Allergy to quince

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Modulation of TNF-α, TNF-α receptors and IL-6 after treatment with AM3 in professional cyclists.

AIM: Changes in IL-6, TNF-α, and TNF-α receptors - sTNFRI and sTNFRII - were evaluated in a group of professional cyclists treated with immunomodulator AM3 (Inmunoferón®) for 6 months of training and competition. METHODS: Sixteen male professional cyclists with a similar training program participated in the study which was designed as a randomized, placebo-controlled, double-blind clinical trial. Venous blood samples were collected in basal conditions, before beginning the supplementation program, and after 90 and 180 days of training and competition season. RESULTS: No significant differences in biochemical parameters or in IL-6 were evidenced between placebo and AM3-treated groups throughout the study. Plasma TNF-α levels significantly decreased (P<0.05) after 90 days of training in the AM3 treated group. TNF-α receptors increased during training season in both placebo and AM3 treated groups, although the increase was significantly higher (P<0.05) in the AM3 group with respect to the placebo group. CONCLUSION: The changes produced by regular training and competition were modified throughout the season by AM3 treatment which could reduce the inflammatory response to excessive exercise.

[Effect of immunomodulator AM3 on the exacerbations in patients with chronic bronchitis: a systematic review of controlled trials]. / Efecto del inmunomodulador AM3 sobre las agudizaciones en enfermos con bronquitis crónica: una revisión sistemática de estudios controlados.

OBJECTIVE: Analyze the effect of AM3, an oral immunomodulator, on the exacerbations and on the use of antibiotics in patients with chronic obstructive pulmonary disease (COPD). DESIGN: Systematic search of controlled clinical trials that used AM3 in some treatment group and that included data on the clinical effects of this drug on patients with COPD. SELECTED VARIABLES: Nine studies were detected in which the clinical effectiveness of AM3 was evaluated in relation to the number of infectious exacerbations, their length, and the length of the antibiotic treatment used. RESULTS: In comparison with placebo group, the average number of excaerbations suffered by the patients treated with AM3 declined significantly in 0.31 units (p < 0.001; 95% confidence interval: 0.20-0.42), without heterogeneity among the different studies (Q = 6.62; p > 0.43). With regard to the average length of the exacerbations and the average length of the antibiotic treatment used for the exacerbations, both variables declined significantly in the group treated with AM3 (3.10 days, p < 0.001, and 8.07 days, p < 0.001, respectively) but this positive effect could not be confirmed because trials were close to heterogeneity. CONCLUSIONS: The results of this systematic review show that AM3 has a clinical effect in the prevention of exacerbations of COPD patients because reduces significantly their number. This could be related to a slowing in the progression of the deterioration in the respiratory function with a potential impact on the quality of life of the patients. Furthermore, these data imply a positive therapeutic result and a possible decline in development of bacterial resistances secondary to the frequent and indiscriminate use of antibiotics in these patients.

Efecto del inmunomodulador AM3 sobre las agudizaciones en enfermos con bronquitis crónica: una revisión sistemática de estudios controlados / Effect of immunomodulator AM3 on the exacerbations in patients with chronic bronchitis: a systematic review of controlled trials

Objetivo. Analizar el efecto de AM3, inmunomodulador oral, sobre las agudizaciones y el uso de antibióticos en pacientes con enfermedad pulmonar obstructiva crónica (EPOC).Diseño. Búsqueda sistemática de estudios clínicos controlados que emplearon AM3 en uno de los grupos de tratamiento y que incluyeron datos sobre los efectos clínicos de esta especialidad farmacéutica en pacientes con EPOC. Variables seleccionadas. Se localizaron 9 estudios en los que se estimó la eficacia clínica de AM3 en función del número de agudizaciones infecciosas, su duración y la del tratamiento antibiótico empleado. Resultados. Comparado con el grupo placebo el número medio de agudizaciones sufridas por los pacientes tratados con AM3 disminuyó significativamente en 0,31 unidades (p0,43).Respecto a la duración media tanto de las agudizaciones como la del tratamiento antibiótico pautado en las mismas, si bien ambas variables disminuyeron significativamente en el grupo tratado con AM3 (3,10 días, p<0,001, y 8,07 días, p<0,001, respectivamente), este efecto positivo no se pudo confirmar al tratarse de estudios cercanos a la heterogeneidad. Conclusiones. Los resultados de esta revisión sistemática muestran que AM3 tiene un efecto clínico en la prevención de las agudizaciones que sufren los pacientes afectos de EPOC al reducir significativamente su número. Esto podría relacionarse con un enlentecimiento en la progresión del deterioro de la función respiratoria y con un potencial impacto en la calidad de vida de los enfermos. Asimismo, estos datos suponen un resultado terapéutico positivo y un posible menor desarrollo de resistencias bacterianas que se produce por el uso frecuente e indiscriminado de antibióticos en estos pacientes (AU)

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Defective natural killer and phagocytic activities in chronic obstructive pulmonary disease are restored by glycophosphopeptical (inmunoferón).

We have investigated both modifications in natural (innate) immunity caused by chronic obstructive pulmonary disease (COPD) and the effects of a glycophosphopeptical immunomodulator (Inmunoferón) treatment on COPD-associated immunoalterations. In a double-blinded clinical trial, 60 patients with COPD received glycophosphopeptical or placebo during 90 consecutive days at oral doses of 3 g/d. Fifty-six sex- and age-matched healthy control subjects were included as a reference group for immunologic parameters. Peripheral blood natural killer (PBNK) cell cytotoxic activity and phagocytic activity of peripheral monocytes/macrophages (Mo/Ma) and polymorphonuclear (PMN) cells were assessed at baseline and then again at the end of treatments. We found both PBNK activity and phagocytic activity to be significantly decreased in patients with COPD compared with levels in healthy volunteers. The treatment with glycophosphopeptical provoked significant stimulatory effects on PBNK cytotoxic activity. This stimulation was not mediated by an increase in CD3(-)CD56(+) NK cells. Further, glycophosphopeptical significantly increased the percentage of monocytes and PMNs that phagocytize Escherichia coli in vitro, as well as increased phagocytic indices. We conclude that peripheral blood cells of patients with COPD show clear defects in natural immunity that are partially rescued by glycophosphopeptical.

An extract of the fern Polypodium leucotomos (Difur) modulates Th1/Th2 cytokines balance in vitro and appears to exhibit anti-angiogenic activities in vivo: pathogenic relationships and therapeutic implications.

In the present study we show the capacity of an extract of the fern Polypodium leucotomos (PLE) to partially inhibit the production of cytokines showing a Th1 pattern (IL-2, IFN-gamma and TNF-alpha) in human PHA-stimulated peripheral blood mononuclear cells. The percentage of inhibition was 24% for IL-2, 72% for INF-gamma and 53% for TNF-alpha. With regard to Th2 cytokines, the addition of PLE resulted in a significant increase (33%) in IL-10 production. Surprisingly, the production of the inflammatory cytokine IL-6 was completely abolished (100% inhibition) by PLE at all doses tested. In a second experiment in vivo we show that, the topical application of PLE to the skin of hairless albino mice (Skh-1) significantly diminished the mast cell infiltrate as well as the number of blood vessels triggered by chronic ultraviolet B (UVB) irradiation. These data show that PLE moderately inhibits the immunological Th1 responses, thus explaining the immunosuppressive as well as the anti-inflammatory and antioxidant activities reported in other studies carried out with PLE. The clear inhibitory effect on TFN-alpha and IL-6 production strongly suggest that this may be the mechanism by which PLE: (a) inhibits angiogenesis in vivo in the mouse model described here, and (b) prevents Langerhans' cells depletion caused by solar irradiation in humans. Taken together, these data suggest that PLE works through the induction of suppressive/anti-inflammatory cytokines such as IL-10 and/or TGF-beta which in turn appear to allow the partial deactivation of macrophages or other accessory cells. These features suggest that PLE could be useful in the treatment of autoaggressive/inflammatory conditions due to an exacerbation of Th1 responses.

Liposomal amphotericin B and amphotericin B-deoxycholate show different immunoregulatory effects on human peripheral blood mononuclear cells.

Conventional preparations of amphotericin B (AmB) at established therapeutic doses are known to increase nonspecific immune responses. It remains to be established whether higher doses of the less toxic liposomal preparation of AmB maintains a beneficial effect on the immune response to fungal infections. Examination of the effect of treatment of human peripheral blood mononuclear cells from healthy subjects with various doses of both liposomal AmB (L-AmB) and deoxycholate AmB (d-AmB) on proliferation, cell viability, and percentage of apoptosis demonstrated that, although both L-AmB and d-AmB at low doses significantly increased nonspecific proliferative responses, L-AmB, but not d-AmB, treatment maintained this beneficial effect at higher doses. High doses of d-AmB, but not L-AmB, resulted in significantly decreased cell viability and increased apoptosis. This study provides further evidence in healthy human subjects for choosing L-AmB over conventional preparations in the clinical treatment of fungal infections requiring systemic high-dose treatment with AmB.

[Evaluation of the hemodynamic effects of tumor necrosis factor alpha factor in rats with portal hypertension using the radioactive microsphere technique]. / Evaluación de los efectos hemodinámicos del factor de necrosis tumoral alfa en ratas con hipertensión portal mediante le técnica de las microesferas radiactivas.

UNLABELLED: This study was aimed at investigating the effects of blocking circulating TNF on the hyperdynamic circulatory state developed in rats with portal vein stenosis (PVS), and the factors mediating the hemodynamic action of this cytokine in this setting. MATERIALS AND METHODS: Murine antiTNF polyclonal antibodies (100 microgram) or placebo were intravenously injected into PVS rats (n = 24) before and 4 days after PVS. Hemodynamic studies were performed the day after the last antiTNF injection. RESULTS: Short-term TNF inhibition led to reductions in cardiac index (p < 0.05) and portal venous inflow (p < 0.01), and significant increases in splanchnic and systemic vascular resistances. Portal pressure was unchanged, but portal-systemic shunting was decreased (p < 0.05). CONCLUSION: TNF plays a key role in promoting the development of the hyperdynamic state of portal hypertension. The effect of TNF is mediated through an increased release of nitric oxide.

The immunosenescent phenotype in mice and humans can be defined by alterations in the natural immunity reversal by immunomodulation with oral AM3.

The reactivities of monocyte/macrophages and natural killer (NK) cells (natural immunity) were evaluated following the administration of the biological response modifier AM3. The lower number of macrophages and NK cells in middle-aged mice (MAM) compared to young adult mice (YAM) were significantly elevated following AM3 treatment to equal or greater than YAM values. Both macrophage and NK cell cytotoxicity peaked at two days following AM3 treatment and remained elevated over control values for up to 8 days following a four days treatment regimen by the oral route. Of particular interest was the clinical effect of AM3 treatment in chronic bronchitis (CB) patients and various aged volunteers. In middle-aged patients with chronic bronchitis (MACBpts) AM3 treatment resulted in significant increases in the number of monocytes as well as their phagocytic and chemotactic activity. Differential NK cell cytotoxicities were observed in MACBpts compared to middle-aged healthy adults (MAHA) and young healthy adults (YHA). Cytotoxicity in YHA was 2-fold higher than MAHA and 5-fold higher than MACBpts. The depressed number of NK cells in MACBpts was reversed following the AM3 treatment to near NK cell levels in YHA. These observations help to explain how AM3 aids in the restoration of natural cellular immunity and its possible application as an adjuvant to bacterial & viral vaccines as well as in the treatment CB.

An extract of the fern Polypodium leucotomos inhibits human peripheral blood mononuclear cells proliferation in vitro.

An alcoholic extract of the fern polypodium leucotomos (PLE) has been empirically used as an immunosuppressor for the treatment of several autoimmune diseases. In this paper, we investigated the effects of PLE on activation and proliferative responses of peripheral blood mononuclear cells (PBMNC) from healthy donors to T lymphocyte polyclonal mitogens. PLE shows a significant inhibitory effect on the proliferative response of PBMNC to stimulation with phytohaemagglutinin (PHA) or anti CD3 monoclonal antibodies (p < 0.05). In contrast, PLE did not modify the proliferative response of PBMNC to phorbol esters (p > 0.05). The inhibitory effect of PLE upon mitogen induced PBMNC proliferation is time dependent and can be overcome by the exogenous addition of interleukin-2 to the culture medium (p < 0.05). The decreased proliferative response of PBMNC to PHA stimulation in the presence of PLE is not associated with a significant modification of expression of the alpha chain (CD25) of the IL-2 receptor (p > 0.05). In conclusion, PLE shows an inhibitory effect on the polyclonal proliferative response of PBMNC to T lymphocyte mitogens that interact with cytoplasmic membrane molecules.

Cyclosporine A shows immunosuppressor activity on T lymphocytes from the peripheral blood and synovial fluid of patients with autoimmune arthritis.

OBJECTIVE: This work studies the effects of Cyclosporine A (CsA) upon the activation and proliferation of mononuclear cells (MNC) from the peripheral blood (PB) of patients with chronic autoimmune arthritis and from healthy controls, and from the synovial fluid (SF) of patients. METHODS: In vitro studies of activation, proliferation, mRNA expression and lymphokine production were carried out. RESULTS: We found in the PB and SF MNCs from patients with autoimmune arthritis that CsA inhibits the proliferative response, activation antigen expression, IL-2 mRNA expression and IL-2 production induced by polyclonal mitogens in a dose dependent manner. CONCLUSION: CsA blocks lymphocyte activation in PB and SF MNCs from patients with autoimmune arthritis.