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Meningitis bacterium is viable without endotoxin
TLDR
A mutant of Neisseria meningitidis is isolated which is viable in spite of an early block in lipid A biosynthesis that causes a loss of endotoxin activity. Expand
Identification of a novel gene involved in pilin glycosylation in Neisseria meningitidis
TLDR
Insertional mutations were constructed in pglA in a range of meningococcal strains with well‐defined lipopolysaccharide (LPS) or pilin‐linked glycan structures to determine whether p glA had a role in the biosynthesis of these molecules, suggesting that PglA is a glycosyltransferase involved in the addition of galactose of the trisaccharide substituent of pilin. Expand
A lipopolysaccharide-deficient mutant of Neisseria meningitidis elicits attenuated cytokine release by human macrophages and signals via toll-like receptor (TLR) 2 but not via TLR4/MD2.
TLDR
Evidence is provided that N. meningitidis contains components other than LPS that can elicit biological responses via pathways that are independent of the TLR4/MD2 receptor system, and TLR2 is one of these alternate pathways. Expand
Modification of Lipid A Biosynthesis inNeisseria meningitidis lpxL Mutants: Influence on Lipopolysaccharide Structure, Toxicity, and Adjuvant Activity
TLDR
Modification of meningococcal lipid A biosynthesis can lead to novel LPS species more suitable for inclusion in human vaccines, as the combination of reduced toxicity and retained adjuvant activity has not been reported before for either lpxL or lpxM mutants from other bacterial species. Expand
Neisseria meningitidis expressing lgtB lipopolysaccharide targets DC‐SIGN and modulates dendritic cell function
TLDR
The use of lgtB LPS may provide a powerful instrument to selectively induce the desired arm of the immune response and potentially increase vaccine efficacy. Expand
The Omp85 protein of Neisseria meningitidis is required for lipid export to the outer membrane
TLDR
It is demonstrated, by fractionation of inner and outer membranes, that lipopolysaccharide and phospholipids mostly disappeared from the outer membrane and instead accumulated in the inner membrane, upon depletion of Omp85. Expand
Contributions of Neisseria meningitidis LPS and non‐LPS to proinflammatory cytokine response
TLDR
It is concluded that non‐LPS parts of N. meningitidis may play a role in the pathogenesis of meningococcal sepsis by inducing substantial TNF‐α, IL‐1β, and IFN‐γ production. Expand
Outer membrane composition of a lipopolysaccharide‐deficient Neisseria meningitidis mutant
TLDR
The presence of the capsular polysaccharide turned out to be essential for viability without LPS, as demonstrated by using a strain in which LPS biosynthesis could be switched on or off through a tac promoter‐controlled lpxA gene. Expand
Altered Linkage of Hydroxyacyl Chains in Lipid A of Campylobacter jejuni Reduces TLR4 Activation and Antimicrobial Resistance*
TLDR
Results indicate that lipid A modification resulting in amide-linked acyl chains in the lipid A is an effective mechanism to evade activation of the innate host defense and killing by antimicrobial peptides. Expand
Teasing apart structural determinants of `toxicity' and `adjuvanticity': implications for meningococcal vaccine development
TLDR
The ability of LPS to stimulate pro-inflammatory cytokine induction is not necessarily linked to its adjuvant activity, suggesting that the availability of this novel set of lipid A variants with improved pharmacological properties will be of great importance for the improvement of future outer membrane vesicle vaccines against N. meningitidis. Expand
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