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)

Sepsis and septic shock account for substantial morbidity and mortality in the intensive care units. NF-kappaB activation, and elevated concentrations of macrophage migration inhibitory factor (MIF), tumor necrosis factor-a (TNF-alpha), interleukin-1 (IL-1), IL-6, free radicals, inducible nitric oxide (iNO), and stress hyperglycemia are some of the factors that induce systemic inflammatory response and myocardial depression seen in sepsis. Conversely, adenosine, activated protein C, oxidized phospholipids, w-3 fatty acids, and insulin have beneficial effects in sepsis and septic shock. These molecules and in particular insulin have the ability to suppress synthesis of MIF, TNF-alpha, IL-1, IL-6, and free radicals, enhance endothelial NO production, and enhance the production of anti-inflammatory cytokines IL-10, and IL-4. In addition, insulin corrects stress hyperglycemia and improves myocardial function. Thus insulin, adenosine, activated protein C, oxidized phospholipids, and w-fatty acids show anti-inflammatory actions and explain why and how they are useful in sepsis and septic shock and possibly, other inflammatory conditions. Hence, their combined use may be of significant benefit in sepsis and septic shock.
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PMID:Current advances in sepsis and septic shock with particular emphasis on the role of insulin. 1294 44

NF-kappaB activation, and elevated concentrations of macrophage migration inhibitory factor (MIF), tumor necrosis factor-alpha (TNF-alpha), interleukin-1(IL-1), IL-6, free radicals, inducible nitric oxide (iNO), and stress hyperglycemia occurs in sepsis and this leads to systemic inflammatory response and myocardial depression seen in sepsis and septic shock. Conversely, insulin suppresses production of MIF, TNF-alpha, IL-1, IL-6, and free radicals, enhances endothelial NO generation, and enhances the production of anti-inflammatory cytokines IL-4, and IL-10, corrects stress hyperglycemia and improves myocardial function. This supports my earlier proposal that insulin (with or without glucose and potassium) therapy to maintain euglycemia suppresses the inflammatory response, improves myocardial function, and thus, is of benefit in acute myocardial infarction, sepsis andseptic shock.
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PMID:Insulin in sepsis and septic shock. 1462 Oct 41

Some studies suggest that inaccuracy in recognizing and describing emotional states, combined with a highly descriptive mode of expression, as in alexithymia, may influence the immune response. We therefore investigated in healthy women the relationship between alexithymia and circulating levels of IL-1, IL-2 and IL-4. Seventeen mentally and physically healthy women aged between 20 and 25 years completed psychological questionnaires to assess alexithymia (Toronto Alexithymia Scale: TAS) and depressed mood (Hospital Anxiety and Depression Scale: HAD). Serum concentrations of IL-1, IL-2 and IL-4 were measured by ELISA. We found a significant positive correlation between serum levels of IL-4 and TAS score (r=0.55; p=0.021) and between factor 1 of the TAS (difficulty in identifying feelings) and IL-4 (r=0.57; p=0.017) while serum IL-1 and IL-2 were not detected in ten and six patients, respectively. Although there was a significant correlation between age and IL-4 levels, a linear regression with BMI, age, depressed mood and TAS as independent variables showed that only alexithymia could predict significantly increased levels of IL-4. Alexithymia and difficulty in identifying feelings could be associated with increased levels of IL-4 which may result in chronic impairment of pro/anti-inflammatory cytokine balance with psychological and somatic consequences. Nevertheless, these intriguing findings would deserve replication and extension in a larger sample of subjects.
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PMID:Correlation between serum levels of interleukin-4 and alexithymia scores in healthy female subjects: preliminary findings. 1474 98

The major purpose of this study was to quantify hypergravity-induced changes in erythrocyte and thrombocyte characteristics, spontaneous and mitogen-induced lymphoblastogenesis, and capacity of splenocytes to secrete immunoregulatory cytokines. C57BL/6 mice were subjected to chronic 1, 2, and 3 G; subsets were euthanized after 1, 4, 7, 10, and 21 days of centrifugation. Erythrocyte counts, hematocrit, and hemoglobin were significantly reduced by day 21 in both centrifuged groups. Hemoglobin concentration and volume per red blood cell were generally low, but an early, transient spike above normal was noted in thrombocyte counts in the 3-G group. Fluctuations above and below normal in blood and spleen cell spontaneous blastogenesis were dependent on the length of centrifugation time and not on the level of gravity. Depression in splenocyte responses to phytohemagglutinin and lipopolysaccharide due to gravity were noted when the data were expressed as stimulation indexes. Cytokine production by spleen cells was primarily affected during the first week of centrifugation: IL-2, IL-4, and tumor necrosis factor-alpha increased, whereas interferon-gamma decreased. These findings, although not identical to those reported for spaceflight, indicate that altered gravity can influence both hematological and functional variables that may translate into serious health consequences during extended missions.
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PMID:Hypergravity-induced immunomodulation in a rodent model: hematological and lymphocyte function analyses. 1497 9

Cytokines are involved in ischemic tolerance, including that triggered by spreading depression (SD), yet their roles in neuroprotection remain incompletely defined. The latter may stem from the pleiotropic nature of these signaling molecules whose complexities for interaction might be better deciphered through simultaneous measurement of multiple targeted proteins. Accordingly, the authors used microsphere-based flow cytometric immunoassays and hippocampal organotypic cultures (HOTCs) to characterize the magnitude, time course, and diversity of cytokine (interleukin [IL] 1alpha, IL-1beta, IL-2, IL-4, IL-6, IL-10, granulocyte-macrophage colony-stimulating factor [GM-CSF], interferon-gamma [IFN-gamma], and tumor necrosis factor-alpha [TNF-alpha]) response to SD. GM-CSF was not detected in HOTCs or media. However, SD triggered a significant, generalized increase in seven cytokines evident in HOTCs 6 hours later, with the remaining cytokine, IL-1beta, becoming significantly different at 1 and 3 days. Additionally, these changes extended to include surrounding media for IL-6 and TNF-alpha by 1 and 3 days. This increase was localized to microglia via immunostaining for IL-1alpha, IL-1beta, and interferon-y. IL-10, although significantly more abundant in HOTCs 6 hours after SD, was significantly less abundant in surrounding media at that time and at 1 day. Finally, the generalized early increase in tissue cytokines later settled to a pattern at 3 days of recovery centering on changes in IL-1alpha, IL-1beta, and TNF-alpha, cytokines capable of modulating ischemic injury.
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PMID:Multiplexed cytokine protein expression profiles from spreading depression in hippocampal organotypic cultures. 1536 13

The mechanisms underlying induction of immune dysregulation and chronic fungal infection by a transient tumor necrosis factor alpha (TNF-alpha) deficiency remain to be defined. The objective of our studies was to determine the potential contribution of neutropenia and immature dendritic cells to the immune deviation. Administration of an anti-TNF-alpha monoclonal antibody at day 0 neutralized TNF-alpha only during the first week of a pulmonary Cryptococcus neoformans infection. Transient neutralization of TNF-alpha resulted in transient depression of interleukin-12 (IL-12), monocyte chemotactic protein 1 (MCP-1), and gamma interferon (IFN-gamma) production but permanently impaired long-term clearance of the infection from the lungs even after the levels of these cytokines increased and a vigorous inflammatory response developed. Early neutrophil recruitment was defective in the absence of TNF-alpha. However, as demonstrated by neutrophil depletion studies, this did not account for the decrease in IL-12 and IFN-gamma levels and did not play a role in establishing chronic pulmonary cryptococcal infection. Transient TNF-alpha neutralization also produced a deficiency in CD11c(+) MHC II(+) cells and IL-12 in the lymph nodes, potentially implicating a defect in mature dendritic cell trafficking. Transfer of cryptococcal antigen-pulsed immature dendritic cells into naive mice prior to intratracheal challenge resulted in the development of a nonprotective immune response to C. neoformans that was similar to that observed in anti-TNF-alpha-treated mice (increased IL-4, IL-5, and IL-10 levels, pulmonary eosinophilia, and decreased clearance). Thus, stimulation of an antifungal response by immature dendritic cells can result in an immune deviation similar to that produced by transient TNF-alpha deficiency, identifying a new mechanism by which a chronic fungal infection can occur in an immunocompetent host.
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PMID:Transient neutralization of tumor necrosis factor alpha can produce a chronic fungal infection in an immunocompetent host: potential role of immature dendritic cells. 1561 39

Anti-inflammatory effect of desloratadine (DL), including, but not limited to depression of production of IL-4, IL-6 and IL-8, has been shown in several in vitro experiments but only a few in vivo studies refer to this findings. The purpose of our study was to evaluate the influence of DL on levels of IL-4, IL-10, IL-18 and TGF-beta in sera of patients with seasonal allergic rhinitis (SAR). Sixty-nine subjects suffering from SAR with hypersensitivity to grass pollen were included into the evaluation of clinical efficacy of DL (5mg once daily). None of them was taking any H(1) receptor antagonist during the pollen season before inclusion into the study. Samples of peripheral blood were taken before and after 4 weeks of treatment. Levels of cytokines were determined using the ELISA method. The mean level of IL-4 was 0.212+/-0.07pg/ml before and 0.221+/-0.1pg/ml after the treatment (p=0.52); IL-10 5.13+/-3.14 and 4.71+/-0.88 (p=0.69); IL-18 54.45+/-26.09 and 44.80+/-22.42 (p=0.48); TGF beta 949.17+/-401.5 and 955.7+/-391.2 (p=0.97)pg/ml before and after the treatment, respectively. Unless in vitro DL demonstrates not only anti-allergic but also anti-inflammatory activities data from this in vivo study in a group of patients suffering from SAR do not support previous pre-clinical findings.
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PMID:The effect of 4 weeks treatment with desloratadine (5mg daily) on levels of interleukin (IL)-4, IL-10, IL-18 and TGF beta in patients suffering from seasonal allergic rhinitis. 1653 Apr 40

Posttraumatic stress disorder (PTSD) may increase cardiovascular risk but the psychophysiological mechanisms involved are elusive. We hypothesized that proinflammatory activity is elevated in patients with PTSD as diagnosed by the Clinician Administered PTSD Scale (CAPS) interview. Plasma levels of proinflammatory C-reactive protein (CRP), interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, and of anti-inflammatory IL-4 and IL-10 were measured in 14 otherwise healthy PTSD patients and in 14 age- and gender-matched healthy non-PTSD controls. Levels of TNF-alpha (p=0.038; effect size Cohen's d=0.58) and of IL-1beta (p=0.075, d=0.68) were higher in patients than in controls. CRP (d=0.10), IL-6 (d=0.18), IL-4 (d=0.42), and IL-10 (d=0.37) were not significantly different between groups. Controlling for traditional cardiovascular risk factors, mood, and time since trauma revealed lower IL-4 in patients than in controls (p=0.029) and rendered group differences in TNF-alpha and IL-1beta insignificant. In all subjects, TNF-alpha correlated with total (frequency and intensity) PTSD symptom cluster of re-experiencing (r=0.49, p=0.008), avoidance (r=0.37, p=0.050), and hyperarousal (r=0.42, p=0.026), and with PTSD total symptom score (r=0.37, p=0.054). Controlling for time since trauma attenuated these associations. The correlation between IL-1beta and total avoidance symptoms (r=0.42, p=0.028) became insignificant when controlling for anxiety and depression. IL-4 correlated with total hyperarousal symptoms (r=-0.38, p=0.047), and after controlling for systolic blood pressure and smoking status, with PTSD total symptom score (r=-0.41, p=0.035). PTSD patients showed a low-grade systemic proinflammatory state, which, moreover, was related to PTSD symptom levels suggesting one mechanism by which PTSD could contribute to atherosclerotic disease.
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PMID:Evidence for low-grade systemic proinflammatory activity in patients with posttraumatic stress disorder. 1690 5

Toxoplasma gondii has been shown to result in life-threatening encephalitis in immunocompromised patients after reactivation of dormant parasites. In order to obtain information on immune responses related to this phenomenon, BALB/c mice were infected with 25 cysts of the 76K strain of T. gondii, then, treated orally with dexamethasone (Toxo/Dexa-treated group) in order to reactivate the chronic toxoplasmosis. None of the T. gondii-infected mice died during the experimental periods, whereas the Toxo/Dexa-treated mice evidenced a significant attenuation of survival periods. Toxoplasma-specific IgG2a, IgA and IgM titers in sera were significantly depressed in the Toxo/Dexa-treated mice; however, the IgG1 sera titers were similar to those seen in the Toxoplasma-infected mice. The percentages of CD4+ and CD8 alpha + T cells in the Toxo/Dexa-treated mice were significantly reduced 2 weeks after dexamethasone treatment. IFN-gamma and IL-10 production levels in the Toxo/Dexa-treated mice were depressed significantly, whereas IL-4 production was increased temporarily. The expression levels of the Toxoplasma-specific P30 and B1 genes were found to have been increased in the Toxo/Dexa-treated mice in comparison with the Toxoplasmainfected mice. Collectively, the findings of this study demonstrate that reactivation of murine toxoplasmosis as the result of dexamethasone treatment induced a depression in Th1 immune responses, whereas Th2 immune responses were not significantly influenced.
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PMID:Cytokine and antibody responses of reactivated murine toxoplasmosis upon administration of dexamathasone. 1696 58

To clarify the relationship between cellular immune status and nutritive condition in periparturient dairy cows, feeding content, blood profiles, and immune condition were observed in cows from two dairy herds with different types of feed content. Immunological analyses such as leukocyte population and peripheral blood mononuclear cell (PBMC) mRNA of IFN-gamma, TNF-alpha, IL-4, and IL-10, quantified by real-time RT-PCR were performed. With regard to feed content during dry periods, there were six cows in the herd with insufficient non-structural carbohydrate (NFC) intake (group I) and six cows in the herd with sufficient NFC intake (group II). Significantly lower levels of blood glucose were observed in group I between weeks -12 and 16 compared with group II. Serum cholesterol level was significantly lower in group I between weeks 2 and 10 than in group II. The numbers of CD3+ and CD4+ T cells in group I were significantly lower than those in group II in weeks 6 and 14. The numbers of CD21+ B cells were significantly lower in group I than in group II in weeks -16, -12, 2, and 10. On the other hand, the CD4+/CD8+ ratio in group II was significantly higher than group I between weeks 2 and 14. The IFNgamma/IL-4 mRNA rate in group I was significantly lower than group II in week 6. We concluded that cellular immune depression occurrs after calving in dairy cows with low nutritional status in the periparturient period.
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PMID:Comparison of two different nutritive conditions against the changes in peripheral blood mononuclear cells of periparturient dairy cows. 1714 72


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