Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to elucidate the biological effects of photochemical smog on the tonsil, lymphocytes from human tonsil were exposed to ozone and rabbits were exposed to ozone or photochemical oxidants. The tonsillar lymphocytes were studied for interferon production by Newcastle disease virus and blastoid transformation by PHA. Both interferon production by and blastoid transformation of the human tonsillar lymphocytes decreased markedly on exposure to ozone. Tonsillar lymphocytes from rabbits exposed to photochemical oxidants showed a significant decrease in interferon production. The decrease in interferon production in tonsillar lymphocytes from the rabbit exposed to photochemical oxidants was greater in magnitude than the decrease in interferon production in tonsillar lymphocytes exposed to ozone or non-irradiated automobile exhaust gas. The difference in blastoid transformation between the exposed groups and controls was not significnat. The results suggest that exposure to photochemical oxidants causes some functional changes in tonsillar lymphocytes.
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PMID:The effect of ozone and photochemical oxidants on the interferon production by tonsillar lymphocytes. 46 28

A synthetic complex of poly (I)-poly (C) with poly-L-lysine and carboxymethyl cellulose (poly ICLC), as well as UV-inactivated Newcastle disease virus, B-1 strain, was used to induce interferon production in dogs. Several criteria were used for interferon specificity. The interferon response depended on dosage and route of inoculation. Serum interferon concentrations usually reached a peak by 8 hours after inoculation (AI), rapidly declined thereafter, and were nondetectable in most instances at 24 hours AI. Dogs responded less to interferon inducers when reinoculated 2 days after primary induction. The interferon response was biphasic (2 and 8 hours AI) when reinoculated 1 week after primary inoculation. Reinoculation 2 weeks after primary inoculation simulated the first response. Although both inducers caused severe lymphopenia in dogs, the toxic side effects would limit clinical use (in dogs) of poly ICLC, but not of UV-inactivated Newcastle disease virus.
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PMID:Interferon induction in dogs. 47 87

Inoculation of mice with Newcastle disease virus (NDV) alters the course of infection with the Thogoto-like arbovirus Tho-Ar-126. The Tho-Ar-126 content of liver, spleen, and lymph nodes was approximately 10 times greater in mice treated with NDV 24 h before infection; the mortality was somewhat increased, but liver damage (as indicated by serum transaminase levels) did not seem to be potentiated. Lymphocytopenia was observed in NDV-inoculated mice, and in the spleen and lymph nodes the proportion of lymphocytes susceptible to lysis by anti-theta (a marker for thymus-derived lymphocytes) was markedly decreased in these animals. This suggests that NDV potentiates infection by Tho-Ar-126 through its action on thymus-derived lymphocytes.
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PMID:Effects of Newcastle disease virus (NDV) on infection of adult mice with the Thogoto-like Ar-126 arbovirus. 108 12

Acemannan, a complex carbohydrate shown to stimulate interleukin-1, tumor necrosis factor alpha and prostaglandin E2 production by macrophages, has also demonstrated antiviral activity in vitro against human immunodeficiency virus, Newcastle disease virus and influenza virus. A pilot study was undertaken to determine acemannan's effect in 49 feline immunodeficiency virus (FIV) infected cats with clinical signs of disease (Stage 3, 4 or 5), 23 of which had severe lymphopenia. Cats received acemannan either by intravenous (Group 1) or subcutaneous (Group 2) injection once weekly for 12 weeks, or by daily oral (Group 3) administration for 12 weeks. Upon entry into the study, cats were randomly assigned to one of the three groups. Laboratory analyses were performed at the beginning of the study and at Weeks 6 and 12. Cats were allowed to continue with a predetermined maintenance regimen of acemannan after completing the 12-week study. Thirteen cats died during the course of treatment. Upon necropsy, the most frequent histopathologic findings were neoplastic, kidney and pancreatic disease. Friedman's two-way ANOVA test showed no significant differences in efficacy among groups administered acemannan by the different routes. Therefore, groups were combined and a signed-ranks test was used to determine changes over time. A significant increase was seen in lymphocyte counts (P < 0.001). Neutrophil counts decreased significantly (P = 0.007), as did incidence of sepsis (P = 0.008). When cats entering with lymphopenia were analyzed separately, a much greater increase in lymphocyte counts was noted (235%) compared with non-lymphopenic cats (42%). A survival rate of 75% was found for all three groups. Thirty-six of 49 animals are alive 5-19 months post-entry. These results suggest that acemannan therapy may be of significant benefit in FIV-infected cats exhibiting clinical signs of disease.
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PMID:Pilot study of the effect of acemannan in cats infected with feline immunodeficiency virus. 133 96

The effect of vitamin A deficiency and Newcastle disease virus (NDV)-infection on peripheral blood lymphocytes (PBL) was studied by differential cell counting and flow cytometry. Day-old chickens were fed purified diets containing either marginal or adequate levels of vitamin A and at 26 days of age half of the chickens in each group were infected with NDV. The absolute numbers of PBL and their subpopulations were studied until 10 days after infection. Vitamin A deficiency resulted in significantly lower numbers of PBL throughout the experiment. NDV-infection produced lymphopenia during the first 3 days, followed by a strong increase in PBL numbers after 6 days. Both changes in PBL were less pronounced in vitamin A-deficient birds. For flow cytometric analysis monoclonal antibodies reacting specifically with B-cells or a subpopulation of T-cells were used. Vitamin A-induced lymphopenia could be attributed to a decreased number of PBL, negative for both antibodies, and to the absence of an increase in B-cells which normally occurs at this age. The negative cells are suggested to represent, at least partially, cytotoxic T-cells, which may explain the impaired cytotoxic T-cell-activity found in earlier studies. NDV-induced lymphopenia and subsequent increase of PBL could be attributed to all cell types investigated. However, in vitamin A-deficient birds negative cells did not show these reactions. Therefore, it can be concluded that vitamin A deficiency has a detrimental effect on PBL, negative for both antibodies used, and on the normal growth of the number of B-cells at this age.
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PMID:Effects of vitamin A deficiency and Newcastle disease virus infection on lymphocyte subpopulations in chicken blood. 157 Jun 76

The effect of vitamin A deficiency in the presence or absence of Newcastle disease virus infection (NDV, La Sota strain) on weight of lymphoid organs and on the number and type of circulating white blood cells (WBC) was investigated in chickens. Day-old chickens with limited vitamin A reserves were fed purified diets containing either marginal (ad libitum) or adequate (pair-fed) levels of vitamin A and at 21-28 days of age; half the chickens in each group were infected with NDV. Vitamin A deficiency resulted only in significantly lower absolute and relative weights of bursa of Fabricius and after infection both weights of bursa and thymus were significantly lower. Relative weight of spleen was significantly higher after infection irrespective of vitamin A status. Liver weights were not affected by vitamin A status and/or NDV infection. Both vitamin A deficiency and NDV infection resulted in lymphopenia, while the lowest number of WBC were observed in vitamin A-deficient chickens during the acute phase of NDV (5 days after infection). Subsequent to lymphopenia due to NDV infection, a marked lymphocytosis was observed in controls and to a lesser extent in vitamin A-deficient birds. These results indicate that vitamin A deficiency, which is aggravated by concomitant NDV infection, affects lymphoid cell systems.
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PMID:Changes in lymphoid organs and blood lymphocytes induced by vitamin A deficiency and Newcastle disease virus infection in chickens. 177 59

Domperidone, anti-emetic drug, given to healthy female volunteers, induced an elevation of plasma prolactin (PRL) concentration with the peak in 1-4 h. The release of prolactin had a transient stimulating effect on theophylline sensitive T lymphocytes and on concanavalin A induced mitogenic activity, suggesting an enhanced activity of T suppressor lymphocytes. The relative number of CD4+ lymphocytes decreased markedly one hour after domperidone administration and returned to normal values within 2 h (that means 3 h after taking the drug). The number of lymphocytes positive for dipeptidyl peptidase IV exhibited similar transient increase and normalization of activity. No change was observed in the number of CD8+ lymphocytes. The production of interferon by leukocytes treated with Newcastle disease virus was found to be significantly increased 2 h after domperidone administration. The results suggest that prolactin can selectively stimulate some functions of cellular immunity as well as the release of cytokines (IFN). The present study may contribute to the understanding of the role of the immune system in endogenous hyperprolactinemia.
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PMID:Effect of domperidone-induced hyperprolactinemia on selected immune parameters in healthy women. 874

Forty, newly hatched, unsexed broiler chicks were fed diets containing 10 ppm cyclopiazonic acid (CPA) and 1 ppm T-2 toxin (T2) either individually or in combination for 28 days to study the immunopathological effects. Lymphoid organs revealed lymphocytolysis and lymphoid depletion in all toxin fed birds. Thymic and splenic CD+4 and CD+8 lymphocytes decreased significantly (p<0.01) in toxin fed birds when compared to the control. Thymic CD+8 lymphocytes of T2 and CPA-T2 showed significant (p<0.01) decrease from that of CPA and control groups. Splenic CD+4 and CD+8 lymphocytes showed significant (p<0.01) decrease in CPA and CPA-T2 fed groups when compared to the control. The T2 group did not differ significantly from that of control. The stimulation index (SI) of splenocytes to concavalin A revealed significant (p<0.01) decrease in all toxin fed birds. Significant (p<0.01) decrease were observed for the haemagglutination inhibition (HI) titres to Newcastle disease virus vaccine F strain (NDV) of birds fed CPA, T2 and in combination. Significant (p<0.01) interaction was found for lymphocyte subsets, SI and HI titres to NDV. The study indicated the immunosuppressive effect of these toxins either alone or in combination in broiler chicks.
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PMID:Immunopathological effect of the mycotoxins cyclopiazonic acid and T-2 toxin on broiler chicken. 1577 Apr 54

The intravenous injection of the PR8 strain of influenza A virus, the Lee strain of influenza B, and the "B" strain of Newcastle disease virus produces fever in rabbits. This phenomenon has been studied in relation to certain in vitro properties of these viruses. Saline suspensions of virus prepared by centrifugation or elution from chicken erythrocytes produced fever. Fluids from which most of the virus particles had been removed were non-pyrogenic. Exposure to temperatures which destroyed the infectivity of the virus for chick embryos did not prevent fever. However, heating sufficient to destroy the hemagglutinin also rendered virus non-pyrogenic. The injection of erythrocytes onto which virus had been adsorbed produced fever. Heated virus adsorbed onto erythrocytes, which failed to elute, produced no elevation of temperature, although heated virus alone was pyrogenic. Neutralization of virus with specific immune serum prevented fever. Antipyrine was capable of abolishing the febrile response to virus. Certain differences between the febrile response in rabbits to the injection of viruses and that following bacterial pyrogens were noted. The period between injection and beginning of temperature rise is longer with virus than with bacterial pyrogens. Relatively low temperatures inactivate the fever-producing capacity of viruses, whereas bacterial pyrogens withstand prolonged autoclaving, and the neutralization of viral fever by specific immune serum contrasts sharply with the failure of antibody to affect the response to bacterial pyrogens. Certain previous observations on the lymphopenia produced in rabbits by the injection of influenzal viruses were confirmed. The capacity of virus preparations to induce fever in rabbits closely parallels their capacity to induce lymphopenia. It was concluded that the fever-producing property of influenzal viruses is closely associated with the capacity to agglutinate erythrocytes.
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PMID:The production of fever by influenzal viruses; factors influencing the febrile response to single injections of virus. 1814 Jun 65