Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
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Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UNIPROT:P43026 (
lipopolysaccharide
)
62,215
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Reactive arthritis
is usually self-limiting polyarthritis, which develops after certain gastrointestinal or urogenital tract infections, mostly in susceptible HLA B27-positive individuals. In the pathogenesis of this arthritis, it is probably important that structures of the causative bacteria are found in the affected joints. The structure found in the synovial fluid phagocytes of the patients with reactive arthritis after Yersinia, Salmonella, and Shigella infections has always been
lipopolysaccharide
(
LPS
) of the causative bacteria. It has been in a highly processed form but still immunoreactive. To follow the degradation process of
LPS
, we fed peripheral blood monocytes of healthy blood donors with heat-killed Yersinia enterocolitica O:3 bacteria in vitro and monitored the fate of
LPS
by immunofluorescence and immunoblotting methods. Heat-killed bacteria were used since Y. enterocolitica O:3 bacteria are able to live inside monocytes in vitro and dividing intracellular bacteria would have made it impossible to monitor the degradation process of
LPS
with these methods. Both the core region and the O-polysaccharide chain of
LPS
persisted in cytoplasmic vacuoles and on plasma membrane of monocytes through the 7-day follow-up time. Migration properties of processed
LPS
in sodium dodecyl sulfate-polyacrylamide gel electrophoresis suggested structural modifications of
LPS
. We also demonstrated that core epitopes appearing on the surface of Yersinia-fed monocytes on day 4 of incubation were processed intracellularly, suggesting that
LPS
-containing phagocytes are a constant source of membrane-active
LPS
in their microenvironment as well as in the joints of arthritic patients.
...
PMID:Yersinia lipopolysaccharide is modified by human monocytes. 769 97
Reactive arthritis
(ReA) has been recognized as a clinical disease entity for nearly 100 years. The prevalence is estimated to be 30-40/100,000 adults. The HLA-B27-associated form is part of the spondyloarthritis concept. According to the current hypothesis the arthritis follows a primary extra-articular infection and is characterized by the presence of bacterial antigen and/or of viable but non-culturable bacteria persisting within the joint. Pathogenesis involves the modification of host cells by pathogen-associated molecular patterns (PAMPs, e.g.
lipopolysaccharide
), bacterial effector proteins, the adaptive immune system, and the genetic background. Up to 30% of patients develop chronic symptoms, and therapeutic options for these patients are still limited. Data for recommendations to apply conventional disease-modifying anti-rheumatic drugs (DMARDs) are rare; however, sulfasalazine seems to be effective, and first reports on agents that block tumour necrosis factor (TNF) are promising. Combination therapy of several antibiotics might open the window to curing the disease; however, controlled clinical studies are needed.
...
PMID:Infection and musculoskeletal conditions: Reactive arthritis. 1712
Reactive arthritis
(ReA) is a sterile arthritis triggered by distal mucosal infection, which suggests a contribution from bacterial products. The pathogenesis of ReA is unclear. There are no international standards for the serological methods used to confirm ReA. In the present work, we analyzed the predominant bacterial component that triggered an immune response in a 24-year-old woman with acute ReA. The candidate bacterial trigger was investigated by measuring the antibacterial antibodies (all immunoglobulin classes and IgA) to Salmonella enteritidis, Shigella flexneri and Yersinia enterocolitica. ELISA for Salmonella gave a positive result. To identify the bacterial component triggering ReA, antibodies to crude lysate, outer membrane proteins (OMP), cytosolic fraction, supernatant proteins and
lipopolysaccharide
of S. enteritidis were analyzed in sera and synovial fluid (SF) by ELISA, dot blot, and Western blot. Among the antigen preparations, the antibody response to OMP was dominant in both serum and SF; a strong reaction to seven OMP bands (50-21 kDa) was observed. We concluded that OMP were the main bacterial antigens that trigged ReA in the reported case. Determining the triggering bacterial components in each case can help elucidate the precise causes of ReA and will contribute to the designing of a specific serological diagnostic method for this arthritis.
...
PMID:Study of predominant bacterial antigens triggering antibody response in Salmonella reactive arthritis: apropos of a case. 1764 39