Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Immune function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMedDate not supplied

Influence of carbohydrate on immune function following 2 h cycling.

The influence of carbohydrate compared with placebo ingestion on changes in immune cell counts and functions following 2 h intensive cycling was studied in 12 trained cyclists who functioned as their own controls. The subjects performed two tests 2 weeks apart where they cycled for 2 h at approximately 64% Watts(max) while receiving 4 mL x kg(-1) x 15 min(-1) carbohydrate (6%) (Cho) or placebo (Pla) beverages. Blood samples were collected 30 min preexercise, and immediately and 1 h postexercise. The samples were assayed for plasma cortisol and epinephrine, blood leukocyte subset counts, PHA-induced lymphocyte proliferation, and natural killer cell activity (NKCA). Compared with Pla ingestion, Cho attenuated exercise-induced changes in plasma cortisol, blood neutrophil, and monocyte counts, but not in total blood lymphocyte, T cell, and NK cell counts, PHA-induced lymphocyte proliferation, and NKCA. Thus despite a strong attenuating influence of carbohydrate ingestion on exercise-induced changes in plasma cortisol and blood neutrophil and monocyte counts, other immune measures related to lymphocyte subset counts, and function were unaffected.

Adult↗
PubMed1989

Nutrition, immune function, and inflammation: an overview.

The collective evidence suggests that nutritional insult to both cell-mediated and humoral immunity in the presence of protein-energy malnutrition contributes to abnormalities of inflammation. The primary goal of nutritional support in inflammatory disease is to provide adequate energy and protein to meet endogenous requirements for tissue repair, IL-1 production, and restored cellular function, thus preventing secondary infection. Substrate provision should aim at improving the acute phase of injury while avoiding immune dysfunction. This goal may be achieved by altering the eicosanoid pathway toward a more regulated inflammatory state. In the context of allograft response, macrophages are central to the initiation of allosensitization by virtue of their ability to present antigen to T-cells. Activated T-cells may further modulate macrophage function by the secretion of lymphokines. Manipulation of macrophage eicosanoid production by dietary omega-3 PUFA may reduce cellular immune response. (table; see text) Nutritional support should also focus on providing essential micronutrients, with their potentially immunomodulating role, as adjunctive therapy in order to protect the host from toxic effects of free-radicals and chemicals released during inflammatory events. (Feeding regimens currently under investigation and development are presented in Table 4.) By integrating dietary immunotherapy with the use of recombinant hormones, monoclonal antibodies, and various available monokines, an optimal outcome for each patient may be achieved. However, effective application of immunotherapy to nutritional supplementation will require accurate monitoring of immune function in individual patients in order to avoid inappropriate treatment.

Animals↗
PubMed1998

Introduction of adhesive and costimulatory immune functions into tumor cells by infection with Newcastle Disease Virus.

We demonstrate in this study that infection of tumor cells by Newcastle Disease Virus (NDV) leads to changes in tumor cell surface adhesiveness and tumor immune costimulatory function. While adsorbtion of virions to the cell surface occurs after short-term (10 min) incubation and leads to cells expressing viral antigens at low antigen density (LAD), viral replication in the cytoplasm occurs within 5-24 h leading to tumor cells expressing viral antigens at high antigen density (HAD) as shown by quantitative FACS flow cytometry. Virus infected tumor cells showed an increased adhesiveness for erythrocytes and lymphocytes. When IL-2 preactivated human lymphocytes with cytotoxic potential were coincubated with 51Cr-labeled NDV-infected or non-infected human colon carcinoma cells increased lysis of the virus infected targets was observed. The virus mediated cell adhesion could be inhibited by monoclonal antibody (mAb) against the hemagglutinin-neuraminidase (HN) molecule but not by antibody against the fusion protein. HN cDNA transfectants also mediated increased lymphocyte adhesion in comparison to wild-type or neo-vector transfected control cells. Further experiments demonstrated that not only the adhesion domain of HN but also the neuraminidase plays a role in cell-cell interactions. A comparison of an NDV neuraminidase mutant of the strain Australian Victoria (AV-L1) with the parental AV strain revealed pronounced differences in their capacity to mediate lymphocyte binding and costimulatory activity. The mutant with highly decreased neuraminidase activity was very similar to NDV Ulster in adhesive and costimulatory activity while the parental line with high neuraminidase activity was negative for both functions. Costimulatory effects of NDV Ulster and AV-L1 were revealed when virions and suboptimal concentrations of anti-CD3 mAbs were coated to microtiter plates for induction of murine CD4 T cell proliferation. In human autologous mixed lymphocyte-tumor cell cultures up-regulation of T cell activation markers CD69 and CD25 was seen with NDV modified but not with non-modified tumor cells.

Animals↗
PubMed1989

[Influence of aminophylline on immune function of mice].

The effects of aminophylline (Ami) on immune systems in normal NIH mice were studied. Ami ig 25, 50 and 100 mg/(kg.d) x 8-10 d increased hemolytic ability of plaque forming cells and antibody concentration while it decreased the delayed type hypersensitivity (DTH) reaction and peripheral white blood cells phagocytosing function. Ami 1, 5, 10 micrograms/ml also promoted lymphocyte transformation of [methyl-3H] TdR incorporation induced by PHA in vitro.

Aminophylline↗
PubMed1983

Circulating immune complexes and serum lysozyme levels in untreated Hodgkin's disease. Their relationship to immune function.

Complement-fixing and non-complement-fixing circulating immune complexes were determined in 42 previously untreated Hodgkin's disease patients by Pl.A.T., C1qB-ELISA and KgB tests. The functional status of the monocyte-macrophage system was evaluated by measuring the serum lysozyme levels. These parameters were then correlated with the patient's immunocompetence, as assessed by the percentage of E-rosette forming cells and the PHA response. The Pl.A.T. was positive in 35.7% patients, the KgB-test in 34.3% and the C1qB-ELISA in 19%. There was overlapping of positive results in 37.5% patients. No correlation was found between CIC levels and stage, unfavourable histology or B symptoms. The PHA response was significantly depressed in CIC + patients, as detected by the C1qB-ELISA technique (p less than 0.0025). The data on serum lysozyme offer an insight into the possible mechanism regulating serum levels of CICs in Hodgkin's disease. Two distinct situations seem to exist: in the first, high CIC levels are associated with normal or low serum lysozyme values (p versus normal controls: n.s.); in the second, serum lysozyme levels are high and CIC absent (p less than 0.005 versus control values). The lowest lysozyme levels are also associated with a depressed lymphocyte PHA response. It could, therefore, be concluded that, in Hodgkin's disease, the presence, or absence, of CICs is directly correlated to the degree of monocyte-macrophage clearance activity and that the host's immunocompetence plays an important role in the induction and/or maintenance of this functional defect.

Antigen-Antibody Complex↗
PubMed1997

Release of calreticulin from neutrophils may alter C1q-mediated immune functions.

Calreticulin is an abundant intracellular protein which is involved in a number of cellular functions. During cytomegalovirus infection, as well as inflammatory episodes in autoimmune disease, calreticulin can be released from cells and detected in the circulation, where it may act as an immunodominant autoantigen in diseases such as systemic lupus erythematosus. Calreticulin is known to bind to the molecules of innate immunity, such as C1q, the first subcomponent of complement. However, the functional implications of C1q-calreticulin interactions are unknown. In the present study we sought to investigate, in greater detail, the interaction between these two proteins following the release of calreticulin from neutrophils upon stimulation. In order to pinpoint the regions of interaction, recombinant calreticulin and its discrete domains (N-, P- and C-domains) were produced in Escherichia coli. Both the N- and P-domains of calreticulin were shown to bind to the globular head regions of C1q. Calreticulin also appeared to alter C1q-mediated immune functions. Binding of calreticulin to C1q inhibited haemolysis of IgM-sensitized erythrocytes. Both the N- and P-domains of calreticulin were found to contain sites involved in the inhibition of C1q-induced haemolysis. Full-length calreticulin, and its N- and P-domains, were also able to reduce the C1q-dependent binding of immune complexes to neutrophils. We conclude that calreticulin, once released from neutrophils during inflammation, may not only induce an antigenic reaction, but, under defined conditions, may also interfere with C1q-mediated inflammatory processes.

Autoantigens↗
PubMed1992

Prolonged increase of corticosterone secretion by chronic social stress does not necessarily impair immune functions.

The influence of a chronic social stress upon immunity was investigated in Wistar rats, submitted for four weeks to two different behavioral situations, balanced in a factorial design: housing with three females and membership rotation. The combination of these two factor led to adrenal enlargement (43.3%), thymus involution (39.5%) and increased basal corticosterone levels, all indices of activation of the hypothalamic-hypophysis-adrenal axis. However, neither natural killer cell activity, splenocyte reactivity to mitogen nor the rate of spontaneous development of antibodies against Mycoplasma pulmonis, a common pathogen of the respiratory tract, were changed in the endocrine activated animals. Analysis of the data on kinetics of stress at 1, 7 and 28 days after the initial mixing of the animals gave the same results. These data question the immunosuppressant activity usually conferred to corticosteroids, at least when adrenal hyperactivity is induced by chronic environmental stressors.

Adrenal Glands↗
PubMed1994

The effect of radiation therapy on immune function in patients with squamous cell lung carcinoma.

The immune response is impaired in patients with malignancy, and radiation therapy (RT) can exacerbate the cancer induced-attenuation of immune response. In order to search for the fine mechanisms behind the RT-induced attenuation of cell-mediated immune response, we measured the number of lymphocytes in peripheral blood, its subsets, and lymphoblast transformation induced by phytohemagglutinin (PHA), purified protein derivatives (PPD), mitogenic monoclonal antibody anti-CD3, and mitogenic combination of anti-CD2 antibodies 9-1 and 9.6 before and after RT in 19 patients with squamous cell lung cancer. Radiation therapy significantly decreased the total numbers of lymphocytes, CD-3, CD-4, and CD8-positive lymphocytes in peripheral blood. However, RT did not change the percentages of lymphocytes and its subsets. Radiation therapy increased the percentage of interleukin 2 (IL-2) receptor-positive lymphocytes, and RT significantly decreased in vitro lymphoblast transformation by PHA, PPD, or monoclonal antibodies to T-cell surface antigens (anti-CD2 or anti-CD3). In vitro incubation with IL-2 did not increase lymphoblast transformation by anti-CD3 before RT but significantly increased after RT. In conclusion, we suggest that one of the fine mechanisms behind the RT-induced suppression of immune responsiveness of patients with lung cancer is a defect in IL-2 synthesis by lymphocytes.

Adult↗
PubMed1996

Effects of Coriolus versicolor polysaccharides peptides on electric activity of mediobasal hypothalamus and on immune function in rats.

AIM: The nervous mechanism of the immune potentiating effect of Coriolus versicolor polysaccharides peptides (PSP) was studied in Wistar rats. METHODS: The unit discharge of the mediobasal hypothalamus (MBH) neurons was recorded extracellularly and the lymphocyte proliferation was measured. RESULTS: PSP 1 g.kg-1 ig for 5 d increased the T-lymphocytes and promoted T-lymphocyte proliferation in spleen and peripheral blood. This promoting effect of PSP was blocked by MBH lesion. PSP increased the discharge frequency of MBH neurons, but no increase in discharge frequency was observed after treatment of PSP plus immune inhibitor, cyclosporin A. CONCLUSION: MBH is involved in the immune-potentiating effect of PSP.

Adjuvants, Immunologic↗
PubMedDate not supplied

Handedness and immune function.

Geschwind, Galaburda, and Behan (GBG) have suggested that in utero levels of testosterone influence both cerebral and immune system developments (Geschwind and Behan, 1982; Geschwind and Galaburda, 1984; Geschwind and Galaburda, 1985). According to this theory, high levels of testosterone result in greater incidences of left-handedness, deviations from standard distribution of cerebral functions (known as anomalous dominance), and increased autoimmune dysfunction. While the original data supported these assertions, more recent tests of the hypothesis have been equivocal. One criticism of these studies is that the definition of both handedness and anomalous dominance are too vague. It was one of the aims of this project to investigate and clarify the GBG model by examining four different aspects of handedness as well as a more direct measure of anomalous dominance. In order to extend the GBG model, degree of left-handedness, general immune system functioning, and current testosterone levels were also examined. First, it was predicted and found that left handers had a higher incidence of autoimmune diseases in their immediate families than did right handers. Second, those left handers with an incidence of at least one autoimmune disease were more strongly left-handed than were those with no incidence of autoimmunity. Finally, it was observed that higher testos terone levels were supportive of general immunity. The present findings both support and expand the GBG model.

Adult↗
PubMed1998

Zinc and immune function: the biological basis of altered resistance to infection.

Zinc is known to play a central role in the immune system, and zinc-deficient persons experience increased susceptibility to a variety of pathogens. The immunologic mechanisms whereby zinc modulates increased susceptibility to infection have been studied for several decades. It is clear that zinc affects multiple aspects of the immune system, from the barrier of the skin to gene regulation within lymphocytes. Zinc is crucial for normal development and function of cells mediating nonspecific immunity such as neutrophils and natural killer cells. Zinc deficiency also affects development of acquired immunity by preventing both the outgrowth and certain functions of T lymphocytes such as activation, Th1 cytokine production, and B lymphocyte help. Likewise, B lymphocyte development and antibody production, particularly immunoglobulin G, is compromised. The macrophage, a pivotal cell in many immunologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular killing, cytokine production, and phagocytosis. The effects of zinc on these key immunologic mediators is rooted in the myriad roles for zinc in basic cellular functions such as DNA replication, RNA transcription, cell division, and cell activation. Apoptosis is potentiated by zinc deficiency. Zinc also functions as an antioxidant and can stabilize membranes. This review explores these aspects of zinc biology of the immune system and attempts to provide a biological basis for the altered host resistance to infections observed during zinc deficiency and supplementation.

Animals↗
PubMed1994

Influenza virus host resistance models in mice and rats: utilization for immune function assessment and immunotoxicology.

Each year influenza viruses are responsible for epidemic respiratory diseases with excess morbidity and mortality. The severity of influenza diseases ranges from mild upper respiratory tract infections to severe lower respiratory tract infections involving pneumonia, bronchiolitis and coincidental bacterial super-infections. The immune response to influenza viruses can be schematically divided into a cascade of non-specific and specific functions. These functions are involved at different well defined time points after infection. We describe in this manuscript three influenza models utilized in our laboratory: (i) a highly virulent influenza virus (influenza A/Hong Kong/8/68 (H3N2) virus) adapted to B6C3F1 mice, (ii) a mouse-adapted influenza A/Port Chalmers/1/73 (H3N2) virus, and (iii) a rat-adapted influenza virus (RAIV) model (influenza A/Port Chalmers/1/73 (H3N2)). This rat-adapted influenza model has been mainly utilized as a model to assess local immunotoxic effects of inhaled environmental pollutants such as phosgene. These host resistance models are also useful for assessing the effect of systemically-induced immunosuppression or immunomodulation by drugs or chemicals on the local pulmonary immune response to influenza virus. The comparison of these different models allowed two major conclusions: (a) viral replication and mortality are two different endpoints and are not necessarily linked (no mortality was observed with Port Chalmers virus in the mouse although the virus replicates to high titers in the lung with a kinetic pattern comparable to the one obtained with Hong Kong virus), (b) mortality, viral replication, and immune function assessment are different endpoints that can be used, depending on the question addressed.

Animals↗
PubMed2004

Defective immune function of primary effusion lymphoma cells is associated with distinct KSHV gene expression profiles.

Primary effusion lymphomas (PEL) are uniformly infected with Kaposi's sarcoma-associated herpesvirus (KSHV), and thus likely present both tumor and viral antigens to the immune system. In order to grow unrestricted and cause disease, multiple immune evasion strategies may be utilized by PEL to evade immune surveillance. Using six well-established PEL cell lines and comparing these to Epstein-Barr virus-transformed B cell lines and peripheral blood B cells, significant differences were found in the surface expression of molecules involved in antigen presentation, T cell activation and cell-cell adhesion. Significantly reduced stimulation of cytotoxic T lymphocytes, lowered sensitivity to natural killer cell-mediated lysis and impaired function as antigen presenting cells in mixed leukocyte reactions were found for three PEL cell lines with particularly low CD54, CD58 and CD81 expression. Comparative microarray analysis demonstrated specific patterns of KSHV-encoded gene expression that were associated with the different immune functions of these cell lines. Thus, the present data suggest that distinct patterns of KSHV gene expression may be associated with particular phenotypic and functional characteristics of PEL cells, which may influence PEL pathogenesis.

Adult↗