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CC16 drives VLA-2-dependent SPLUNC1 expression.

Natalie Iannuzo¹, Holly Welfley², Nicholas C Li³

¹Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.

Frontiers in Immunology

|December 6, 2023

Summary

This summary is machine-generated.

Club Cell Secretory Protein (CC16) enhances lung antimicrobial defenses by upregulating SPLUNC1 via the VLA-2 receptor. This pathway is crucial for reducing bacterial burden in the lungs.

Keywords:

CC16 SPLUNC1 airway epithelia mass spectrometry mycoplasma pneumoniae

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Area of Science:

Pulmonary immunology
Epithelial biology
Host-pathogen interactions

Background:

Club Cell Secretory Protein (CC16) protects against obstructive lung diseases and reduces pathogen burden.
The precise mechanisms of CC16's action within pulmonary epithelial cells remain unclear.
Understanding CC16's role in epithelial responses is vital for developing new therapeutic strategies.

Purpose of the Study:

To investigate if CC16 deficiency impairs epithelial host responses.
To identify novel receptors mediating CC16's activity in the pulmonary epithelium.

Main Methods:

Quantitative proteomics and mass spectrometry were used to analyze secreted proteins in CC16-deficient mouse tracheal epithelial cells (MTECs) and human nasal epithelial cells (HNECs).
Studies were conducted in both naive conditions and following *Mycoplasma pneumoniae* (Mp) challenge.
Validation of key findings was performed using Severe Asthma Research Program (SARP) cohorts.

Main Results:

CC16 deficiency led to a significant decrease in 8 antimicrobial proteins, including Short Palate Lung and Nasal Epithelial Clone 1 (SPLUNC1).
CC16 enhances SPLUNC1 expression in MTECs and HNECs through signaling via the Very Late Antigen-2 (VLA-2) receptor complex.
Administration of recombinant CC16 (rCC16) to mice reduced Mp burden and increased pulmonary SPLUNC1 production, an effect dependent on the VLA-2 binding site.

Conclusions:

CC16 plays a novel role in epithelial-driven host defense by increasing antimicrobial protein production.
VLA-2 is identified as a novel epithelial receptor for CC16, mediating enhanced SPLUNC1 production and antimicrobial activity.
These findings elucidate a critical molecular pathway for CC16 in lung immunity and host defense.