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 1,531 records · Page 85Linked to original sources

Pulmonary surfactant proteins A and D: innate immune functions and biomarkers for lung diseases.

Pulmonary surfactant, a complex of lipids and proteins, functions to keep alveoli from collapsing at expiration. Surfactant proteins A (SP-A) and D (SP-D) belong to the collectin family and play pivotal roles in the innate immunity of the lung. Pulmonary collectins directly bind with broad specificities to a variety of microorganism and possess anti-microbial effects. These proteins also exhibit both inflammatory and anti-inflammatory functions, which occur through interactions with pattern recognition receptors including Toll-like receptor and CD14, signal inhibitory regulatory protein alpha and a receptor complex of calreticulin and CD91. The collectins enhance phagocytosis of microbes by macrophages through opsonic and/or non-opsonic activities. The proteins stimulate cell surface expression of phagocytic receptors including scavenger receptor A and mannose receptor. Since the expression of SP-A and SP-D is abundant and restricted within the lung, the proteins are now clinically used as biomarkers for lung diseases. The levels of SP-A and SP-D in bronchoalveolar lavage fluids, amniotic fluids, tracheal aspirates and pleural effusions reflect alterations in alveolar compartments and epithelium, and lung maturity. The determination of SP-A and SP-D in sera is a non-invasive and useful tool for understanding some pathological changes of the lung in the diseases, including pulmonary fibrosis, collagen vascular diseases complicated with interstitial lung disease, pulmonary alveolar proteinosis, acute respiratory distress syndrome and radiation pneumonitis.

Animals↗

Age- and disease-related decline in immune function: an opportunity for "thymus-boosting" therapies.

The thymus is the site of production of mature T lymphocytes and thus is indispensable for the development and maintenance of the T cell-mediated arm of the immune system. Thymic production of mature T cells is critically dependent on an influx of bone marrow-derived progenitor T cells that undergo replication and selection within the thymus. Thymus cellularity and thymic hormone secretion reach a peak during the first year of life and then decline gradually until the age of 50-60 years, a process known as "thymic involution." A rapid reduction of thymus cellularity occurs in young patients following injuries, chemotherapy, and other forms of stress. The mechanisms underlying the involution process appear to be dependent on factors intrinsic to the thymic tissue, such as the local production of cytokines and chemoattractants, promoting the recruitment, growth, and differentiation of bone marrow-derived T cell progenitors in the thymus, as well as extrinsic factors, such as systemic levels of endocrine hormones and mediators released by intrathymic nerves of the autonomic nervous system. Knowledge of these factors provides a rational basis for the development of an approach based on tissue engineering that could be used to provide either temporary or permanent reconstitution of thymic function.

Aging↗

Low level chromium (VI) inhalation effects on alveolar macrophages and immune functions in Wistar rats.

In inhalation chambers, 5-week-old male Wistar rats of the strain TNO-W-74 were continuously exposed to submicron aerosols of sodium dichromate in concentrations from 25 (low level) to 200 micrograms/m3 Cr (high level). Subacute exposure (28 days) to 25 and 50 micrograms/m3 Cr resulted in "activated" alveolar macrophages with stimulated phagocytic activities, and significantly elevated antibody responses to injected SRBC's. After subchronic (90 days) low level exposure there was a more pronounced effect on activation of the alveolar macrophages, with increased phagocytic activities. However, at high Cr (VI) exposure level (200 microgram/m3), inhibited phagocytic function of the alveolar macrophages was seen. In rats which were exposed to this chromium aerosol concentration for 42 days, the lung clearance of inert iron oxide was reduced significantly. The humoral immune system was still stimulated at subchronic low chromium aerosol concentrations of 100 micrograms/m3, but significantly depressed at 200 micrograms/m3 Cr. These results show that respiratory defence and immunologic functions were stimulated or inhibited depending on dose and time of chromium (VI) inhalation.

Aerosols↗

Complement proteins C1q and MBL are pattern recognition molecules that signal immediate and long-term protective immune functions.

C1q and mannose binding lectin, members of the "defense collagen" family, are pattern recognition molecules that can trigger rapid enhanced phagocytosis resulting in efficient containment of pathogens or clearance of cellular debris, apoptotic cells and immune complexes. In addition, interaction of C1q and mannose binding lectin with the phagocyte alters subsequent phagocyte cytokine synthesis, and thus may have important implications in directing acute inflammation as well as long-term protective immunity. The importance of the role of defense collagens in phagocytosis of apoptotic cells is highlighted by studies in vivo of mice deficient in C1q, pulmonary surfactant D and mannose binding lectin in which there is delayed clearance of apoptotic cells. Indeed, deficiency of C1q is a risk factor for the development of autoimmunity in both humans and mice, consistent with the hypothesis that inefficient clearance of apoptotic cells results in release of autoantigens and contributes to the pathology associated with autoimmune diseases such as systemic lupus erythematosus. Further understanding of the importance of C1q and mannose binding lectin in the clearance of apoptotic cells and regulation of cytokine synthesis and identification of the receptors implicated in mediating these processes should provide novel targets for therapeutic intervention in the control and manipulation of the immune response in terms of both host defense against infectious disease and tissue repair and remodeling.

Animals↗

The effects of nonsteroidal anti-inflammatory drugs on immune functions of human peripheral blood mononuclear cells.

It is generally accepted that the nonsteroidal anti-inflammatory drugs (NSAIDs) exhibit anti-inflammatory effects primarily through inhibition of prostaglandin (PG) synthesis. However, effects of NSAIDs on immune responses are not fully understood. This study investigated effects of indomethacin and a new NSAID (d-2-[4-(3-methyl-2-thienyl)phenyl]propionic acid, termed as M-5011 in this study) on cytokine production, lymphocyte proliferation, activities of natural killer (NK) and lymphokine activated killer (LAK) cells and secretion of immunoglobulin (Ig). Both indomethacin and M-5011 augmented interleukin (IL)-2 production, whereas they suppressed IL-6 production both at the protein and mRNA levels. These two NSAIDs augmented proliferation of phytohemagglutinin (PHA)-stimulated PBMC and enhanced NK and LAK cell activities. In contrast, indomethacin was more potent than M-5011 in inhibition of both PG synthesis and Ig secretions by pokeweed mitogen (PWM)-stimulated PBMC. These results suggest that these two NSAIDs equally augment cell-mediated immunity, whereas indomethacin was more potent than M-5011 in the inhibition of humoral immunity and PG synthesis.

Anti-Inflammatory Agents, Non-Steroidal↗

Stress-induced enhancement of skin immune function: A role for gamma interferon.

Contrary to the widespread belief that stress is necessarily immunosuppressive, recent studies have shown that, under certain conditions, stress can induce a significant enhancement of a skin cell-mediated immune response [delayed-type hypersensitivity (DTH) or contact hypersensitivity]. Adrenal stress hormones and a stress-induced trafficking of leukocytes from the blood to the skin have been identified as systemic mediators of this immunoenhancement. Because gamma interferon (IFNgamma) is an important cytokine mediator of DTH, the studies described here were designed to examine its role as a local mediator of the stress-induced enhancement of skin DTH. The effect of acute stress on skin DTH was examined in wild-type and IFNgamma receptor-deficient (IFNgammaR-/-) mice that had previously been sensitized with 2,4-dinitro-1-fluorobenzene. Acutely stressed wild-type mice showed a significantly larger DTH response than nonstressed mice. In contrast, IFNgammaR-/- mice failed to show a stress-induced enhancement of skin DTH. Immunoneutralization of IFNgamma in wild-type mice significantly reduced the stress-induced enhancement of skin DTH. In addition, an inflammatory response induced by direct IFNgamma administration to the skin was significantly enhanced by acute stress. Our results suggest that IFNgamma is an important local mediator of a stress-induced enhancement of skin DTH. These studies are clinically relevant because, depending on the nature of the antigen, DTH reactions mediate numerous protective (e.g., resistance to viral, bacterial, parasitic, and fungal infections) or pathological (e.g., autoimmune reactions and contact sensitivity reactions such as that to poison ivy) immune responses.

Animals↗

Modification of immune function through exposure to dietary aflatoxin in Gambian children.

Aflatoxins are immunotoxins that frequently contaminate staple foods in The Gambia and other parts of sub-Saharan Africa, resulting in high exposure throughout life. Impaired infant immune system development may be a key predictor of mortality from infectious disease. In this study we aimed to determine the effect of dietary aflatoxin exposure on a number of immune parameters in Gambian children. A cohort of 472 Gambian children 6-9 years of age was recruited. Serum aflatoxin-albumin (AF-alb) adducts were analyzed to provide a measure of exposure. Immune parameters included secretory IgA (sIgA) in saliva, cell-mediated immunity (CMI), determined using the CMI multitest where test antigens are applied to the skin, and antibody responses to both rabies and pneumococcal polysaccharide vaccines. Birth weight, current anthropometry, and micronutrient status were also recorded. AF-alb adducts were detected in 93% of the children (geometric mean level 22.3 pg/mg; range 5-456 pg/mg). AF-alb level was strongly influenced by month of sampling. In a multivariable analysis, sIgA was markedly lower in children with detectable AF-alb compared with those with nondetectable levels [50.4 micro g/mg protein (95% confidence interval [CI] 48.0-52.8) and 70.2 micro g/mg protein (95% CI 61.1-79.2), respectively; p < 0.0001]. Antibody response to one of four pneumococcal serotypes, but not rabies vaccine, was weakly associated with higher levels of AF-alb. There was no association between CMI responses to test antigens and AF-alb. These data confirm that children in rural Gambia are frequently exposed to high levels of aflatoxin. The study provides evidence that sIgA in saliva may be reduced because of dietary levels of aflatoxin exposure. Given the high burden of infection-related mortality in West Africa, further investigation of the immune effects of aflatoxin exposure in children is merited.

Aflatoxins↗

Dietary fat and immune function. I. Antibody responses, lymphocyte and accessory cell function in (NZB x NZW)F1 mice.

The influence of dietary fat on autoimmunity in lupus-prone (NZB x NZW)F1 mice has been demonstrated. In defining further the effects of dietary lipid on the immune system of this strain, female weanling mice were placed on four diets differing in quantity and type of fat. Their immunologic response was then studied by a variety of tests at 4 and 7 mo of age. Few differences were seen among the four groups at 4 mo of age. At 7 mo of age, however, the mice receiving diets high in saturated and unsaturated fats had a reduced mitogenic response to T cell mitogens and an enhanced response to the B cell mitogen LPS. Immunoglobulin levels and delayed hypersensitivity responses did not show any consistent differences among the diet groups. At 7 mo, however, mice receiving diets high in unsaturated fat demonstrated hyperresponsiveness to injected sheep red blood cells as measured by the hemolytic plaque technique. In addition, peritoneal leukocytes from the same diet group exhibited an increased response to bromelain-treated autologous erythrocytes which was decreased after treatment with anti-Thy-1 antiserum and complement. Phagocytosis by peritoneal macrophages was significantly decreased in the animals fed high-fat diets, particular high saturated fat. Similarly, natural killer cell activity was markedly reduced in the mice with a high intake of saturated lipid, a finding which correlated with the in vitro production of interferon. These results indicate that diets high in fat influence immune responses and thus can affect the onset and severity of autoimmune disease. A low-fat diet can reduce the development of disease by maintaining normal immune responses. The data also suggest that unsaturated fat may influence T helper cell activity and therefore antibody production, whereas saturated fats may affect cellular immune responses which are dependent on membrane contact.

Animals↗

[Age-related changes of B-cell immune function in patients with subacute myelo-optico-neuropathy (SMON)].

Several kinds of immunological abnormalities have been found more frequently in patients with subacute myelo-optico-neuropathy (SMON). To investigate whether the B-cell immune system is implicated in aging in patients with SMON, we examined serum levels of immunoglobulin including IgG, IgM, and IgA, and the number of CD20+ cells (B lymphocytes) and CD20+ CD23+ cells (activated B lymphocytes) using flow cytometry, and compared them with those in age-matched controls. We also investigated whether the number of HLA-DR+ cells was correlated with those of CD20+ cells, CD20+ CD23+ cells, or HLA-DR+CD3+ cells (activated T lymphocytes) in patients with SMON. Serum levels of IgG, IgM and IgA were decreased with aging both in the patients with SMON and in the controls, and no significant difference was found between the two groups. Although the patients with SMON tended to show higher levels of CD20+ and CD20+ CD23+ cells than the age-matched controls, there were no significant differences between the two groups. The number of HLA-DR+ cells was correlated not with that of CD20+ cells or CD20+ CD23+ cells, but with that of HLA-DR+CD3+ cells. In patients with SMON, it is likely that the B-cell immune system is mainly implicated in the effect of aging, but it is unlikely that other factors than aging are associated with the B-cell immune system. The increase in the number of HLA-DR+ cells associated with aging in patients with SMON reflects the increase in the number of activated T lymphocytes, and is not correlated with the changes of B lymphocytes.

Age Factors↗