism control.
  • While EphA2 signaling aids in controlling Pneumocystis, it also contributes to lung inflammation.
  • Targeting EphA2 presents a potential strategy to modulate inflammation in severe PCP while preserving antimicrobial defense.
Keywords:
PneumocystisEphA2alveolar macrophage (AMs)inflammation

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