Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042961 (volvulus)
 4,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two horses with clinicopathologic evidence of endotoxic shock were randomly selected for a double-blind trial of hyperimmune lipopolysaccharide (LPS) core antigen plasma. Horses were suffering from acute toxic enteritis (n = 15), 360 degrees volvulus of the large colon (n = 9), proximal jejunitis/duodenitis (n = 6), or strangulating obstruction of the small intestine (n = 2). Plasma was harvested from suitable equine plasma donors (preimmune plasma) and horses were immunized with a whole-cell bacterin of an Rc mutant E. coli (J5). Plasma was again harvested from these horses when IgG ELISA titers recognizing LPS core antigen were greater than 1:32,000. All horses included in the trial received either preimmune or hyperimmune plasma in addition to traditional therapy (fluids, antimicrobials, antiinflammatory agents, etc.) as dictated by the attending clinician. The mortality rate in the group of horses receiving hyperimmune plasma was 13%; in the control group receiving preimmune plasma, the mortality rate was 47% (P = .045). Horses receiving J5 hyperimmune plasma had a significantly improved clinical appearance 48 hours after plasma administration (P less than .05) and a shorter period to recovery than control horses (P = .069).
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PMID:Protection against clinical endotoxemia in horses by using plasma containing antibody to an Rc mutant E. coli (J5). 267 Mar 8

Toll-like receptor 4 (TLR4) has been shown to be important for the induction of Th2-dependent immune responses in mice. Protective immunity against larval Onchocerca volvulus in mice depends on the development of a Th2 immune response mediated by both interleukin-4 (IL-4) and IL-5. In addition, O. volvulus contains the rickettsial endosymbiont Wolbachia, which has molecules with lipopolysaccharide-like activities that also signal through TLR4. We therefore hypothesized that protective immunity to O. volvulus would not develop in C3H/HeJ mice which have a mutation in the Tlr4 gene (TLR4 mutant), either because of a decreased Th2 response to the larvae or because of the absence of a response to Wolbachia. TLR4-mutant mice were immunized against O. volvulus with irradiated third-stage larvae, and it was observed that Th2 responses were elevated based on increased IL-5 production, total immunoglobulin E (IgE) levels, antigen-specific IgG1 response, and eosinophil recruitment. Protective immunity, however, did not develop in the TLR4-mutant mice. The Th1 response, as measured by gamma interferon production from spleen cells, was comparable in both wild-type and TLR4-mutant mice. Furthermore, antibody responses to Wolbachia were absent in both wild-type and TLR4-mutant mice. Therefore, the defect in the development of a protective immune response against O. volvulus in TLR4-mutant mice is not due to loss of Th2 immunity or the response to Wolbachia but is due to an unidentified TLR4-dependent larval killing mechanism.
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PMID:Protective immunity to the larval stages of onchocerca volvulus is dependent on Toll-like receptor 4. 1629 26