Community-Acquired Respiratory Distress Syndrome Toxin: Unique Exotoxin for M. pneumoniae.

Xiaoling Su,Wei Tian,Jun He,Zufeng Ye,Keying Liang,Haodang Luo,Li Chen,Xiaoxing You

doi:10.3389/fmicb.2021.766591

Abstract

Mycoplasma pneumoniae infection often causes respiratory diseases in humans, particularly in children and adults with atypical pneumonia and community-acquired pneumonia (CAP), and is often exacerbated by co-infection with other lung diseases, such as asthma, bronchitis, and chronic obstructive pulmonary disorder. Community-acquired respiratory distress syndrome toxin (CARDS TX) is the only exotoxin produced by M. pneumoniae and has been extensively studied for its ADP-ribosyltransferase (ADPRT) activity and cellular vacuolization properties. Additionally, CARDS TX induces inflammatory responses, resulting in cell swelling, nuclear lysis, mucus proliferation, and cell vacuolization. CARDS TX enters host cells by binding to the host receptor and is then reverse transported to the endoplasmic reticulum to exert its pathogenic effects. In this review, we focus on the structural characteristics, functional activity, distribution and receptors, mechanism of cell entry, and inflammatory response of CARDS TX was examined. Overall, the findings of this review provide a theoretical basis for further investigation of the mechanism of M. pneumoniae infection and the development of clinical diagnosis and vaccines.

Highlights

Mycoplasma are cell wall-less and self-replicating prokaryotic microorganisms capable of causing diseases in animals and plants (Baseman et al, 1995; Rottem, 2003)
This review focused on the structures and features of CARDS TX, a unique exotoxin produced by M. pneumoniae, which is responsible for acute or chronic infections
Previous studies have suggested that CARDS TX can bind to the mammalian cell surface receptors such as surfactant protein-A (SP-A), annexin A2 (AnxA2), and non-proteinaceous receptors [phosphatidylcholine (PC), and sphingomyelin (SM)], which play an important role in cytopathology (Kannan et al, 2005; Kannan and Baseman, 2006; Somarajan et al, 2014; Becker et al, 2015)

Summary

Introduction

Mycoplasma are cell wall-less and self-replicating prokaryotic microorganisms capable of causing diseases in animals and plants (Baseman et al, 1995; Rottem, 2003). CARDS TX can independently cause cilia stagnation, vacuolization, nuclear fragmentation, and the release of inflammatory factors in infected mammalian cells, similar to the cytopathic pathology induced by M. pneumoniae. The expression of CARDS TX devoid of the N-terminal domain in M. pneumoniae caused a decrease in vacuolization of mammalian cell lines during infection, indicating an important role of N-terminus in maintaining the conformational integrity of the C-terminus (Kannan et al, 2014).

Results

Conclusion