A Comprehensive Review on the Manipulation of the Sphingolipid Pathway by Pathogenic Bacteria.

Monica Rolando,Carmen Buchrieser

doi:10.3389/fcell.2019.00168

Abstract

Bacterial pathogens have developed many different strategies to hijack host cell responses to promote their own survival. The manipulation of lipid biogenesis and cell membrane stability is emerging as a key player in bacterial host cell control. Indeed, many bacterial pathogens such as Legionella, Pseudomonas, Neisseria, Staphylococci, Mycobacteria, Helicobacter, or Clostridia are able to manipulate and use host sphingolipids during multiple steps of the infectious process. Sphingolipids have long been considered only as structural components of cell membranes, however, it is now well known that they are also intracellular and intercellular signaling molecules that play important roles in many eukaryotic cell functions as well as in orchestrating immune responses. Furthermore, they are important to eliminate invading pathogens and play a crucial role in infectious diseases. In this review, we focus on the different strategies employed by pathogenic bacteria to hijack the sphingolipid balance in the host cell to promote cellular colonization.

Highlights

Sphingolipids constitute an important class of lipids that are structural modules in eukaryotic membranes
The main hub in the sphingolipid pathway is ceramide that can be synthesized de novo from serine and palmitate, present in the endoplasmic reticulum (ER) and in ER-associated membranes, or from the breakdown of sphingomyelin (SM) into ceramide and phosphatidylcholine catalyzed by sphingomyelinase enzymes (SMases) (Figure 1)
The ceramide generated by acidic SMase (ASM), for example, resides either in the lysosome or at the plasma membrane, where ceramide aggregates into microdomains

Summary

Introduction

Sphingolipids constitute an important class of lipids that are structural modules in eukaryotic membranes. They modulate the reorganization of cellular membrane receptors and regulate the internalization of bacteria in the host cell, as well as the subsequent fusion of phagosomes and lysosomes. Many bacterial pathogens have acquired the ability to counteract the cellular response and to change the sphingolipid balance of the cell they infect.

Results

Conclusion