Sentence examples for murine macrophage model from inspiring English sources

To demonstrate this, we used an M. smegmatis infected RAW 264.7 murine macrophage model system.

Following a similar approach, Wilson et al. analyzed the in vivo transcriptional response when Listeria monocytogenes infected a murine macrophage model [ 99].

In a murine macrophage model, M. avium-containing phagosomes acquired the preform of cathepsin D but this protein was not processed to the cleaved active form due to the blockage of pH reduction in mycobacterial phagosomes [ 33].

In this study, as a part of our on-going screening program to evaluate the anti-inflammatory potentials of medicinal mushrooms, we investigated the anti-inflammatory properties of an ethanol extract of P. cocos (EEPC) and the responsible underlying molecular mechanisms involved in an LPS-stimulated RAW 264.7 murine macrophage model.

Interestingly, the Δ metH mutant was not attenuated in the J774 murine macrophage model of infection, leading to the conclusion that this amino acid was available in the Brucella-containing vacuoles and that the intracellular attenuation of the rsh mutant was not due to amino acid starvation.

This is a relevant aspect because it has been demonstrated that iron depletion limits intracellular bacterial growth in murine macrophage models [ 50]. > -wrap-foot> The bacterial load (in arbitrary units) was measured by qPCR in infected head kidneys from fish from LS and HS families.

Hypoxia signalling is upregulated in cell-line and in murine macrophage models of bacterial infection, and HIF-1α overexpression is known to upregulate the antimicrobial activities of leukocytes, including phagocytosis, bacterial killing and leukocyte lifespan (Peyssonnaux et al., 2005; Walmsley et al., 2006; Zarember and Malech, 2005).

The results of our study reveal a pattern of H37Rv and H37Ra gene expression in broth and inside a murine macrophage infection model that is consistent with this hypothesis.

As proof of this principle, we tested the hypothesis that bacterial NO detoxification mechanisms can affect the abundance of host cell SNO, using a murine macrophage infection model.

In conclusion, our study demonstrated that EEPC is a potent inhibitor of pro-inflammatory mediators and cytokines in an LPS-stimulated RAW 264.7 murine macrophage cell model via down-regulating the NF-κB signaling pathway to attenuate their corresponding gene activations.

Setting: In vitro model of murine macrophage M. tuberculosis infection.