Cytokine natural killer cells production

DiaZepin Nucleosides. Four naturally occurring dia2epin nucleosides, coformycin (58), 2 -deoxycoformycin (59), adechlorin or 2 -chloro-2 -deoxycoformycin (60), and adecypenol (61), have been isolated (1—4,174,175). The biosynthesis of (59) and (60) have been reported to proceed from adenosine and C-1 of D-ribose (30,176,177). They are strong inhibitors of adenosine deaminase and AMP deaminase (178). Compound (58) protects adenosine and formycin (12) from deamination by adenosine deaminase. Advanced hairy cell leukemia has shown rapid response to (59) with or without a-or P-interferon treatment (179—187). In addition, (59) affects interleukin-2 production, receptor expression on human T-ceUs, DNA repair synthesis, immunosuppression, natural killer cell activity, and cytokine production (188—194). 

Based upon recent controlled studies, there is considerable evidence that opioids such as morphine induce substantial effects on immune status. For example, it has been shown that morphine administration is associated with alterations in a number of immune parameters, such as natural-killer cell activity [12,13], proliferation of lymphocytes, [13, 14] antibody production [15,16], and the production of interferon [17]. Studies in our laboratory have shown that acute morphine treatment in rats suppresses splenic lymphocyte proliferative responses to both T- and B-cell mitogens, splenic natural-killer cell activity, blood lymphocyte mitogenic responsiveness to T-cell mitogens, and the in vitro production of the cytokines interleukin-2 and interferon-y [18-22], Furthermore, the immune alterations induced by morphine are dose-dependent and antagonized by the opioid-receptor antagonist, naltrexone (e.g., [22]). 

Perez, L. and Lysle, D.T., Corticotropin-releasing hormone is involved in conditioned stimulus-induced reduction of natural killer cell activity but not in conditioned alterations in cytokine production or proliferation responses, J. Neuroimmunol., 63, 1, 1995. 

The effect of echinacea on the immune system is controversial. In vivo human studies using commercially marketed formulations of E purpurea have shown increased phagocytosis, total circulating white blood cells, monocytes, neutrophils, and natural killer cells but not immunostimulation. In vitro, Epurpurea juice increased production of interleukins-1, -6, and -10, and tumor necrosis factor- by human macrophages. Enhanced natural killer cell activity and antibody-dependent cellular toxicity was also observed with E purpurea extract in cell lines from both healthy and immunocompromised patients. Studies using the isolated purified polysaccharides from Epurpurea have also shown cytokine activation. Polysaccharides by themselves, however, are unlikely to accurately reproduce the activity of the entire extract. 

Pycnogenol reduces the production of interleukin-6 and restores the activity of natural killer cells in retrovirus-infected animals. Pycnogenol delays the development of immune dysfunctions secondary to retrovirus infection by restoring the imbalanced cytokine secretion by T helper 1 and T helper 2 cells. 

The most relevant bioassays measure specific activities on immune function, either as effector or regulatory, for example, assay of cytokine IL-12 by the augmentation of the cytolytic function of natural killer cells (B9), IL-10 by the inhibition of the production of TNF-o from stimulated monocytes (B13), and IL-8 and eotaxin by the chemotaxis of neutrophils and eosinophils, respectively (C2). 

Conneely, 2001). LF has the ability to bind to the surface of several types of immune cells, which suggests that it can modulate immune functions. Both stimulatory and inhibitory effects of LF on lymphocyte proliferation have been described in the literature. LF has been reported to induce in vitro maturation of T- and B-lymphocytes, to modulate the activity of natural killer cells and to enhance the phagocytic activity of neutrophils. In mice, bovine LF has been shown to induce both mucosal and systemic immune responses (Debbabi et al., 1998). Cell-culture studies have demonstrated that LF and peptides derived from LF influence the production of various cytokines which regulate the immune and inflammatory responses of the body (Crouch et al., 1992 Shinoda et al., 1996). 

Recent studies further suggest that LF may have a role in the development and progression of tumors (Tsuda et al., 2002). Orally administered bovine LF has been found to inhibit the development of tumors in the colon, oesophagus and lung carcinogenesis in a rat or mouse model, but the mode of action remains to be resolved (Sekine et al., 1997 Ushida et al., 1999 Kuhara et al., 2000). The anti-tumor activity may be mediated by the enhanced cytokine production or the activating effect on natural killer cells and be independent of the iron-saturation level. 

The effects of marijuana on immune function have been reviewed (122). The studies suggest that marijuana affects immune cell function of T and B lymphocytes, natural killer cells, and macrophages. In addition, cannabis appears to modulate host resistance, especially the secondary immune response to various infectious agents, both viral and bacterial. Lastly, marijuana may also affect the cytokine network, influencing the production and function of acute-phase and immune cytokines and modulating network cells, such as macrophages and T helper cells. Under some conditions, marijuana may be immunomodulatory and promote disease. 

One reasonably thorough study examined immune function in rats orally dosed at up to 400 mg/kg/day 2-butoxyethanol twice after immunization with trinitrophenyl-lipopolysaccharide (TNP-LPS) (Smialowicz et al 1992). Compared with controls, the 2-butoxyethanol had no adverse effect on antibody production, delayed B type hypersensitivity, natural killer cell function, or splenocyte production of cytokines. 

In a mouse vaccination model adapted to study the effect of prebiotics, the animals were vaccinated twice with the Influvac Orthomyxovirus influenza) vaccine (booster vaccination after 21 days). The response to the vaccination was measured at day 30 after the first vaccination. Parameters used to identify the response to vaccination were DTH response (skin response after local subcutaneous vaccine injection as an in vivo measure for Thl-mediated immunity), plasma titers of specific antibodies, ex vivo lymphocyte stimulation, T-cell prohferation, cytokine production, and natural killer cell activity. A specific prebiotic mixture (GOS/lcFOS) significantly stimulated the vaccination response in a dose-dependent manner and increased the DTH response indicating a modulation of the immune system toward a Thl-dominated immune response. This effect only... 

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