Lipopolysaccharide (LPS)-related damage by H. pylori

Abstract

The outer membrane of the cell wall of Gram-negative bacteria is a protective layer that controls the entry of many large molecules and protects the cell from potentially damaging agents. For those bacteria that come in contact with animals an important component of the Gram-negative outer membrane is lipopolysaccharide (LPS), a complex molecule not found elsewhere in nature. LPS, also termed endotoxin, represents the main surface antigen (O-antigen) for Gram-negative bacteria. The term endotoxin was coined by Pfeiffer in 1982, when he noted that certain toxic material was not excreted from living bacteria, as an exotoxin, but rather was released when the bacteria underwent lysis¹. LPS is firmly bound to the bacterial cell and is composed of three main domains² (Fig. 1). An outer polysaccharide chain, called the O-specific chain, contributes to the antigenicity and serospecificity of the molecule and is composed of repeating units that may contain up to seven different sugars. This O-specific chain is thus a polymer of identical repeating units, and is of large size since it can be up to 50 repeating units in length. The second component of the molecule is a short series of core sugars (approximately 10–15) while the innermost lipid component, termed lipid A, anchors LPS in the outer leaflet of the membrane. The fatty acids in lipid A vary with the microbial species, and endow hydrophobicity to the molecules. Thus LPS is an essential structure of all Gram-negative bacteria whether their natural habitat is salt lakes, ocean sediments, root nodules or the human gut. LPS is not a specific component to bacterial pathogens, rather it is a universal component of these organisms, be they friend or foe.