The effects of subinhibitory concentrations of costus oil on virulence factor production in Staphylococcus aureus.

AIM: To determine the antimicrobial activity of costus (Saussurea lappa) oil against Staphylococcus aureus, and to evaluate the influence of subinhibitory concentrations of costus oil on virulence-related exoprotein production in staph. aureus. METHODS AND RESULTS: Minimal inhibitory concentrations (MICs) were determined using a broth microdilution method, and the MICs of costus oil against 32 Staph. aureus strains ranged from 0.15 to 0.6 µl ml(-1) . The MIC(50) and MIC(90) were 0.3 and 0.6 µl ml(-1) , respectively. Western blot, haemolytic, tumour necrosis factor (TNF) release and real-time RT-PCR assays were performed to evaluate the effects of subinhibitory concentrations of costus oil on virulence-associated exoprotein production in Staph. aureus. The data presented here show that costus oil dose dependently decreased the production of α-toxin, toxic shock syndrome toxin 1 (TSST-1) and enterotoxins A and B in both methicillin-sensitive Staph. aureus (MSSA) and methicillin-resistant Staph. aureus (MRSA). CONCLUSION: Costus oil has potent antimicrobial activity against Staph. aureus, and the production of α-toxin, TSST-1 and enterotoxins A and B in Staph. aureus was decreased by costus oil. SIGNIFICANCE AND IMPACT OF THE STUDY: The data suggest that costus oil may deserve further investigation for its potential therapeutic value in treating Staph. aureus infections. Furthermore, costus oil could be rationally applied in food products as a novel food preservative both to inhibit the growth of Staph. aureus and to repress the production of exotoxins, particularly staphylococcal enterotoxins.

Omega-3 fatty acids: investigations from cytokine regulation to pancreatic cancer gene suppression.

Omega-3 (omega-3) fatty acids have been clinically and experimentally associated with the amelioration of chronic and acute inflammation; however, the mechanisms for these observations have not been well defined. During the past decade, laboratories of nutrition and inflammation have demonstrated that the anti-inflammatory activities of omega-3 fatty acids occur at least in part through the inhibition of macrophage-elaborated tumor necrosis factor production and through inactivation of the nuclear factor-kappaB signaling pathway subsequently altering proinflammatory cytokine transcription. These observations led to further experiments that support a role for omega-3 fatty acids in the restoration of apoptosis in various chemoresistant tumor models through a similar inactivation of the nuclear factor-kappaB signaling pathway. The potential for nutritional modulation of host inflammation has been an ongoing and expanding area of investigation. An increased emphasis has been placed on the potential for diet and dietary supplements to serve as modulators of host response to disease, injury, and infection.

Restoration by dietary glutamine of reduced tumor necrosis factor production in a low-protein-diet-fed rat model.

Tumor necrosis factor-alpha (TNF) production by peritoneal macrophages and its dietary modification were investigated by using rats fed on a low-protein diet. The rats were given a 20% casein (control) diet or a 3% casein diet for 21 days, and TNF production was measured in activated macrophages of these animals. TNF production was significantly lower in macrophages from rats fed on the low-protein diet than that in macrophages from rats fed on the control diet. Oral administration of a cabbage extract, a known modulator of TNF production, to the low-protein-diet-fed rats significantly enhanced TNF production by macrophages. Glutamine supplementation to the low-protein diet significantly enhanced TNF production as well as TNF mRNA expression. These results indicate that the 3%-casein-diet-fed rat would be useful as a model for reduced TNF production in protein malnutrition. These results also suggest that glutamine administration restored the reduced TNF production associated with protein malnutrition.

Interleukin-15 and interferon-gamma participate in the cross-talk between natural killer and monocytic cells required for tumour necrosis factor production.

We have characterized the lymphocyte subset and the receptor molecules involved in inducing the secretion of TNF by monocytic cells in vitro. The TNF secreted by monocytic cells was measured when they were co-cultured with either resting or IL-15-stimulated lymphocytes, T cells, B cells or natural killer (NK) cells isolated from the peripheral blood of healthy subjects and from the synovial fluid from patients with inflammatory arthropathies. Co-culture with IL-15-activated peripheral blood or synovial fluid lymphocytes induced TNF production by monocytic cells within 24 hours, an effect that was mainly mediated by NK cells. In turn, monocytic cells induced CD69 expression and IFN-gamma production in NK cells, an effect that was mediated mainly by beta2 integrins and membrane-bound IL-15. Furthermore, IFN-gamma increased the production of membrane-bound IL-15 in monocytic cells. Blockade of beta2 integrins and membrane-bound IL-15 inhibited TNF production, whereas TNF synthesis increased in the presence of anti-CD48 and anti-CD244 (2B4) monoclonal antibodies. All these findings suggest that the cross-talk between NK cells and monocytes results in the sustained stimulation of TNF production. This phenomenon might be important in the pathogenesis of conditions such as rheumatoid arthritis in which the synthesis of TNF is enhanced.

AIP1, a water-soluble fraction from Artemisia iwayomogi, suppresses thymocyte apoptosis in vitro and down-regulates the expression of Fas gene.

The AIP1 fraction, a small water-soluble fraction purified from Artemisia iwayomogi, was shown to increase antibody production and suppress transplanted tumor cell growth in mice. In order to understand its immuno-modulating activity, we have examined the effect of the AIP1 on mouse thymocytes in vitro. Treatment of mouse thymocytes in culture with the fraction resulted in the suppression of the cell death and the extension of the cell survival. A mouse gene array provided a profile of gene expression change showing the pattern of up- and down-regulated genes by the AIP1 treatment, suggesting that the Fas/FasL-dependent apoptosis pathway might be modulated by the fraction.

[The influence of Bazhen decoction on hematopoietic modulator in anaemic mice].

This study was designed to evaluate the effect of Bazhen decoction on bone marrow depression induced by cyclophosphamide (CY) in mice. An experimental model of mouse bone marrow injury was established through cyclophosphamide induced and the following phenomena were observed. The techniques of culture of hematopoietic progenitor cell and hematopoietic growth factor assay were used. Bazhen decoction could obviously promote the proliferation of bone marrow cells of anaemic mice. The culture media of spleen cell, macrophage, lung and skeletal muscle treated with Bazhen decoction had much stronger stimulating effects on hematopoietic cells. The bone marrow cells of the anaemic mice could yield TNF through Bazhen decoction treatment. It was suggested that Bazhen decoction is clinically a hopeful drug used to cure bone marrow depression and attenuate the side effects of CY.