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PubMed1990

[Immune function of cancer patients with spleen-deficiency syndrome].

According to this study, the immunological function was aberrant in cancer patients with Spleen-deficiency syndrome. The TII cell in normal persons (n = 26) was 30, 86 +/- 9.70% (means +/- S) and in these cases (n = 43) was 22.62 +/- 9.92%, P less than 0.002. The cytotoxicity of NK cell in patients (n = 59) was 17.65 +/- 10.58%, in normal controls (n = 43) was 25.51 +/- 14.10%. The combining ability of NK cell in patients (n = 48) was 39.11 +/- 19.43%, the normal persons (n = 41) was 55.88 +/- 17.94%. It showed that the immune function of the cancer patients with Spleen-deficiency syndrome were markedly lower than that of normal persons. The serum IgA in saliva of patients (n = 37) was 0.44 +/- 0.17 microgram/ml. It was much higher than that of normals' (n = 24, 0.30 +/- 0.06 microgram/ml), P less than 0.001. Some patients' NK cell function and the level of level of SIgA in saliva were recovered to normal after treatment of Shengxue Tang which could strengthen the Spleen and replenish the Kidney. These studies proved that the TCM played an important role for modulating immune function in treating cancer patients.

Adult↗
PubMed1996

Innate immune function as a bioindicator of pollution stress in fish.

Immunotoxicological studies, based on processing of samples in the field and laboratory, were conducted on fish collected from a stream receiving point-source contaminants near its headwaters. Previous studies in this stream have revealed that cytochrome P4501A activity, liver somatic indices, macrophage aggregates, and parasitic liver lesions are significantly elevated in sunfish with the degree of impact decreasing with distance from the contaminant source. Fish collected from each sampling site were equally divided, One group was sacrificed in the field and the spleen and anterior kidney tissues were removed and placed in buffer on ice. The other group was kept in MS-222 for 2 hr and transported to the laboratory for processing. The spleen and anterior kidney from each fish were then prepared as a single cell suspension and shipped overnight to Mississippi State University. Cells were then evaluated for PMA-stimulated phagocyte oxidative burst and non-specific cytotoxic cell (NCC) activity against K562 tumor targets. Oxidative burst responses were dramatically suppressed in both groups at sampling sites near the headwaters but returned to reference levels further downstream. There were no differences between processing strategies at each station. NCC activities did not follow gradient-response patterns observed with phagocyte oxidative burst data and there were inconsistent differences between processing strategies at each site. These data indicate that simple immune function assays, such as phagocyte oxidative burst responses, can be used as a ancillary bioindicator in fish health monitoring and that immune function in these fish can be reliably assessed even if samples are not immediately processed.

Analysis of Variance↗
PubMed1996

Pharmacological profile of SB 203580, a selective inhibitor of cytokine suppressive binding protein/p38 kinase, in animal models of arthritis, bone resorption, endotoxin shock and immune function.

SB 203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4- pyridyl)imidazole], a selective cytokine suppressive binding protein/p38 kinase inhibitor, was evaluated in several models of cytokine inhibition and inflammatory disease. It was demonstrated clearly to be a potent inhibitor of inflammatory cytokine production in vivo in both mice and rats with IC50 values of 15 to 25 mg/kg. SB 203580 possessed therapeutic activity in collagen-induced arthritis in DBA/LACJ mice with a dose of 50 mg/kg resulting in significant inhibition of paw inflammation and serum amyloid protein levels. Antiarthritic activity was also observed in adjuvant-induced arthritis in the Lewis rat when SB 203580 was administered p.o. at 30 and 60 mg/kg. Evidence for disease-modifying activity in this model was indicated by an improvement in bone mineral density and by histological evaluation. Additional evidence for beneficial effects on bone resorption was provided in the fetal rat long bone assay in which SB 203580 inhibited 45Ca release with an IC50 of 0.6 microM. In keeping with the inhibitory effects on lipopolysaccharide-induced tumor necrosis factor-alpha in mice, SB 203580 was found to reduce mortality in a murine model of endotoxin-induced shock. In immune function studies in mice treated with SB 203580 (60 mg/kg/day for 2 weeks), there was some suppression of an antibody response to ovalbumin, whereas cellular immune functions measured ex vivo were unaffected. This novel profile of activity strongly suggests that cytokine inhibitors could provide significant benefit in the therapy of chronic inflammatory disease.

Animals↗
PubMed2004

Effects of aging on immune function.

A variety of changes are observed in the immune system in both animals and humans with increasing age. There is a decline in the functional capacity of the cell populations that mount generalized and focused immune responses, and decreasing production and response of these cells to regulatory signals and proteins. These changes translate into less effective innate and adaptive immune responses, increased reactivity against self-antigens in vivo, and an increased incidence of infection. There may also be an increased risk of mortality. The mechanisms underlying age-related changes in immune function are not fully understood, but are likely to be multifactorial, including environmental and behavioral factors that affect over-all immune function from the molecular level to that of the entire organism.

Aged↗
PubMed2001

Obesity and immune function relationships.

The immunological processes involved in the collaborative defence of organisms are affected by nutritional status. Thus, a positive chronic imbalance between energy intake and expenditure leads to situations of obesity, which may influence unspecific and specific immune responses mediated by humoral and cell mediated mechanisms. Furthermore, several lines of evidence have supported a link between adipose tissue and immunocompetent cells. This interaction is illustrated in obesity, where excess adiposity and impaired immune function have been described in both humans and genetically obese rodents. However, limited and often controversial information exist comparing immunity in obese and non-obese subjects as well as about the cellular and molecular mechanisms implicated. In general terms, clinical and epidemiological data support the evidence that the incidence and severity of specific types of infectious illnesses are higher in obese persons as compared to lean individuals together with the occurrence of poor antibody responses to antigens in overweight subjects. Leptin might play a key role in linking nutritional status with T-cell function. The complexities and heterogeneity of the host defences concerning the immune response in different nutritional circumstances affecting the energy balance require an integral study of the immunocompetent cells, their subsets and products as well as specific and unspecific inducer/regulator systems. In this context, more research is needed to clarify the clinical implications of the alterations induced by obesity on the immune function.

Adipose Tissue↗
PubMed2004

Expression of non-neuronal acetylcholine in lymphocytes and its contribution to the regulation of immune function.

Lymphocytes express most components of the cholinergic system including acetylcholine (ACh), muscarinic and nicotinic ACh receptors (mAChRs and nAChRs, respectively), choline acetyltransferase (ChAT), high affinity choline transporter and acetylcholinesterase. ACh and mAChR agonists elicit intracellular Ca2+ signaling, up-regulation of c-fos expression and nitric oxide synthesis within T and B cells probably via M3 and M5 mAChRs. Stimulation of nAChRs with ACh or nicotine causes a rapid and transient Ca2+ signaling in T and B cells, probably via alpha7 nAChR subunit-mediated pathways. Phytohemagglutinin- or antigen-induced T cell activation via cell surface molecules (e.g., T cell receptor/CD3 complexes) enhances lymphocytic cholinergic transmission by up-regulating ChAT and M5 mAChR expression. It is thus likely that a local lymphocytic cholinergic system is involved in regulating immune function. This idea is supported by the findings that lymphocytic cholinergic activity is altered in animal models exhibiting immunological abnormalities. In addition, it appears likely that during interactions mediated by cell surface molecules T cells communicate via ACh with thymic epithelial cells and vascular endothelial cells, which also express ChAT and nAChRs or mAChRs. This interaction leads to T cell selection and maturation in the thymus and local vascular smooth muscle relaxation. Collectively, these data provide a compelling picture in which lymphocytes constitute a cholinergic system that is independent of cholinergic nerves, and which is involved in the regulation of immune function and local circulation.

Acetylcholine↗
PubMed2004

Low dose gamma-rays activate immune functions via induction of glutathione and delay tumor growth.

We examined whether the increase of glutathione level induced by low dose gamma-ray irradiation is involved in the appearance of enhanced natural killer (NK) activity and antibody-dependent cellular cytotoxicity (ADCC), leading to delayed tumor growth in Ehrlich solid tumor-bearing mice. NK activity in ICR mouse splenocytes significantly increased from 4 h to 6 h after whole-body gamma-ray irradiation at 0.5 Gy, and thereafter decreased almost to the zero-time level by 24 h post-irradiation. ADCC also increased significantly in a similar way. Reduced glutathione exogenously added to splenocytes obtained from normal mice enhanced both NK activity and ADCC in a dose-dependent manner. Since immune functions were enhanced through the induction of cellular glutathione after low-dose irradiation, the inhibitory effect of the radiation on tumor growth was then examined in Ehrlich solid tumor-bearing mice. Tumor growth after inoculation was significantly delayed by the radiation. These results suggest that low-dose gamma-rays activate immune functions via an induction of glutathione, leading to a delay of tumor growth.

Animals↗
PubMed2004

Postoperative epidural anesthesia preserves lymphocyte, but not monocyte, immune function after major spine surgery.

UNLABELLED: Extensive spine surgery is associated with postsurgical pain. Epidural pain therapy may reduce postoperative stress responses and thereby influence immune functions. In a randomized, controlled, double-blinded prospective trial, 54 patients received either conventional patient-controlled IV analgesia (PCIA; morphine 3 mg/15 min) or patient-controlled epidural analgesia (PCEA; 0.125% ropivacaine plus sufentanil 1 microg/mL at a base rate of 12 mL/h and bolus application of 5 mL/15 min). Circulating cytokines, C-reactive protein (CRP), cortisol, and cell-surface receptor expression of immune cells (cluster of differentiation [CD]14, human leukocyte antigen-DR, CD86, CD71, CD3, CD4, CD8, CD16, and CD19) were measured perioperatively to characterize immunological functions. PCEA, compared with PCIA, had no influence on altered levels of circulating cytokines (interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and macrophage inhibitory factor) or indicators of the stress response (CRP and cortisol). Also, no significant difference was found in monocyte numbers or their human leukocyte antigen-DR, CD86, or CD71 expression. In contrast, the postoperative decrease in B lymphocytes and T-helper cells was significant in the PCEA group. Natural killer cells decreased significantly in patients receiving PCEA compared with PCIA. Therefore, postoperative epidural pain therapy has no influence on monocyte functions but reduces natural killer cells and preserves B-cell and T-helper cell populations. Epidural analgesia thus influences the specific rather than the innate immune system and potentially blunts the postsurgical lymphocyte depression, which is relevant for infectious resistance. IMPLICATIONS: Epidural analgesia affects the immune system. Postoperative epidural analgesia, compared with conventional IV opioid therapy, preserves lymphocyte rather than monocyte functions. An improvement of postoperative immune function by epidural analgesia therefore may improve postoperative resistance to infectious complications or to chronic pain states.

Adult↗
PubMed1999

Effects of 6 months of moderate aerobic exercise training on immune function in the elderly.

The purpose of this study was to determine the effects of 6 months of moderate aerobic exercise on age-dysregulated measures of T lymphocyte and natural killer (NK) cell number and function. Previously sedentary elderly (age = 65 +/- 0.8 years) subjects were randomly assigned to supervised 3 time/week exercise intervention group (EXC, n = 14) or flexibility/toning control group (FT-CON, n = 15). Fasting resting blood samples were drawn prior to and after the 6 month intervention. The EXC group exhibited a significant (P < 0.05) 20% increase in VO2 max, whereas the FT-CON group had a smaller non-significant (P = 0.07) increase (9%). Immune results revealed that, in general, changes in immune function in response to 6 months of exercise training at an average intensity of 52% heart rate reserve (HRR) were similar when compared to FT-CON who exercised at approximately 21% HRR. There were no intervention-induced changes in total white blood cell, neutrophil, lymphocyte, monocyte, eosinophil, or basophil blood counts. Furthermore, the percentage and number of CD3+, CD4+ and CD8+ T cells in the blood remained unchanged. There was a tendency for the percentage and number of CD4+ and CD8+ näive cells (CD45RA+) to increase and for CD4+ memory cells (CD45RO+) to decrease post-intervention, especially in FT-CON. Both groups exhibited a small intervention-induced increase in the T-cell proliferative response to mitogenic stimulation: the percentage change of which was higher in the EXC group at several doses of Con A. Unstimulated NK cell cytolysis versus K562 cells tended to increase (P < 0.1) in the EXC group with little change in FT-CON. We conclude that 6 months of supervised exercise training can lead to nominal increases in some measures of immune function, while not affecting others, in previously sedentary elderly.

Aged↗
PubMed2002

Modulatory effects of compound polysaccharide erweikang on the immune function of mice.

In order to study the modulatory effects of compound polysaccharide Erweikang on the immune function of the immunosuppressive mice, the positive immune modulation of Erweikang at different doses and different time points was compared when normal saline and cyclophosphamide served as controls. The results showed that different doses of Erweikang could effectively reverse the decreased induction levels of NK, IL-2, gamma-IFN and the contents of TNF and IgF of the immunosuppressive mice after administration of Erweikang for 7 to 14 days. It was suggested that compound polysaccharide Erweikang presents positive immune modulation in dose- and time-dependent manners.

Adjuvants, Immunologic↗
PubMed2003

Immune function, mitogenicity, and angiogenic growth factor concentrations in lean and obese rodent sera: implications in obesity-related prostate tumor biology.

Some studies suggest that several tumors have a greater incidence in those patients with a high fat diet, such as colon, breast, and prostate. However, we wanted to determine the effects of obesity alone, independent of diet, on the progression of prostate tumor growth. Using a genetic model of obese and lean Zucker rats, we wanted to demonstrate any sera differences in the concentration of basic fibroblast growth factor (FGF-2) and vascular endothelial cell growth factor (VEGF), two important factors involved in the growth and progression of prostate cancer. We also wanted to investigate if there were any differences in immune function between the two sera, which could also account for uninhibited tumor growth, as well as differences in mitogenic stimulation. Female Zucker rat obese and lean sera were analyzed using ELISA assays for FGF-2, VEGF, and macrophage inflammatory protein-1 alpha (MIP-1a), as a measure of macrophage function. In addition, the sera of lean and obese sera were plated on wells growing LNCaP prostate cancer cells to determine differences in mitogenicity. We found a greater concentration of FGF-2 in the sera from obese Zucker rats compared to lean Zucker rats: 6.32+/-0.56 vs 3.48+/-0.34 pg/ml, respectively, P<0.05). We also demonstrated a greater concentration of VEGF in obese rat sera compared to lean sera: 54.4+/-4.1 vs 38.0+/-2.9 pg/mL, respectively, P<0.05). We detected a trend in mitogenic stimulation among LNCaP cells along the higher concentrations of the dose-response curve (0.72+/-0.06 vs 0.51+/-0.5). However, this was not statistically significant. In addition, we did not find a significant difference in MIP-1a macrophage activity levels between sera. To conclude, we speculate that the greater concentrations of VEGF and FGF-2 in the sera of obese rodents vs lean rodents may account for some of the differences seen in obesity-related tumor growth seen in the human condition. However, the lack of any sera differences of immune function, as measured by macrophage activity, as well as no significant differences on mitogenic proliferation on LNCaP prostate cancer cells, suggests that other mechanisms may exist to explain differences seen in obesity-related prostate tumor biology.

Angiogenesis Inducing Agents↗
PubMed2000

Endocrine-immune interaction: alteractions in immune function resulting from neonatal treatment with a GnRH antagonist and seasonality in male primates.

PROBLEM: The effect of neonatal gonadotropin releasing hormone (GnRH) antagonist (Ant) treatment and seasonality on immune system development and function was investigated in male primates. METHOD OF STUDY: Neonatal male rhesus monkeys and marmosets were treated with Ant, and its effect on immune system morphology, circulating lymphocyte subsets, and cell- and humorally-mediated immune responses was assessed during development. In adult rhesus monkeys, we correlated seasonal changes in immune function with circannual fluctuations in immunoactive hormones. RESULTS: In neonatal marmosets, Ant reduced the number of B cells and T cells in the thymic medulla and T cells in the periarterial lymphatic sheaths (PALS) of the spleen. Ant also altered the development of, but did not permanently impair, the proliferative index (PI) of blood lymphocytes to mitogens. In vitro treatment of control lymphocytes with GnRH analogues altered their response to these proliferative agents. In neonatal rhesus monkeys, Ant treatment increased the frequency of clinical problems, lowered circulating levels of lymphocytes, total T cells, CD8+ T cells and B cells, and altered the PI of lymphocytes to mitogens. As adults, the cell- and humorally-mediated immune responses remained impaired. We also documented seasonal fluctuations in the prevalence of diseases, circulating immune cells and immune function in rhesus monkeys. The number of cases of campylobacteriosis and shigellosis was lowest in the winter and highest in the spring. Circulating numbers of white blood cells (WBC) and neutrophils and the PI of lymphocytes to mitogens were higher in the winter than in the summer. Natural killer cell activity also varied with season. Cortisol and leptin secretion exhibited circannual rhythms, rising in concert with decreasing photoperiod and increasing testicular activity in the fall. Conversely, prolactin levels declined with decreasing photoperiod and then rose in the spring. CONCLUSION: Neonatal exposure of male primates to Ant appears to alter early postnatal programming of immune function. In the rhesus monkey, immune function shows seasonal fluctuations that may be driven by circannual changes in the secretion of immunoactive hormones.

Animals↗
PubMed2004

CD26/dipeptidyl peptidase IV: a regulator of immune function and a potential molecular target for therapy.

CD26 is a 110 kDa surface-bound ectopeptidase with intrinsic dipeptidyl peptidase IV (DPP IV) activity, which has multiple biological functions. In this review, we will focus specifically on work demonstrating that CD26 has a key role in immune function as a T cell activation molecule and a regulator of the functional effect of selected biological factors through its DPP IV enzyme activity. As further evidence of the important role played by this multifaceted molecule in immune regulation, we will also discuss experimental attempts from our laboratory and others to influence immune-mediated conditions through CD26 monoclonal antibodies and DPP IV activity with various agents, including anti-CD26 monoclonal antibodies and DPP IV chemical inhibitors. Of special significance from a clinical perspective is also CD26 effect on glucose metabolism through its DPP IV activity and its potential role as a therapeutic target in diabetes. In addition, we will review recent studies that describe the physical and functional interaction of CD26 with other essential cellular structures and the biological consequences of their association. In particular, we will present recent data from our laboratory that demonstrates the correlation between CD26, especially its DPP IV activity, and the key nuclear protein topoisomerase II alpha, an interaction that has important clinical implications. In summary, we will examine the biology of the multifaceted CD26/DPP IV molecule, focusing particularly on its function in immune regulation and its potential role as a molecular target for novel treatment modalities for a number of disease states, ranging from autoimmune diseases, diabetes to malignancies.

Animals↗
PubMed1984

Studies of immune function and host resistance in B6C3F1 mice exposed to formaldehyde.

A series of immune function and host resistance parameters were examined in female B6C3F1 mice following a 21-day (6 hr/day) inhalation exposure to 15 ppm of formaldehyde (HCHO). Immune parameters examined included delayed hypersensitivity to keyhole limpet hemocyanin, antibody plaque-forming cell response to sheep erythrocytes (T-lymphocyte-dependent antigen) and TNP-Ficoll (T-lymphocyte-independent antigen), lymphoid organ weights and histopathology, routine hematology, bone marrow cellularity and CFU progenitor cell enumeration, lymphocyte subpopulation quantitation by cell surface markers, mitogen-induced lymphocyte blastogenesis, macrophage function parameters, and host resistance to challenge with the bacterium Listeria monocytogenes and transplantable tumor cells. Lymphoid organ weight, bone marrow cellularity, and hematology parameters were unchanged in HCHO exposed mice. Similarly, the percentage of T and B lymphocytes and their proliferative responses to mitogens were not significantly altered. Antibody (IgM) plaque-forming cell response following antigen challenge was unchanged. Macrophage function was normal although some evidence of enhanced H2O2 production associated with elevated bactericidal activity was observed in resident macrophages. Resistance to challenge with the bacteria Listeria monocytogenes was significantly enhanced, while resistance to tumor challenge remained unchanged. No evidence of immunosuppression following short-term exposure to HCHO was observed.

Animals↗
PubMed2004

Effect of hypertonic saline infusion on postoperative cellular immune function: a randomized controlled clinical trial.

BACKGROUND: Previous studies found hypertonicity to affect immune responses in intact laboratory animals and in human blood cell cultures. In this study, the authors investigated the cellular immune response to surgery after preoperative infusion of hypertonic saline in humans. METHODS: Sixty-two women scheduled to undergo abdominal hysterectomy were randomly assigned to single-blinded infusion of 4 ml/kg NaCl, 7.5%; 4 ml/kg NaCl, 0.9%; or 32 ml/kg NaCl, 0.9%, over 20 min. Blood was collected at baseline, during surgery, and 1, 24, and 48 h after surgery for the determination of leukocyte and differential counts, flow cytometric phenotyping of mononuclear cells, and natural killer cell activity against K 562 tumor cells. Phytohemagglutinin-induced lymphocyte proliferation, plasma elastase, and neutrophil chemotaxis were measured at the same time points except during surgery. The authors tested cell-mediated immune function in vivo by delayed-type hypersensitivity reaction in the skin. RESULTS: Surgery induced well-known changes in the cellular immune response, which were unrelated to the tonicity or volume of the infused fluids. CONCLUSION: Infusion of a clinically relevant dose of hypertonic saline did not seem to modify the postoperative cellular immune response after elective abdominal hysterectomy.

Adult↗
PubMed2002

[Effect of coal-burning air pollution on children immune function].

Study of effect of coal-burning air pollution on children immunity function was hold in Taiyuan city which is one of typical coal-burning air pollution city in China. The children of grade 4-5 who dwell more than 3 years were screened in three different pollution areas. The test includes the observation on the T lymphocyte subpopulations classes (CD3+, CD4+ and CD8+), saliva lysozyme contents and immunoglobulin content. The results showed that the contents of saliva lysozyme and immunoglobulin were lower than those in control area respectively(P < 0.05), and T lymphocyte subpopulations class (the percent ages of CD3+, CD4+ and CD8+) had the same trend, but it was not marked. The results suggested that coal-burning air pollution could affect children by nonspecific immunity and sap immunity. The effect on cell immunity was not marked.

Air Pollutants↗
PubMed2001

Neonatal chlorpyrifos administration elicits deficits in immune function in adulthood: a neural effect?

Neural input plays a key role in the establishment of immune function, and environmental agents or drugs that interfere with the development of the nervous system elicit corresponding immunologic deficits. In the current study, we gave neonatal rats the widely used organophosphate pesticide, chlorpyrifos (CPF), and determined the immediate and long-term effects on T-lymphocyte function. Exposure of neonatal rats to 1 mg/kg of CPF daily on postnatal days (PN) 1-4 had no immediate effect (PN5) on T-cell mitogenic responses to concanavalin A challenge. However, once the animals reached adulthood, T-cell responses were significantly impaired. There were no deficits in basal T-cell replication rates, implying that the adverse effect of CPF exposure was specific to mitogenic activation. Treatment during a later neonatal period (PN11-14) elicited similar deficits in adulthood. CPF administration leads to inhibition of cholinesterase, and a cholinergic connection is supported by the fact that the results seen here correspond to those seen with a direct cholinergic stimulant (nicotine) administered during gestation or adolescence. These results indicate that exposure to CPF during a developmental period in which this organophosphate pesticide is known to produce lasting changes in neural function, elicits corresponding, long-term deficits in immune competence.

Age Factors↗