Sentence examples for mouse peritonitis model from inspiring English sources

Also the tpx mutant was attenuated in a mouse peritonitis model [26].

The mouse peritonitis model supported the SOD3-derived reduction in the number of infiltrating leukocytes (Figure 3A), which was predominantly due to reduced macrophage numbers (Figure 3B).

To confirm the findings and to further analyze the SOD3-derived selective inhibition of cell migration we examined leukocyte migration in a mouse peritonitis model, which provides an efficient way to analyze leukocyte traffic in an acute inflammatory response.

We used mouse peritonitis model, a well-documented experimental animal model for studying pathogenesis of inflammatory stimuli and evaluating in vivo efficacy of anti-inflammatory and anti-infectious treatments.

Furthermore the tpx mutant was attenuated in a mouse peritonitis model [26], In addition, in vitro enzymatic analysis of M. tuberculosis TpX and AhpC with different hydroperoxides including peroxynitrite showed that the TpX was more efficient and faster in peroxynitrite reduction than AhpC [21].

Two R-IVET systems with different levels of sensitivity have been constructed in a E. faecalis V583 derivative strain and tested in the insect model Galleria mellonella, during growth in urine, in a mouse bacteremia and in a mouse peritonitis model.

No differences in pathogenicity of E. faecalis were detected using a mouse bacteraemia and a mouse peritonitis models (tail vein and intraperitoneal injection).

In the present work the effect of SOD3 on the inflammatory cell extravasation was studied in vivo in rat hind limb ischemia and mouse peritonitis models by identifying the migrated cells and analyzing SOD3-derived response on inflammatory cytokine and adhesion molecule expression.

The fsr quorum sensing system has been shown to coordinate expression of the virulence factors gelE (encoding a gelatinase) and sprE (encoding a serine protease) during infection of C. elegans and in mouse peritonitis models [25], [101], and several other genes were differentially expressed in wild type OG1RF compared to an fsrB mutant, indicating a more complex regulatory network [103].

Other virulence genes detected correspond to msrA and msrB, encoding methionine sulfoxide reductases important for the oxidative stress response, macrophage survival, and persistent infection [ 51]; and gls genes encoding general stress proteins (Gls33 and Gls20), important for adaptation to the intestinal environment and in mouse peritonitis models [ 52].

Over 99% of S. suis cells were killed within 4 h in blood, lung, liver and spleen with dosage of 10, 20, and 40 mg/kg in mice peritonitis models and no pathogen were detected after 24 h of treatment.