Abstract: The invention relates to the innate immune pathway and anti-inflammatory molecules with therapeutic properties. In some embodiments, the invention relates to compounds and pharmaceutical compositions and methods of using the compounds and compositions to treat inflammatory diseases including inflammation associated with auto-immune diseases.

Abstract: The invention relates to the innate immune pathway and anti-inflammatory molecules with therapeutic properties. In some embodiments, the invention relates to compounds and pharmaceutical compositions and methods of using the compounds and compositions to treat inflammatory diseases including inflammation associated with auto-immune diseases.

Abstract: Provided are methods for recombinant production of an O-acetyltransferase and methods for acetylating capsular polysaccharides, especially those of a Serogroup A Neisseria meningitidis using the recombinant O-acetyltransferase, and immunogenic compositions comprising the acetylated capsular polysaccharide.

Abstract: Provided herein are mutant strains of Neisseria meningitidis which produce Kdo-free lipid A as well as the Kdo-free lipid A molecules and immunogenic compositions containing such Kdo-free lipid A molecules from a Neisseria strain containing a genetically stable mutation which inactivates a gene selected from the group consisting of genes encoding arabinose-5-phosphate isomerase, CMP-Kdo synthetase and CMP-Kdo transferase. N. meningitidis NMB206 is a specifically exemplified strain which harbors a stable insertion mutation in the gene (kpsF) encoding A5P isomerase; strain NMB-249 is a specifically exemplified strain with a stable insertion mutation in the gene (kdtA) encoding CMP-Kdo synthetase, and strain NMB259 is specifically exemplified strain with a stable insertion mutation in the gene (kdsB) encoding CMP-Kdo transferase. Also provided by the present invention are methods for the production of Lipid A flee of 3-keto-3-deoxyoctanoic acid using these genetically stable N. meningitidis mutants.

Abstract: Provided are methods for recombinant production of an O-acetyltransferase and methods for acetylating capsular polysaccharides, especially those of a Serogroup A Neisseria meningitidis using the recombinant O-acetyltransferase, and immunogenic compositions comprising the acetylated capsular polysaccharide.

Abstract: Provided are recombinant DNA molecules that do not occur in nature encoding a Lot3 O-acetyltransferase, vectors that direct expression of a Lot O-acetyltransferase, recombinant host cells which express a Lot3 O-acetyltransferase, methods for recombinant production of a Lot3 O-acetyltransferase, methods for acetylating lipooligosaccharides, especially those of a Neisseria meningitidis using a recombinant Lot O-acetyltransferase, and immunogenic compositions comprising the acetylated lipooligosaccharide.

Abstract: Macrolide resistance associated with macrolide efflux (mef) in Streptococcus pneumoniae has been defined with respect to the genetic structure and dissemination of a novel mefE-containing chromosomal insertion element. The mefE gene is found on the 5?-end of a 5.5 kb or 5.4 kb insertion designated mega (macrolide efflux genetic assembly) found in at least four distinct sites of the pneumococcal genome. The element is transformable and confers macrolide resistance to susceptible S. pneumoniae. The first two open reading frames (ORFs) of the element form an operon composed of mefE and a predicted ATP-binding cassette homologous to msrA. Convergent to this efflux operon are three ORFs with homology to stress response genes of Tn5252. Mega is related to mefA-containing element Tn1207.1. Macrolide resistance due to mega has been rapidly increased by clonal expansion of bacteria containing it and horizontally by transformation of previously sensitive bacteria.

Abstract: Genes isolated from Neisseria memingitidis, as well as isolated nucleic acids, probes, expression cassettes, polypeptides, antibodies, immunogenic compositions, antisense nucleic acids, amplification mixtures, and new invasion deficient swains of Neisseria meningitidis are provided Methods of detecting Neisseria meningitidis and Neisseria meningitidis nucleic acids, and methods of inhibiting the invasion of mammalian cells by Neisseria meningitidis are also provided.

Abstract: The present invention is based on the discovery of meningococcal isolates having genetic markers of a particular serogroup but expressing a capsular polysaccharide of a different serogroup. These isolates and prototype serogroup A, B, C, Y and W-135 strains were used to define the capsular biosynthetic operon of the major meningococcal serogroups and to show that capsule switching occurs as a result of allelic exchange of, for example, the polysialyl-transferase gene. Findings of capsule switching in vivo indicate that closely related virulent meningococcal clones may not be recognized by traditional serogroup-based surveillance and can escape vaccine-induced or natural protective immunity by capsule switching.

Abstract: Provided herein are mutant strains of Neisseria meningitidis which produce lipooligosaccharide (LOS) differing from the wild-type LOS in structure as well as the mutant LOS molecules and immunogenic compositions containing truncated LOS molecules from a Neisseria strain containing a genetically stable in a gene selected from the group consisting of genes encoding .alpha.-1,2-N-acetylglucosamine transferase and a gene homology to an Escherichia coli gene encoding 1-acyl-sn-glycerol-3-phosphate acyltransferase. N. meningitidis NMB-559 harbors an insertion mutation in the gene encoding .alpha.-1, 2-N-acetylglucosamine transferase, and N. meningitidis NMB-469 harbors an insertion mutation in an nlaB gene, the protein product of which has significant amino acid sequence homology to the E. coli gene encoding 1-acyl-sn-glycerol-3-phosphate acyltransferase.