Lipopolysaccharide in bacterial chronic infection: Insights from Helicobacter pylori lipopolysaccharide and lipid A

Identification and Characterization of a Lipopolysaccharide ,2,3-Sialyltransferase from the Human Pathogen Helicobacter bizzozeronii

“…The results are summarized in Tables 3 and 4. H. bizzozeroni contains a core oligosaccharide linked via one 3-deoxy-D-manno-oct-2-ulosonic acid (Kdo) molecule to a lipid A molecule, as observed for H. pylori LPS (38). Mass spectrometry showed that the core oligosaccharide of H. bizzozeronii is composed of heptoses (Hep), hexoses (Hex), hexosamines (HexNAc), and deoxysugars (dHex).…”

Identification and Characterization of a Glycosyltransferase Involved in Acinetobacter baumannii Lipopolysaccharide Core Biosynthesis

“…In general, the lipid A region is considered the most toxic or inflammatory region of LPS, although the polysaccharide portion of the molecule also has potent immunomodulating and immunostimulating properties (24,33). LPS has been shown to contribute both to bacterial evasion of host immune responses, affecting both innate and acquired host responses to infection, and to initiation of an overwhelming host inflammatory response that significantly correlates with the morbidity and mortality of infected patients (15,24,32). Moreover, the cell surface location of LPS contributes to the interaction between the bacterium and its environment.…”

Helicobacter and Salmonella Persistent Infection Strategies

“…In addition, H. pylori evade signaling through TLR4, which recognizes lipopolysaccharide (LPS). H. pylori make an LPS that is 1000 times less pyrogenic and 500-fold less toxic than other Gram-negative enteric bacteria, such as Salmonella (Moran 2007). This evasion is thought to be due to underphosphorylation, underacylation, and substitution of long-chain fatty acids in the lipid A moiety of H. pylori (Moran 2007).…”

“…H. pylori make an LPS that is 1000 times less pyrogenic and 500-fold less toxic than other Gram-negative enteric bacteria, such as Salmonella (Moran 2007). This evasion is thought to be due to underphosphorylation, underacylation, and substitution of long-chain fatty acids in the lipid A moiety of H. pylori (Moran 2007). In addition, modifications in the H. pylori LPS may act as molecular mimics of human glycans to avoid immune recognition.…”