Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differences in the levels of immune cell subsets present in peripheral blood have been demonstrated based on sociodemographic factors such as age and race. Postpartal women, who are recovering from the immune changes that are concomitant with pregnancy, have lymphocyte and monocyte values that differ from other populations. A subgroup of postpartal women, mothers who deliver preterm very-low-birth-weight (VLBW) (< or = 1,500 g) infants, may have further differences in values of immune cell subsets and in immune functioning either because of hormonal factors or lifestyle changes or because of the stress they experience after their infant's birth and for the first few months of infant caretaking. This study examined anxiety, depression, and immune cell phenotypes in 30 mothers of VLBW infants and in 30 mothers of healthy term infants over the first 4 postpartal months to determine if mothers of preterm VLBW infants differed from mothers of healthy term infants in psychological and immunologic parameters. Additionally, lymphocyte proliferation and natural killer cell functional assays were performed in a subset of mothers. Mothers of VLBW infants had increased anxiety and decreased lymphocyte proliferation compared to mothers of term infants. When lymphocyte and monocyte subsets were compared over time between the two groups of mothers differences were found in CD8, CD20, CD3-/CD56+, CD14, and HLA class II Ia on monocytes. Mothers with high-fat diets had lower percentages of some monocytes (CD14), lymphocytes (CD4+/CD45RA+), and natural killer cells (CD3-/CD57+) during the first 4 postpartal months.
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PMID:Immune responses in mothers of term and preterm very-low-birth-weight infants. 930 6

Mothers of preterm, very low birthweight (< or = 1500 g; VLBW) infants experience the stress of caring for small, fragile infants at the same time that they are recovering from the relative immunosuppression of pregnancy and when many health behaviour changes (e.g., nutrition) occur which also may influence immune status. The purpose of this study was to examine changes in anxiety and depression and in health behaviors, as well as lymphocyte proliferation and natural killer cell activity in mothers of preterm, VLBW infants compared to mothers of healthy term infants. Mothers of preterm VLBW infants have decreased in vitro lymphocyte response to mitogens compared to mothers of healthy term infants over time, and this difference could not be explained by anxiety, depression, or health behaviors. However, among mothers of VLBW infants, anxiety was related to decreased lymphocyte proliferation response at 1 month postpartum. There was no relationship between maternal depression and lymphocyte proliferative response in mothers of term infants. Natural killer cell activity did not differ between the two groups of mothers, nor was there a relationship between natural killer cell activity and maternal anxiety, depression, or health behaviors. Thus, lymphocyte proliferative response to mitogens may be an important biologic market of increased stress in mothers of VLBW infants in the first couple of months postpartum.
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PMID:Caregiving to very low birthweight infants: a model of stress and immune response. 941 5

Fluoxetine (FLX) and other specific serotonin uptake inhibitors (SSRIs) have become the drugs of choice for treating depression. However, only a limited number of studies have addressed the effects of FLX on immune cell function. Our lab has measured the effects of both acute and chronic FLX administration on two functions of cell-mediated immunity, mitogen-induced lymphocyte proliferation (MILP) and natural killer cell cytolytic activity (NKCA). In this article we report that acute FLX administration (10 mg/kg) resulted in a dose- and time-dependent decrease in MILP and NKCA. MILP was more sensitive than NKCA to FLX, requiring lower doses for inhibition; however, the effects were more transient. Following chronic FLX administration, these effects were no longer observed, suggesting that an apparent tolerance to these particular measures of cell-mediated immunity had developed. Finally, a single microinjection of FLX directly into the lateral ventricle produced similar suppressive effects on MILP and NKCA, suggesting that the immunomodulatory mechanism may have a central component.
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PMID:Modulation of immune cell function following fluoxetine administration in rats. 944 50

Recently there has been considerable conjecture in the literature concerning a possible relationship between stress, depression and bereavement, and carcinoma. We shall propose a causal model in which the relationship between stress, depression and carcinoma is clarified. This relationship is grounded on dysregulation of the inflammatory cytokines in stress and depression. Stress is associated with increased expression of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), and reduced expression of IL-2, interferon-gamma (IFN-gamma), major histocompatability complex (MHC) class II molecules and natural killer cell activity (NKA). Depression is associated with elevated IFN-gamma and IL-1 beta, downregulated IL-2, and reduced NKA. Most organ-related carcinomas are associated with elevated TNF-alpha, which inhibits the activity of protein tyrosine phosphatase (PTPase), the enzyme that initiates activation of the MHC class I pathway. Sustained elevation of TNF-alpha inhibits the activity of PTPase which results in diminished expression of the MHC class I antigen on the cell surface and thus, malignant cells escape immune surveillance. Therefore, stress and depression can foster tumor progression by means of inhibiting the expression of MHC class I and II molecules and through the reduction of NKA.
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PMID:An immunological model connecting the pathogenesis of stress, depression and carcinoma. 982 37

Depressed mood has been associated with reduced natural killer cell activity (NKCA). Further, amelioration of depressive symptoms by pharmacotherapy has resulted in augmented NKCA. Serotonin, an indoleamine implicated in the pathophysiology of affective disorders, enhances NKCA in vitro and lymphocytes possess serotonin transporters and receptors. The present study evaluated NKCA in depressed outpatients before and during treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Prozac(R)). Further, the SSRIs, fluoxetine and paroxetine (Paxil(R)), were also incubated in vitro with lymphoid cells to evaluate possible direct effects of SSRIs on NKCA. Depressed outpatients were administered fluoxetine (20 mg/day) for 4 weeks. NKCA and severity of depression were evaluated at weeks 0, 1, 2, and 4. Serum concentrations of fluoxetine and norfluoxetine were obtained as well. Mononuclear cells obtained from nonpatient volunteers were incubated with pharmacologic concentrations of fluoxetine or paroxetine and NKCA measured with a standard chromium release assay. Fluoxetine treatment resulted in decreased symptoms of depression and increased serum concentrations of fluoxetine and norfluoxetine. Further, fluoxetine treatment was associated with augmented NKCA in a subgroup of depressed outpatients exhibiting low NKCA at baseline. Fluoxetine had no effect on NKCA in depressed individuals exhibiting high NKCA at baseline. Incubation of mononuclear cells with fluoxetine and paroxetine augmented NKCA in vitro. The enhancing effects of antidepressants on NKCA in vivo and in vitro indicate a possible direct drug interaction with lymphoid cells during pharmacotherapy, suggesting that pharmacologic treatment of depression may result in enhanced immune competence as indexed by enhanced NKCA and that NKCA could be pharmacologically augmented with antidepressants in individuals with compromised immune function.
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PMID:Antidepressants augment natural killer cell activity: in vivo and in vitro. 989 55

Xeroderma pigmentosum group A gene-deficient mice easily develop skin cancers by ultraviolet radiation. Natural killer cells play an important part in tumor surveillance. To study whether ultraviolet radiation-induced suppression of natural killer cell function is involved in the high incidence of skin tumors in patients with xeroderma pigmentosum, we analyzed the number and activity of natural killer cells in ultraviolet B-irradiated xeroderma pigmentosum A model mice. The number of natural killer cells in peripheral blood significantly decreased after ultraviolet B-irradiation only in xeroderma pigmentosum A mice, but those in the spleen were not affected. As compared with the wild-type mice, the xeroderma pigmentosum A mice displayed a higher level of spontaneous splenic natural killer cell activity (10%-15% vs 3%) and inducible natural killer activity (30%-50% vs 20%-25%) after injection of polyinosinic:polycytidylic acid. At 24 h after the last irradiation of three and five daily consecutive exposures to 500 mJ per cm2-ultraviolet B, however, the natural killer activity in xeroderma pigmentosum A mice decreased to 60 and 30% of the preirradiated level, respectively, but it did not in the wild-type mice. The depression of natural killer activity in xeroderma pigmentosum A mice recovered to a normal level at 10 and 15 d after the last irradiation, respectively. The high incidence of skin cancers in xeroderma pigmentosum patients may be mainly due to a defect in the repair of ultraviolet-damaged DNA of cutaneous cells, and possibly also due to an intensified ultraviolet-induced immunosuppression. Moreover, the present study suggests that the enhanced ultraviolet-induced impairment of natural killer function could be partially involved in cancer development.
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PMID:Ultraviolet radiation-induced suppression of natural killer cell activity is enhanced in xeroderma pigmentosum group A (XPA) model mice. 1038 46

Recent evidence suggests that depression of immune function occurs early after spinal cord injury (SCI) and is maintained thereafter. Deviations from immune function observed in healthy persons with intact neuraxes include natural killer cell number and cytotoxicity, T cell function and activation, macrophage phagocytosis, levels of interleukins (IL)-2 and -6, the soluble IL-2R receptor, and intracellular adhesion molecules. While a single etiology explaining these abnormalities has not been identified, decentralization of the autonomic nervous system is the most likely cause. Otherwise, many persons with SCI, who sustain episodic autonomic overstimulation, are among the most physically deconditioned of all humans, and often select a diet rich in fat and low in protein. All of these are associated with suppressed immune function in persons without SCI. Those with SCI may also be (over)exposed to drugs and medications that suppress immune function, including methylprednisolone administered immediately after traumatic injury. No evidence suggests that the immune profiles of persons with SCI favor disease and illness resistance. As opportunistic infections of the urinary tract, lungs, and skin represent major causes of morbidity for those aging with SCI, attention to, or intervention on, immune suppressive states, traits, behaviors, diets, and medications may represent a means through which host defenses of persons with SCI can be fortified and their illness proclivities reduced.
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PMID:Known and plausible modulators of depressed immune functions following spinal cord injuries. 1091 52

Epidemiological evidence suggests that heavy acute or chronic exercise is related to an increased incidence of upper respiratory tract infections in athletes, while moderate exercise is believed to be protective. During the past years, many groups have investigated the association between changes within the immune system and exercise at different intensity levels. Although following strenuous exercise, some immunologic alterations were quite consistent and reproducible, e.g. neutrophilia, lymphopenia, and depression of natural killer cell activity, some findings were divergent or strongly dependent on the study design and athletes investigated. Lately, interesting results in the field of psychoneuroimmunolgy as well as new insights in the relationship between macro- and micronutrient and the immune system have brought up new fields of research interest. There is growing evidence that e.g. lifestyle factors, the coping with daily stress, and dietary behavior are important cofactors in the immune response to exercise. The present work gives a short review on the literature dealing with URTI in athletes with special reference to the above mentioned cofactors. In addition, the results of a recent investigation concerning training and associated lifestyle patterns in German athletes are presented.
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PMID:Upper respiratory tract infection in athletes: influence of lifestyle, type of sport, training effort, and immunostimulant intake. 1091 64

MDMA (3,4-methylenedioxymethamphetamine) use can cause neurochemical, behavioral and endocrine alterations, similar to those produced by exposure to acute stress, suggesting its potential as a "chemical stressor." It is known that stressful stimuli can produce a depression of immune function and an alteration in immune cells distribution. In vitro exposure to MDMA resulted in a modulation of several immune functional parameters such as T-cell regulatory function, cytotoxic T-lymphocyte activity, natural killer cell activity and macrophage function. Administration of MDMA in rats produced a rapid and sustained suppression of induced lymphocytes proliferation and a significant decrease in circulating lymphocytes. These alterations in rat immune function were accompanied by a significant rapid increase in plasma corticosterone concentrations. It was postulated that the result of altered induced proliferation response of lymphocytes could have been due to a combined effect of direct action of MDMA on lymphocytes and to the activation of the hypothalamic pituitary adrenal axis (HPA axis) and/or the sympathetic nervous system (SNS) via central mechanisms. In humans, acute MDMA treatment produced a time-dependent immune dysfunction associated with MDMA plasma concentrations. Although total leukocyte count remained unchanged, there was a decrease in CD4+ T-cells and functional responsiveness of lymphocytes to mitogenic stimulation, while percentage of natural killer cells significantly increased. A rise of cortisol plasma concentrations similar to that observed in the rat model supported the hypothesis of MDMA-induced release of corticotrophin-releasing factor from the median eminence of the hypothalamus and subsequent HPA axis and SNS activation. The present findings indicate that MDMA ingestion may represent a potential health hazard for an increased risk of immune system-related diseases.
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PMID:Immunomodulating activity of MDMA. 1108 23

It is now widely accepted that psychological stress and psychiatric illness can compromise immune function. Furthermore the mechanisms whereby such changes occur are probably associated with the activities of the cytokines and other inflammatory mediators of the immune system which are known to initiate changes in behaviour. This review aims to summarise the experimental and clinical evidence that implicates the pro-inflammatory cytokines in the pathological changes seen in major depression and in Alzheimer's disease (AD). In major depression, evidence is provided to show that both activation (e.g., macrophage activity, acute phase proteins) and inhibition (e.g., natural killer cell activity) of the immune system occur. Many of the behavioural changes seen in depression are simulated by three pro-inflammatory cytokines (IL-1, IL-6 and TNF-alpha), which may produce their impact on the brain by activating cyclooxygenase, nitric acid synthase and corticotrophin releasing factor. Effective antidepressant treatments largely attenuate the immune changes thereby raising the possibility that the normalisation of central biogenic amine function that are conventionally implicated in the cause of depression may be secondary to those of the pro-inflammatory cytokines. With respect to AD, while the cause(s) are unknown, there is both experimental and clinical evidence to suggest that inflammatory processes in the brain caused in particular by TNF-alpha together with the subsequent rise in free radicals, are instrumental in causing the pathological changes which underlie the disease. Evidence in favour of the inflammatory hypothesis is supported by the finding that nonsteroidal anti-inflammatory drugs slow down the progression of the disease.Although, more research is needed into the inter-relationships between the various pro-inflammatory cytokines and the behavioural changes invoked in major depression and AD, the immunological hypothesis has been important in stimulating new concepts regarding the causes of the pathological changes in these diseases and how effective drug treatments may attenuate them.
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PMID:Changes in the immune system in depression and dementia: causal or co-incidental effects? 1133 99


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