39 research outputs found
Lipopolysaccharides of brucella abortus and brucella melitensis induce nitric oxide synthesis in rat peritoneal macrophages
Producción CientíficaSmooth lipopolysaccharide (S-LPS) and lipid A of Brucella abortus and Brucella melitensis induced the
production of nitric oxide (NO) by rat adherent peritoneal cells, but they induced lower levels of production
of NO than Escherichia coli LPS. The participation of the inducible isoform of NO synthase (iNOS) was
confirmed by the finding of an increased expression of both iNOS mRNA and iNOS protein. These observations
might help to explain (i) the acute outcome of Brucella infection in rodents, (ii) the low frequency of septic
shock in human brucellosis, and (iii) the prolonged intracellular survival of Brucella in humans.This work was supported by (grants FIS 96/1017, SAF96-0144, and SAF98-0176
Performance of LTE downlink communication system in presence of electronic warfare spot jamming
Role of plasma, lipopolysaccharide-binding protein, and CD14 in response of mouse peritoneal exudate macrophages to endotoxin
Plasma lipopolysaccharide (LPS)-binding protein (LBP) and membrane CD14 function to enhance the responses of monocytes to low concentrations of endotoxin. Surprisingly, recent reports have suggested that LBP or CD14 may be dispensable for macrophage responses to low concentrations of LPS or may even exert an inhibitory effect in the case of LBP. We therefore investigated whether LBP and CD14 participated in the response of mouse peritoneal exudate macrophages (PEM) to LPS stimulation. In the presence of a low amount of plasma (<1%) or of recombinant mouse or human LBP, PEM were found to respond to low concentrations of LPS (<5 to 10 ng/ml) in an LBP- and CD14-dependent manner. However, tumor necrosis factor production (not interleukin-6 production) by LPS-stimulated PEM was reduced when cells were stimulated in the presence of higher concentrations of plasma or serum (5 or 10%). Yet, the inhibitory effect of plasma or serum was not mediated by LBP. Taken together with previous results obtained with LBP and CD14 knockout mice in models of experimental endotoxemia, the present data confirm a critical part for LBP and CD14 in innate immune responses of both blood monocytes and tissue macrophages to endotoxins