TNF-alpha mRNA expression in diaphragm muscle after endotoxin administration.

Abstract

We studied gene expression and production of TNF-alpha in the diaphragm tissue and changes of muscle contractile properties after endotoxin injection (Escherichia coli, 20 mg/kg) in 88 rats. We assessed the muscle contractile properties by force-frequency curves and twitch kinetics using dissected diaphragm muscle strips. The peak tensions of force-frequency curves decreased from control values (2.15 +/- 0.2 kg/cm2) up to 4 h (0.81 +/- 0.17, p < 0.001), and then increased at 6 h (1.36 +/- 0.19, p < 0.05) after endotoxin injection. The cytotoxic activity on L929 cells in arterial blood samples maximally increased at 2 h (p < 0.001), then decreased to 6 h (p < 0.05). TNF-alpha mRNA in diaphragm tissue was detected by Northern blot method at 1 and 1.5 h, and the immunolocalization of TNF-alpha was evaluated at 2 and 4 h by immunohistochemistry in the muscle tissues. Furthermore, preinjection with anti-m TNF-alpha antibody prevented the decrement of force-frequency curves after endotoxin injection of 10 microliters/kg. From this evidence that TNF-alpha gene expression and production occurred in the diaphragm tissue, but anti-m TNF-alpha antibody preinjection prevented the deterioration of diaphragm muscle contractile properties, we suggest that TNF-alpha may act on muscle cells extracellularly.

Lipopolysaccharide regulates proinflammatory cytokine expression in mouse myoblasts and skeletal muscle

“…LPS is a potent stimulus for cytokine synthesis by a variety of cell types including macrophage, peripheral blood mononuclear cells, and endo-thelial cells. But less is known about the regulation of cytokine mRNAs in skeletal muscle (39,40). We examined the ability of LPS to increase TNF-␣ and IL-6 mRNA in the skeletal muscle of mice injected intraperitoneally with LPS by RPA.…”

Cerium oxide nanoparticle treatment ameliorates peritonitis-induced diaphragm dysfunction

“…15 Whether this increase in survivability following CeO 2 nanoparticle intervention also associated with improvements of diaphragm function is currently unclear. On the basis of previous data demonstrating that rodent diaphragm is particularly susceptible to elevations in oxidative stress and circulating cytokines, [16][17][18] we hypothesized that septic animals that had been treated with CeO 2 nanoparticles would exhibit improved diaphragmatic function compared with that observed in the untreated counterparts. Our findings suggest that CeO 2 nanoparticle treatment improves diaphragm contractility following a severe polymicrobial insult, and that this finding is associated with evidence of diminished muscle damage and inflammation.…”

Tulobuterol Patch Maintains Diaphragm Muscle Contractility for Over Twenty-four Hours in a Mouse Model of Sepsis

“…On the other hand, endotoxin is known to induce a decrease in diaphragm muscle contractility (i.e., diaphragm muscle weakness) due to its cellular damage by superoxides or free radicals and to induce TNF-α mRNA expression (Shindoh et al 1995). Concerning the effect of endotoxin on diaphragm muscle contractility, some cytokines of interleukin-10 (IL-10) (Taneda et al 1998), interleukin-13 (IL-13) (Takahashi et al 1999), and interleukin-12 (IL-12) (Nakahata et al 2001) prevent the depressive effects of endotoxin on diaphragm muscle contractility.…”