Modulation of Airway Expression of the Host Bactericidal Enzyme, sPLA2-IIA, by Bacterial Toxins

Author:

Wu Yongzheng1ORCID,Pernet Erwan2,Touqui Lhousseine34

Affiliation:

1. Unité de Biologie Cellulaire de l’Infection Microbionne, CNRS UMR3691, Institut Pasteur, Université de Paris Cité, 75015 Paris, France

2. Groupe de Recherche en Signalisation Cellulaire, Département de Biologie Médicale, Université du Québec à Trois-Rivières, Trois-Rivières, QC G8Z 4M3, Canada

3. Sorbonne Université, Inserm U938, Centre de Recherche Saint-Antoine (CRSA), 75012 Paris, France

4. Institut Pasteur, Université de Paris Cité, Mucoviscidose et Bronchopathies Chroniques, 75015 Paris, France

Abstract

Host molecules with antimicrobial properties belong to a large family of mediators including type-IIA secreted phospholipase A2 (sPLA2-IIA). The latter is a potent bactericidal agent with high selectivity against Gram-positive bacteria, but it may also play a role in modulating the host inflammatory response. However, several pathogen-associated molecular patterns (PAMPs) or toxins produced by pathogenic bacteria can modulate the levels of sPLA2-IIA by either inducing or inhibiting its expression in host cells. Thus, the final sPLA2-IIA concentration during the infection process is determined by the orchestration between the levels of toxins that stimulate and those that downregulate the expression of this enzyme. The stimulation of sPLA2-IIA expression is a process that participates in the clearance of invading bacteria, while inhibition of this expression highlights a mechanism by which certain bacteria can subvert the immune response and invade the host. Here, we will review the major functions of sPLA2-IIA in the airways and the role of bacterial toxins in modulating the expression of this enzyme. We will also summarize the major mechanisms involved in this modulation and the potential consequences for the pulmonary host response to bacterial infection.

Publisher

MDPI AG

Subject

Health, Toxicology and Mutagenesis,Toxicology

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