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Results for “immune modulation”

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At least 397 records · Page 22Linked to original sources
PubMed2002

Exercise and psychosocial factors modulate immunity to influenza vaccine in elderly individuals.

BACKGROUND: Decreases in immune responsiveness with age contribute to the increased incidence and severity of infectious disease among elderly adults. The immune response to immunization also decreases with advancing age. Lifestyle factors (exercise, diet) have been established to play an important role in immunosenescence, and the practice of "healthy" behavior may minimize the age-associated decline of immune function. The objective of this study was to determine whether exercise, diet, and psychosocial factors were associated with altered immune response to influenza vaccine. METHODS: Adults aged 62 years and older were categorized into one of three groups: active (> or =20 min vigorous exercise three or more times per week), moderately active (regular exercise but with less intensity, frequency, and/or duration), or sedentary (no exercise). Two weeks postimmunization, serum was frozen for antibody analysis, and peripheral blood mononuclear cells (PBMC) were cultured in vitro with influenza vaccine to elicit antigen-specific responses (proliferation and cytokine [IL-2, IFN-gamma, IL-10] production). Cytokines and antibody were measured by enzyme-linked immunosorbent assay. RESULTS: The results demonstrated that anti-influenza IgG and IgM were greater in active as compared with moderately active or sedentary participants. PBMC proliferation was lowest in sedentary subjects. Perceived stress was a significant predictor of IL-2. Greater optimism and social activity were associated with greater IL-10. Daily multivitamin intake was significantly correlated with IL-2. CONCLUSIONS: These results suggest that lifestyle factors including exercise may influence immune response to influenza immunization. The practice of regular, vigorous exercise was associated with enhanced immune response following influenza vaccination in older adults.

Aged↗
PubMed2001

Genistein modulates immune responses and increases host resistance to B16F10 tumor in adult female B6C3F1 mice.

The isoflavone genistein (4,7,4'-trihydroxyisoflavone) is a phytoestrogen found in high levels in soy products that has been associated with decreased incidences of breast and prostate cancers. The potential effects of genistein on the immune system were evaluated in adult female B6C3F1 mice. Groups of mice were exposed to vehicle or genistein by gavage for 28 d. The doses of genistein used were 2, 6 and 20 mg/kg body. Consistent with the chemopreventive effect of genistein, exposure to this compound significantly increased host resistance to B16F10 tumor as reflected by a decrease in the number of lung tumor nodules after tumor cell injection at the middle and high dose levels. Inhibition of B16F10 tumor formation was not due to a direct effect of serum genistein and/or its metabolites on the proliferation of B16F10 tumor cells. When innate and acquired immune responses were evaluated, a dose-related increase of cytotoxic T-cell activity was observed in genistein-treated mice with significant changes observed at the middle and high dose levels. Furthermore, in vitro interleukin (IL)-2-stimulated natural killer (NK) cell activity was significantly enhanced in the high genistein dose group, although the basal NK cell activity was not affected. Although no affect on the mixed lymphocyte responses and anti-CD3 antibody-mediated splenocyte proliferation was observed, exposure to genistein significantly increased basal splenocyte proliferation. Exposure to genistein did not alter the activity of the mononuclear phagocyte system and the cytotoxic/cytostatic function of thioglycollate-recruited peritoneal cells on B16F10 tumor cells. Finally, exposure to genistein did not produce biologically meaningful changes in spleen immunoglobulin (Ig)M and IgG antibody-forming cell responses. In conclusion, genistein enhanced host resistance as evaluated in the B16F10 tumor model, which may be related to the increases in the activities of cytotoxic T cells and NK cells.

Animals↗
PubMed2004

Immune modulation of the pulmonary hypertensive response to bacterial lipopolysaccharide (endotoxin) in broilers.

The lungs of broilers are constantly challenged with lipopolysaccharide (LPS, endotoxin) that can activate leukocytes and trigger thromboxane A2 (TxA2)- and serotonin (5HT)-mediated pulmonary vasoconstriction leading to pulmonary hypertension. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure, whereas others fail to exhibit any response to the same supramaximal dose of LPS. This extreme variability in the pulmonary hypertensive response to LPS appears to reflect variability in the types or proportions of chemical mediators released by leukocytes. Our research has confirmed that TxA2 and 5HT are potent pulmonary vasoconstrictors in broilers and that broilers hatched and reared together consistently exhibit pulmonary hypertension after i.v. injections of TxA2 or 5HT. Previous in vitro studies conducted using macrophages from different lines of chickens demonstrated innate variability in the LPS-stimulated induction of nitric oxide synthase (iNOS) followed by the onset of an LPS-refractory state. The NOS enzyme converts arginine to citrulline and nitric oxide (NO). It is known that NO produced by endothelial NOS serves as a key modulator of flow-dependent pulmonary vasodilation, and it is likely that NO generated by iNOS also contributes to the pulmonary vasodilator response. Accordingly, it is our hypothesis that the pulmonary hypertensive response to LPS in broilers is minimal when more vasodilators (NO, prostacyclin) than vasoconstrictors (TxA2, 5HT) are generated during an LPS challenge. Indeed, inhibiting NO production through pharmacological blockade of NOS with the inhibitor Nomega-nitro-L-arginine methyl ester modestly increased the baseline pulmonary arterial pressure and dramatically increased the pulmonary hypertensive response to LPS in all broilers evaluated. Innate differences in the effect of LPS on the pulmonary vasculature may contribute to differences in susceptibility of broilers to pulmonary hypertension syndrome (ascites).

Animals↗
PubMed2003

The current status of immune modulating therapy for myocarditis: a case of acute parvovirus myocarditis treated with intravenous immunoglobulin.

We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.

Acute Disease↗
PubMed1998

The immune modulator Linomide prevents neuronal death in injured peripheral nerves of the mouse.

Neuronal death after injury or disease could result from imbalanced cytokine expression. Linomide (LS-2616, quinoline-3-carboxamide), a synthetic immunomodulator with effects on cytokine production, suppresses autoimmune diseases of the nervous system. Here adult mice were pre-treated with 200 mg/kg/day of Linomide for 9 days, after which the sciatic nerves were crushed. After another 10 days of Linomide treatment the dorsal root ganglia were dissected out and stained for apoptosis, either immediately or after 2 days in culture, which increases cell death. Superior cervical ganglia were also cultured for 2 days. The Linomide pretreatment profoundly reduced (approximately 60-80%) the injury-induced apoptotic death of neurons and satellite cells in both systems. The results suggest that modulation of the inflammatory cytokine cascade is a promising road to nerve cell rescue.

Adjuvants, Immunologic↗
PubMed2006

Steroids versus other immune modulators in the management of allergic dermatoses.

PURPOSE OF REVIEW: The classic role of topical and systemic corticosteroids for allergic dermatoses is discussed, with special attention to the impact on the current clinical treatment paradigm by newer systemic and topical therapies. These products are reviewed and recommendations presented on how to effectively assimilate them into clinical practice. RECENT FINDINGS: Current knowledge about the etiopathogenesis of atopic dermatitis has resulted in drug development focused on agents with less toxicity than current topical and systemic corticosteroids. Some agents with ceramide/cholesterol/acid combinations demonstrate efficacy in restoring the dysfunctional skin barrier of atopic patients. Concerns resulting from the recent Federal Drug Administration announcement regarding a theoretical risk of cancer associated with topical calcineurin inhibitors are also addressed. Novel therapeutic entities are presented. SUMMARY: Patients seeking relief from atopic dermatitis have historically had few really effective and safe therapeutic options. Topical calcineurin inhibitors represent an exciting new therapy for atopic dermatitis without the side-effect profile associated with topical corticosteroids. Nonsteroidal formulations incorporating glycyrrhetinic acid/telmesteine/Vitis vinifera extract and palmitoylethanolamide as 'active' ingredients recently entered the market, stressing antipruritic, antiinflammatory, and skin barrier repair. This confabulates against previously designed topical therapy paradigms. These new products may be used as monotherapy or alternatives to steroid agents.

Adrenal Cortex Hormones↗
PubMed2025

TYK2 :p.Pro1104Ala Variant Protects Against Autoimmunity by Modulating Immune Cell Levels.

The TYK2:p.Pro1104Ala (rs34536443) hypomorph variant has been associated with protection against numerous autoimmune disorders. Thus, its mechanism of action becomes of great interest. Here, consistent with the participation of activated immune cells in autoimmunity, we show that the variant regulates the levels of immune cells at a human, general population level and is associated particularly with higher levels of T and B lymphocytes, especially the naïve (non-activated) compartment. Also, consistent with a protective function in autoimmunity, the level of regulatory CD4+ T cells was increased. Thus, this variant decreases immune activation thereby protecting from autoimmunity. Our work links the cellular mechanism regulated by the TYK2:p.Pro1104Ala variant to autoimmunity protection and supports TYK2 as a therapeutic target in autoimmunity.

Humans↗
PubMed2006

Role of interleukin (IL-10) in probiotic-mediated immune modulation: an assessment in wild-type and IL-10 knock-out mice.

While the impact of Bifidobacterium infantis 35624 and other probiotics on cytokines has been shown in established colitis, the effects of B. infantis consumption in pre-inflammation of interleukin (IL)-10 knock-out (KO) mice and on the wild-type (WT) C57Bl/6 mice have not been well demonstrated. The objective of this study was to examine cytokine responses in mucosal and systemic lymphoid compartments of IL-10 KO mice early in disease and to compare with control WT mice. Mice were fed B. infantis or placebo for 5 weeks and culled prior to the onset of chronic intestinal inflammation (12-14 weeks). The spleen, Peyer's patches and intestinal mucosa were removed and stimulated with various bacterial stimuli. Cytokine levels were measured by enzyme-linked immunosorbent assay. While basal intestinal and systemic cytokine profiles of WT and IL-10 KO mice were similar, transforming growth factor (TGF)-beta was reduced in the spleen of IL-10 KO mice. Following probiotic consumption, interferon (IFN)-gamma was reduced in the Peyer's patch of both WT and IL-10 KO mice. Alterations in IFN-gamma in the Peyer's patches of WT mice (enhancement) versus IL-10 KO (reduction) were observed following in vitro stimulation with salmonella. Differential IL-12p40, CCL2 and CCL5 responses were also observed in IL-10 KO mice and WT mice. The cytokine profile of IL-10 KO mice in early disease was similar to that of WT mice. The most pronounced changes occurred in the Peyer's patch of IL-10 KO mice, suggesting a probiotic mechanism of action independent of IL-10. This study provides a rationale for the use of B. infantis 35624 for the treatment of gastrointestinal inflammation.

Animals↗
PubMed1992

In vitro immune modulation of polymorphonuclear leukocyte adhesiveness by sodium fluoride.

We investigated the influence of sodium fluoride on polymorphonuclear leukocyte (PMN) adhesiveness in a healthy subject with low serum levels of fluoride. The PMN were separated from venous blood, and the percentages of adhered and unadhered cells were determined in vitro in plastic culture plates. The cells were cultured with five different fluoride concentrations ranging from 6.25 10(-2) microM to 4.0 microM in the presence and absence of autologous serum. PMN adhesiveness in both the presence and in the absence of autologous serum was 98.5%; the addition of fluoride had no effect on the results in the absence of serum. However, in the presence of autologous serum, PMN adhesiveness decreased significantly with the addition of fluoride (P < 0.05) from 0.5 microM. The decrease was smaller (1.1%) at a concentration of 0.125 microM, and larger at 12 times this concentration of fluoride (52.7%). We conclude that sodium fluoride reduces PMN adhesiveness in a dose-dependent manner. The effect is not direct, but should be modulated by a seric factor.

Adult↗