How Salmonella Enteritidis evades the innate immunity mechanisms using the length of lipopolysaccharide molecules

Jacek Rybka

Bacterial resistance to bactericidal activity of the serum is a crucial virulence factor for the development of systemic infections. The most important component of innate immunity in serum is the complement system, which consists of a cascade of proteins activated upon the recognition of foreign antigens. The recognition and activation of complement cascade leads to inflammatory response, attraction of phagocytic cells and elimination of microorganisms. Non-typhoidal Salmonella (NTS) infections are a serious public health problem. Salmonella has the ability to escape bactericidal of the complement system, realized by various mechanisms. Surprisingly, one of the mechanisms is the adaptation of the length of the lipopolysaccharide (LPS) molecule, which influences the complement activity. LPS is a main component of the outer membrane of Gram-negative bacteria. LPS molecule consists of three structural domains: lipid A, core oligosaccharide and O-specific chain (O-antigen). O-antigen is built of varying number repeating oligosaccharide units (from one to over one hundred repeating units). In some bacteria, including Salmonella, the distribution of LPS molecules length creates a distinct modal pattern. In the lecture describes the research of analysis of LPS O-antigen length and modal patterns, creation of research model including a set of bacterial mutants varying in LPS modal distribution and analysis of their ability to evade the complement bactericidal activity.