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)

The use of 129 strain-derived embryonic stem cell lines for targeted gene mutation in mice has led directly to an expanded use of this inbred strain worldwide. It has been noted, however, that the 129 genetic background can make a significant contribution to the severity of a mutant phenotype. In this study, we reveal a specific defect in the IL-5 and Rp105 responses of B lymphocytes from two widely used 129 mouse substrains. The response to stimulation through surface IgM is also diminished, although to a lesser degree, in these mice. The lesion appears to reduce significantly the expression of the alpha-chain of the IL-5R, but may also influence events downstream of the IL-5R. This phenotype displays a codominant inheritance pattern, and is accompanied by a variable but significant depression of peritoneal B-1 cell numbers in 50% of the mice.
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PMID:IL-5 and Rp105 signaling defects in B cells from commonly used 129 mouse substrains. 1057 Feb 67

Environmental exposure to a number of xenobiotics, including pesticides, can have serious effects on the immune system of children, thus rendering them susceptible to infections or other disease states. To study this problem, a recycling chromatographic system for assessing cytokine profiles in humans has been developed and used for the measurement of immune system function in children with documented exposure to residential pesticides. The system is capable of measuring 30 different analytes in a single sample thus enabling the same time examination of representative markers of immune differentiation and function. In the present study, a cohort of 25 exposed children were examined and shown to exhibit a number of features; all subjects demonstrated some abnormalities in cytokines associated with hematopoiesis. Additionally, elevations in pro-inflammatory cytokines and neuropeptides indicated a state of generalized and neurogenic inflammation. Further analysis indicated that a depression of the cellular arm of the immune system that correlated with clinical indicators of lowered host resistance to infection could also be detected in a subgroup of the exposed subjects. All exposed children demonstrated evidence of hyperstimulation of the humoral immune system as indicated by elevated IL-5 concentrations and clinical allergy. The degree of immune dysregulation in the exposed children was found to be quite marked when compared to similar studies performed on age-matched controls.
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PMID:Assessing environmental exposure in children: immunotoxicology screening. 1113 69

Psychological stress can lead to asthma exacerbations in some patients. It is our hypothesis that the stress effect can occur through an enhancement of allergic inflammatory response. To investigate this possibility, airway antigen challenge was evaluated in 20 college students with mild asthma during both a low-stress phase (midsemester or two weeks postfinal examination) and a stress phase (final examination week). Subjects completed questionnaires to assess psychological state and underwent inhaled antigen challenge. Sputum samples were collected before challenge, and six and 24 hours and seven days postchallenge. Leukocytes were counted and eosinophil-derived neurotoxin (EDN) was measured in sputum supernates. Sputum cells were cultured and stimulated ex vivo with phytohemagglutinin (10 microg/ml), and culture supernates were assayed for interleukin-5 (IL-5) and interferon-gamma by enzyme-linked immunosorbent assay. Sputum eosinophils and EDN levels significantly increased at six and 24 hours postchallenge and were enhanced during the stress phase (p < 0.01). IL-5 generation by sputum cells was also increased at 24 hours during stress and correlated with airway eosinophils (r(s) = 0.65, p < 0.05). Students' anxiety and depression scores were significantly higher during the examination period. Our findings suggest that stress associated with final examinations can act as a cofactor to increase eosinophilic airway inflammation to antigen challenge and thus may enhance asthma severity.
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PMID:School examinations enhance airway inflammation to antigen challenge. 1195 39

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

T-bet (T-box expressed in T cells) and GATA-3 are transcription factors that play a critical role in the development of Th1 and Th2 cells, as do genes of the SOCS (suppressor of cytokine signaling) family, albeit indirectly. Another transcription factor, Foxp3, is a master regulator of natural regulatory T cells (Tregs). To identify the role of these factors in impaired Th1 responses of patent filarial infection, analysis of cytokine, SOCS, and transcription factor mRNA expression was performed on purified T cells of filaria-infected individuals (n = 6) and uninfected controls (n = 6). As expected (and in contrast to cells of uninfected individuals), there was a significant depression of gamma interferon (IFN-gamma) and a concomitant increase in interleukin-4 (IL-4), IL-5, and IL-10 mRNA expression following stimulation with parasite antigen (BmA) but not with a polyclonal T-cell (anti-CD3) stimulus. T-bet (but not GATA-3) was expressed at significantly lower levels in cells of filaria-infected individuals in response to BmA compared with those from the uninfected group, accounting, at least partially, for the diminished IFN-gamma expression. Second, we found no significant differences in expression of Foxp3 between the two groups, although induction of Foxp3 expression correlated with induced expression levels of IL-10, implicating Tregs in the IL-10 expression seen. Finally, parasite-specific T-cell expression of SOCS-1, SOCS-5, and SOCS-7 was significantly diminished among infected patients; in contrast, expression of SOCS-3 increased. Our data therefore indicate that the impaired Th1 responses observed in patent lymphatic filariasis are associated with decreased expression of T-bet, SOCS-1, SOCS-5, and SOCS-7 and increased expression of SOCS-3 in T cells.
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PMID:Transcriptional control of impaired Th1 responses in patent lymphatic filariasis by T-box expressed in T cells and suppressor of cytokine signaling genes. 1590 66

The cell-mediated response in BALB/c mice infected either by Trichinella pseudospiralis or Trichinella spiralis was compared at days 30-50 post-infection (muscle phase). The former species is non-encapsulated, whereas the latter is encapsulated in host muscles. The pattern of response against the two species was similar. Both species elicited T(H)0 or T(H)1/T(H)2 response, with the last one being dominant. Productions of interferon gamma (IFN-gamma), interleukin (IL)-4 and IL-5 were observed after antigenic restimulation of splenocytes from infected mice. No significant difference was observed between the levels of response to concanavalin A (Con-A) by the splenocytes from both infected and non-infected animals. There was a significant increase in serum IgG(1) and IgG(2a). Flow cytometric analysis revealed a marked proliferative response of splenocytes from infected mice to worm antigens, dominated by B (CD19) lymphoblasts. Only a few helper (CD4+) and cytotoxic (CD8+) T lymphoblasts were present. This was confirmed by an up-regulation of CD69, with a dominant expression on B lymphoblasts. In conclusion, the minimal or lack of intense cellular response against T. pseudospiralis in muscles is likely not due to depression of cell-mediated immunity.
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PMID:Cell-mediated response at the muscle phase of Trichinella pseudospiralis and Trichinella spiralis infections. 1648 72

The immune response against clinical forms of chronic schistosomiasis mansoni patients with or without HCV infection was evaluated by assays the serum levels of IFN-gamma and IL-5 for estimate the cell mediated immunity and IgE level to estimate the humoral immunity. This study included three patient groups. G.I included 25 patients with intestinal schistosomiasis, G.II included 15 patients with hepatosplenic schistosomiasis and G.III included 40 patients hepatosplenic schistosomiasis co-infected with HCV. Control G.IV included 15 healthy persons with matched age and sex. The intestinal group had high IFN-gamma (92%), normal level of IL-5 and IgE. The immune response was mainly 100% Th-1 response. The hepatosplenic patients had high IFN-gamma (26.7%), IL-5 (86.7%) and IgE (73.3%). The immune response was 73.4% Th-0, 13.3% Th-1 and 13.3% Th-2. The co-infected group had high IFN-gamma (62.7%), IL-5 (100%) and IgE (92.5%). The immune response was 62.5% Th-0 and 37.5% Th-2 immunity. The shift to Th-0 and Th-2 immunity as well as associated depression of Th-1 in mixed group of patients may be playing a role in the persistence and severity of both diseases. Such immunity defects add to decrease challenge against HCV clearance.
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PMID:INF-gamma, IL-5 and IgE profiles in chronic schistosomiasis mansoni Egyptian patients with or without hepatitis C infection. 1660 10

The non-cytopathic hepatitis B virus (HBV) can induce chronic infections characterized by weak and limited T cell responses against the virus. The factors contributing to the failure to clear HBV and subsequent development of chronic HBV infections are not clearly understood, but a strong interferon-gamma (IFN-gamma) response by CD4+ T cells against the nucleocapsid hepatitis B core antigen (HBcAg) of the virus appears to be important for viral clearance. The present study documents depressed numbers of CD4+ T cells secreting IFN-gamma and interleukin-2 (IL-2) in enzyme-linked immunospot assay (ELISPOT) assays restimulated for 24 hr with antigen following both primary and secondary immunizations of mice with recombinant hepatitis B core antigen (rHBcAg). The kinetics of these responses showed that the depression occurred following a peak response and lasted approximately 2 weeks before returning to the previous peak levels. The depression was abrogated by depletion of CD25+ cells prior to culture in the ELISPOT assay, suggesting inhibition by regulatory T cells. This inhibition of IFN-gamma and IL-2 production was also reversed by in vitro restimulation of the test cells for 48 hr rather than 24 hr in the assay. No such transient, reversible inhibition was detected in the production of IL-5, a Th2-type cytokine. The inhibition in cytokine production did not appear to correlate with the number of antibody-secreting cells or the isotypes produced. This delay by regulatory T cells of Th1-type cytokine production could contribute to viral persistence in chronic HBV infection by interfering with the critical role IFN-gamma plays in protection against viral infections.
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PMID:Transient inhibition of Th1-type cytokine production by CD4 T cells in hepatitis B core antigen immunized mice is mediated by regulatory T cells. 1676 29

Dracunculiasis is a promising candidate for eradication, but transmission of Dracunculus medinensis and recrudescence of the disease have been observed repeatedly. In the present investigation, the D. medinensis-specific cellular cytokine response profiles and the parasite-specific antibody subclass reactivity were evaluated in dracunculiasis patients at distinct states of infection. Analysis of the cellular cytokine response in dracunculiasis patients disclosed a D. medinensis antigen-specific depression of IFN-gamma production with patent D. medinensis infection, while the T helper type 2 cytokine IL-10 was similar in patent, post-patent and control individuals, and IL-5 production was always the highest in controls. In parallel, diminished IFN-gamma and IL-12 responses to antigens from Ascaris lumbricoides, Entamoeba histolytica and mycobacteria were observed in patent and post-patent dracunculiasis cases. The parasite-specific IgG(1) and IgG(4) subclass reactivity profiles corresponded with the D. medinensis infection state, and a clear distinction between patent and post-patent patients and controls was found. Overall a depressed cytokine release was observed with patent D. medinensis, which extended beyond the parasite-specific immune responsiveness. The detection of D. medinensis-specific IgG(1) and IgG(4) isotypes may help to distinguish newly exposed, patent and post-patent D. medinensis infections.
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PMID:Antibody and cytokine responses in Dracunculus medinensis patients at distinct states of infection. 1825 73

Hostility is a risk factor for adverse health outcomes as diverse as cardiovascular disease and post-traumatic stress disorder (PTSD). Cytokines have been suggested to mediate this relationship. We investigated whether in healthy men a relation existed between hostility and T-cell mitogen-induced cytokines and chemokines. Male Dutch military personnel (n=304) were included before deployment. Eleven cytokines and chemokines were measured in supernatants of T-cell mitogen-stimulated whole blood cultures by multiplex immunoassay. Factor analysis was used to identify clusters of cytokines and chemokines. In a regression analysis hostility was related to the cytokine/chemokine clusters, and the potential risk factors age, BMI, smoking, drinking, previous deployment, early life trauma and depression. Explorative factor analysis showed four functional clusters; a pro-inflammatory factor (IL-2, TNFalpha, IFNgamma), an anti-inflammatory factor (IL-4, IL-5, IL-10), IL-6/chemokine factor (IL-6, MCP-1, RANTES, IP-10), and MIF. Hostility was significantly related to decreased IL-6/chemokine secretion and increased pro- and anti-inflammatory cytokines. There was an inverse relation between age and hostility scores. Early life trauma and depression were positively and independently related to hostility as well. This study represents a novel way of investigating the relation between cytokines and psychological characteristics. Cytokines/chemokines clustered into functional factors, which were related to hostility in healthy males. Moreover this relation appeared to be independent of reported depression and early trauma.
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PMID:Hostility is related to clusters of T-cell cytokines and chemokines in healthy men. 1864 Jul 86


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