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 immune response of BALB/c mice to type III pneumococcal polysaccharide (SIII), as measured by splenic PFC, was abolished at the height of an acute self-limiting attack of malaria caused by the murine plasmodium P. yoelii, over a wide range of antigen doses. The response to antigen, given at various times after clinical recovery, gradually reappeared, but did not reach normal levels until 12 weeks after the injection of the parasite. A second injection of P. yoelii given 1 hr before SIII caused a moderate degree of depression, although in this case the plasmodium does not multiply. In chronic malaria the response to SIII was also very poor. Short term under-nourishment was found to reduce only slightly the response to SIII.
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PMID:The immune reponse to type III pneumococcal polysaccharide in mice with malaria. 1 12

Levels of complement proteins and functional activity of the alternate complement pathway were assessed in 39 patients with pneumococcal pneumonia. Mean levels of C3 and properdin and the functional activity of the alternate pathway in acute sera were significantly (P less than 0.05) below normal, whereas levels of components of the early classical pathway were normal. Although levels of factor B were in the normal range, they correlated significantly with C3 levels; there was no significant relation between C3 levels and C4 or C1q levels. The 19 patients iwth pneumococcal pneumonia and bacteremia had significantly lower mean values of properdin and factor B than the 20 patients without bacteremia, suggesting a more severe depression of the alternate complement pathway with bacteremia. During convalescence, complement levels were normal or elevated in most of the patients, but mean levels of properdin remained significantly below normal in bacteremic patients. Functional activity of the alternate pathway also remained below normal. These results indicate that there is a selective depression of the alternate pathway in patients with pneumococcal pneumonia, and they are consistent with the concept that the alternate pathway has an important role in host defenses in pneumococcal infection.
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PMID:Complement levels in pneumococcal pneumonia. 2 Apr 5

Dextran B1355 induces a direct PFC response detectable with dextran B512-sensitized red cells which is directed towards an alpha1--6-linked glucose epitope. This response is distinguishable from the alpha1--3-linked specificity assayed by homologous sensitization in that: (a) it is totally suppressed in donors previously rendered tolerant of B512; (b) the PFC are sensitive to inhibition by B512 and isomaltohexaose. The alpha1--6 epitope of B1355 is less immunogenic in BALB/c mice than that with alpha1--3 linkage, inducing a lower amplitude of response and requiring a 100-fold greater minimal dose, while conversely, it is the more effective tolerogen. No alpha1--6-specific response develops in 50 per cent of mice given 10 mg of B1355 and all become totally unresponsive within 14 days. This tolerant state remains stable when spleen cells are transferred to irradiated recipients. By comparison, parallel depression of the alpha1--3 response is not great and rapidly lost by similar transfer. No correlation was observed between the levels of alpha1--6 suppression and alpha1--3 response induced by 10 mg of B1355 in individual mice. The dissociative aspects of the responses to these two epitopes present on the same molecule are discussed in relation to some current theories of B-cell tolerance induction. It is argued that the present findings are contrary to those models which attribute a causal role to mitogenic overstimulation or failure to generate an extrinsic 'second signal'.
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PMID:Influence of molecular structure of the tolerogenicity of bacterial dextrans. III. Dissociation between tolerance and immunity to the alpha1--6- and alpha1--3-linked epitopes of dextran B1355. 5 14

The intensity of reticuloendothelial blockade by carrageenan, silica and ethyl stearate was measured and its effect studied on the susceptibility to tolerance induction by polysaccharide antigens in mice. The most intense RE depression reduced the tolerance threshold dose of levan only by 3-fold and that of dextran B512 not at all. The genetic resistance of BALB/c mice to tolerization with the alpha1-3 glucose epitope of dextran B1355 was not overcome by carrageenan blockade which did however, render them normally susceptible to tolerance induction by human gamma-globulin. PFC responses to immunization by the polysaccharides were diminished by blockade, relative to its intensity and to the antigen itself. These and other data suggest that severe RE blockade (a) can promote tolerance by suppressing the active role(s) of the macrophages in immune induction rather than by sustaining circulating antigen, and (b) depresses responses to thymus-independent antigens, probably by an immunosuppressive influence mediated by damaged macrophages.
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PMID:Influence of reticuloendothelial blockade on the induction of tolerance and immunity by polysaccharides. 5 95

The ocular inflammation and antibody production that follow intravitreal injection of rabbit eyes with bovine gamma globulin were suppressed by treatment with Cytoxan by the intramuscular (i.m.) route. The drug suppressed PFC responses of uveal tract and corneal cells when it was administered, beginning as late as 5 days after immunization, if treatment was continued until day 12 or 13. Short-term treatments and treatment with smaller Cytoxan doses were less effective. We noted a good correlation between the presence or absence of ocular inflammation, suppression of ocular PFC responses and depression of serum, aqueous humour and vitreous humour antibody titres. In some treatment groups ocular antibody production seemed to be completely suppressed, while in others antibody production was significantly delayed.
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PMID:The effect of cyclophosphamide on an ocular immune response. I. Primary response. 34 57

Prospective sequential studies of the antibacterial function of neutrophils, lymphocyte responsiveness, opsonic capacity of serum and serum levels of C3(B), properdin, factor B, IgG, and albumin were made in 32 patients with severe burn injury (greater than or equal to 45%), 21 patients with severe multisystem traumatic injury, 20 high-risk, infected patients, and 22 renal transplant patients. Fifty-five episodes of bacteremia occurred in 37 of the 95 patients. Abnormal neutrophil function was clearly associated as a predisposing factor to these episodes, whereas there was no association between bacteremia and low serum levels of C3, IgG, factor B, or properdin. C3, factor B, and IgG usually rose following bacteremia as acute phase proteins, but there was evidence of a consumptive opsoninopathy in 11% of episodes. Defective opsonization was associated with a high risk of bacteremia only when there was a coexisting abnormality of neutrophil function (88% of such patients became bacteremic). None of 27 nonburned patients tested with delayed hypersensitivity antigens responded normally, and there was regularly depression of lymphocyte responsiveness to phytohemagglutinin-A and concanavalin-A in a whole blood assay related to serum immunosuppressive factors, but poor responsiveness was not associated with bacteremia.
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PMID:A comparison of immunologic profiles and their influence on bacteremia in surgical patients with a high risk of infection. 37 44

The effects of immunosuppressive ascites fluids from mastocytoma-bearing mice on the primary vs secondary immune response to sheep red blood cells (SRBC) was examined. Injection of mice with ascites fluid from tumor-bearing mice markedly depressed the primary immune response of normal syngeneic mice challenged with SRBC. However, there was a preferential depression of the 19S IgM antibody response as compared with the 7S IgG response. Injection of ascites fluid shortly before secondary immunization of mice with SRBC also resulted in depressed IgM PFC responses but only a slight to moderate depression of IgG PFC. Treatment of mice with the ascites fluid before primary immunization had little if any effect on the secondary IgG PFC response, although the IgM response was moderately depressed. These results indicate that the immunosuppressive factor(s) present in the ascites fluid of mastocytoma-bearing mice has a differential effect on distinct classes of immunocytes. Those immunocytes or their precursors involved in formation of low efficiency 7S IgG antibody are more resistant to immunodepression. Such differences appear due to different sensitivities of cells involved in the immune response system.
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PMID:Differential immunosuppressive effects of ascites fluid from mastocytoma-bearing mice on primary vs secondary immunocyte responses. 41 68

A prospective evaluation of the activity of the complement system was undertaken in 32 patients at the time of diagnosis of inflammatory bowel disease, before the onset of therapy. Serum classical pathway components and function were normal, while significant abnormalities of the alternative pathway were found. Depressions of serum properdin and properdin convertase were noted in association with diminished consumption of C3--C9 after reaction with cobra venom. These abnormalities of alternative pathway integrity were most significant in regional enteritis and in ulcerative colitis with extraintestinal complications. Sequential studies extending into clinical remission revealed resolution of all significant abnormalities.
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PMID:Complement alterations in inflammatory bowel disease. 43 35

Components of the complement system are known to play an important role in the cytolytic process and in chemotaxis of leukocytes. Cobra venom factor specifically cleaves C3 activity via activation of the alternative (properdin) complement pathway. It does not act directly on C3. If C3 is involved in tissue necrosis after ischemic injury, cobra venom factor might reduce tissue damage after acute coronary occlusion. Accordingly, in 14 control dogs occlusion of the left anterior descending artery was carried out for 24 h. Epicardial electrograms were recorded 15 min after occlusion, and 24 h later transmural specimens for creatine phosphokinase activity (CPK) and for histological analysis were obtained from the same sites. In another 14 experimental dogs, 20 U/kg cobra venom factor was given intravenously 30 min after occlusion. Serum complement levels fell within 2-4 h to <20% of normal. In the control dogs, the relationship between ST-segment elevation and CPK activity 24 h later was: log CPK = -0.06 ST + 1.48 (n = 111 specimens, 14 dogs, r = 0.77). In the experimental dogs, log CPK = -0.024 ST + 1.46 (n = 111 specimens, 14 dogs, r = 0.60), showing significantly different slopes (P < 0.001), i.e., less CPK depression for any level of ST-segment elevation. Histologically, 69 of 71 sites (97%) with ST-segment elevation exceeding 2 mV in the control dogs showed signs of necrosis 24 h later, whereas in the experimental group only 43 of 79 sites (54%) with abnormal ST-segment elevations showed signs of necrosis (P < 0.0005). At the same time, it was shown that the administration of cobra venom factor did not alter cardiac performance, collateral blood flow to the ischemic myocardium or the clotting system, but infiltration of polymorphonuclear leukocytes into the myocardium was decreased. It is concluded that cobra venom factor, by reducing the amount of C3 and C5 substrate available for chemotactic factor generation, or other as yet undefined mechanisms, protects the ischemic myocardium from undergoing necrosis, as judged by histology and local CPK activity. Hence, a new approach to limiting the extent of myocardial infarcts after experimental coronary occlusion, based upon inhibition of complement-dependent inflammatory processes, is demonstrated.
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PMID:Reduction by cobra venom factor of myocardial necrosis after coronary artery occlusion. 64 Nov 47

The effect of Lewis lung tumor growth in mice on the induction of primary immune response to SRBC, was investigated by PFC assay for measuring antibody activity and by footpad test as a correlate for delayed type hypersensitivity reactions. With the appearance of micrometastases in the lungs there was a decline in the humoral and cellular immune response to the SRBC. An increase of number and size of metastases in the lungs led to a further depression of the immune reactivity. Since the reduction of general immune response in mice bearing this tumor is not due to a direct influence of tumor cells, it might be assumed that suppressor cells or factors, are actively abrogating the general and also the tumor directed immune reactions.
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PMID:Correlation of immune response with clinical stage in Lewis lung tumor-bearing mice. 70 36


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