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)

For development of an animal model of virus-induced anergy, the effect of canine distemper virus (CDV) upon cell-mediated immunity in dogs was investigated. First, canine cutaneous reactions and in vitro lymphocyte responses to soluble protein antigens were characterized. Dogs immunized with picryl guinea pig albumin and with keyhole limpet hemocyanin (both in complete Freund's adjuvant) responded reproducibly to intracutaneous challenge with these antigens. Reactivity peaked in 20-40 days (maximal induration, 6-50 mm). Lymphocytes from these animals responded in vitro to stimulation with keyhole limpet hemocyanin or purified protein derivative. This stimulation was antigen-specific and was maximal on day 6 of culture. Infection with CDV depressed cutaneous reactivity and lymphocyte response in vitro to antigens and mitogens. This effect was transient in animals previously vaccinated with attenuated CDV; however, gnotobiotic puppies (susceptible to CDV) had prolonged depression of cell-mediated immunity and lymphopenia. Some of these animals developed neurologic symptoms and died. The findings indicate that CDV infection is a potentially useful model for study of virus-induced depression of T (thymus)-cell responses and support the hypothesis that there is more than one mechanism responsible for this phenomenon.
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PMID:A canine distemper model of virus-induced anergy. 5 99

Infection of the peritoneal cavity with cestode larvae, presumptively diagnosed as tetrathyridia of the genus Mesocestoides, was found by exploratory celiotomy in a dog with clinical signs consisting of episodic anorexia, vomiting, and depression. Lymphopenia and hypoalbuminemia were associated clinicopathologic abnormalities. Dystrophic calcification and midline duodenal displacement were found on abdominal radiographs. Therapy with mebendazole was instituted after recurrence of the initial episodic clinical signs postoperatively. Daily use of mebendazole for intermittent periods of up to 3 months led to remission of gastrointestinal signs for 30 months. However, 17 months after the initial diagnosis, infection of the vaginal tunic of the testicle with similar cestode larvae necessitated castration and removal of the vaginal tunic to the inguinal ring. Mebendazole therapy was reinstituted and continued for 31/2 months postoperatively. The dog was free of clinical signs of infection during and for the 16 months since this period of treatment.
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PMID:Diagnosis and treatment of peritonitis caused by a larval cestode Mesocestoides spp., in a dog. 45 93

Eighteen volunteers in tow study groups were inoculated with influenza A (H3N2) and their peripheral blood T, B and null cells enumerated at subsequent intervals. Infection with wild-type virus or with a live, attenuated virus vaccine markedly reduced the proportion and absolute number of T-cell rosettes 24 hours after inoculation. T-Cell depression preceded the onset of clinical illness in symptomatic subjects, continued during illness, and returned to normal with recovery. T-cell lymphopenia was most pronounced in volunteers infected with wild-type virus and was accompanied by an increase in null cells. Lymphocytes from six wild-virus recipients with T-cell leukopenia were incubated in vitro with a calfthymus extract (thymosin), significantly increasing the percentage of T rosettes in all six subjects (P less than 0.0001). These data indicate that influenza is accompanied by pronounced quantitative and functional changes in T cells.
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PMID:Influenza: response of T-cell lymphopenia to thymosin. 108 84

Tumour necrosis factor (TNF), a polypeptide produced by mononuclear phagocytes, has been implicated as an important mediator of inflammatory processes and of clinical manifestations in acute infectious diseases. To study further the potential role of TNF in infectious diseases, recombinant Escherichia coli (E. coli) derived human (r.HuTNF-alpha) and bovine TNF (r.BoTNF-alpha) were intravenously (i.v.) administered in dwarf goats. Rectal temperature, heart rate, rumen motility, plasma zinc and iron concentrations, and certain other blood biochemical and haematological values were studied and compared with the changes seen after E. coli endotoxin (LPS) was administered (dose: 0.1 microgram/kg i.v.). Following a single injection of 4 micrograms/kg of r.BoTNF-alpha, shivering and biphasic febrile response were observed, accompanied by tachycardia, inhibition of rumen contractions, drop in plasma zinc and iron concentrations, lymphopenia, and neutropenia followed by neutrophilia. The i.v. administration of a single injection of 4 micrograms/kg r.HuTNF-alpha induced shivering and biphasic febrile responses, accompanied by anorexia and a similar drop in plasma trace metal concentrations when compared with r.BoTNF-alpha-treated goats. The TNF-alpha-induced symptoms were essentially the same as those that occurred after LPS administration. However, the time of onset of these changes after the injection of TNF-alpha was significantly shorter than after LPS. Moreover, the r.BoTNF-alpha induced a longer lasting neutrophilic leucopenia, less neutrophilia, and a more persistent lymphopenia than after LPS injection. Neither r.BoTNF-alpha nor LPS caused severe haemo-concentration. Furthermore, no cross-tolerance between r.BoTNF-alpha and LPS could be demonstrated. We conclude that both r.BoTNF-alpha and r.HuTNF-alpha induce many of the physiologic, haematologic and metabolic changes that characterize the acute phase response to LPS. The overlapping biological activities of r.BoTNF-alpha, r.HuTNF-alpha and LPS in dwarf goats may indicate that both recombinant tumour necrosis factors have some homology with caprine TNF-alpha.
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PMID:Fever and acute phase response induced in dwarf goats by endotoxin and bovine and human recombinant tumour necrosis factor alpha. 148 32

Feline leukemia virus and feline immunodeficiency virus (FIV) are lymphotropic retroviruses that cause a wide range of diseases in domestic cats. Although it is known that both viruses are capable of infecting T lymphocytes and that infected cats are lymphopenic, it was not known how infection with either virus might alter specific lymphocyte subpopulations. Using a panel of monoclonal antibodies to feline lymphocyte subpopulations, we examined, by use of flow cytometric analysis, lymphocyte changes in cats naturally infected with FeLV or FIV and explored the early stages in the immunopathogenesis of experimentally induced infection with these viruses. Both groups of naturally infected cats had T-cell lymphopenia. In the FIV-infected cats, the T-cell decrease was principally attributable to loss of CD4+ cells, whereas CD8+ and B-cell numbers remained normal. This led to inversion of the CD4+ to CD8+ ratio in these cats. In contrast, the T-cell lymphopenia in FeLV-infected cats resulted from decrease in CD4+ and CD8+ cells, which led to a CD4+ to CD8+ ratio within normal limits. Experimentally induced infection with these 2 viruses supported these findings. Infection with FIV induced early (10 weeks after infection), chronic inversion of the CD4+ to CD8+ ratio. In contrast, infection with FeLV did not alter CD4+ to CD8+ ratio in the first 20 weeks after infection.
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PMID:Early events in the immunopathogenesis of feline retrovirus infections. 166 73

Infection of macaques by the simian immunodeficiency virus (SIV), like HIV infection in humans, results in a variable time course to clinical disease. Developmental studies of macaques have shown that psychosocial disruption, including social separations, can result in both immediate and long-term immunological consequences. Using colony records on a subset of rhesus macaques (Macaca mulatta) inoculated with SIV at the California Primate Research Center, Davis, California, USA, we constructed regression equations to determine whether the animals' psychosocial histories could explain any of the variability observed in measures of disease progression. After controlling for dosage, age at inoculation, sex, and previous inoculation history, psychosocial variables were found to be significantly associated with several indicators of disease, including latencies to display leukopenia and lymphopenia, weight loss, and survival. We believe these preliminary results suggest an important role for psychosocial processes in affecting disease progression in SIV infection in macaques.
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PMID:Psychosocial factors and disease progression in simian AIDS: a preliminary report. 193 Jul 72

Bacterial infections and certain muramyl peptides elicit a variety of pathophysiological effects including increases in body temperature and slow-wave sleep. Bacterial cell wall peptidoglycan is composed of muramyl peptides. To investigate the ability of isolated bacterial cell walls to enhance slow-wave sleep, rabbits were injected intravenously with cell walls isolated from Staphylococcus aureus or with soluble peptidoglycan prepared from Neisseria gonorrhoeae. These injections increased slow-wave sleep, electroencephalographic delta-wave amplitudes, and body temperature, reduced rapid-eye-movement sleep, and induced neutrophilia and lymphopenia. The somnogenic and pyrogenic effects of S. aureus cell walls developed within 1 h and persisted throughout the recording period. Injections of N. gonorrhoeae peptidoglycan induced similar effects but of larger magnitude and shorter duration. We conclude that peptidoglycan is a bacterial component that mediates the increased sleep observed during infectious disease.
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PMID:Somnogenic, pyrogenic, and hematologic effects of bacterial peptidoglycan. 210 68

Infection of macaque monkeys with simian immunodeficiency virus (SIV) has been established as an excellent animal model system for studying the pathogenesis of an HIV-like virus and for evaluating newly developed antiretroviral drugs and vaccines. Based on their genetic, antigenic, and biologic properties, the simian immunodeficiency viruses are the closest known relatives of the human AIDS viruses, and experimental infection of macaque monkeys results in a disease that is remarkably similar to human AIDS. Infected macaques show diarrhea, weight loss, hematologic abnormalities including lymphopenia and thrombocytopenia, lymphadenopathy/lymphoid hyperplasia that progresses to lymphoid depletion, immunosuppression with marked reduction in CD4+ cells and in the CD4+/CD8+ cell ratio, and opportunistic infections. A majority of such macaques die from an AIDS-like disease within one to three years of infection. An acutely lethal variant of SIV has been identified that results in death in susceptible macaques within 7-12 days of infection. Preliminary prophylactic treatment trials with AZT in macaque monkeys exposed to the acutely lethal SIV variant indicate that some protection is provided when AZT treatment is initiated within 24 hours of virus exposure. Other studies with the more chronic SIV infection model, however, failed to show any prophylactic efficacy of CS-87, AZT, D4T, or FDT.
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PMID:Nonhuman primate models for evaluation of AIDS therapy. 212 64

A 6-year-old Jewish Iranian girl with familial hemophagocytic lymphohistiocytosis (FHLH) is described. The course of the disease fluctuated with partial initial response to antibiotics, steroids, and supportive treatment. Subsequent cytotoxic treatment, including VP-16, Velban (vinblastine sulfate), and methotrexate (MTX) controlled the disease for a few months but the child died with a clinical picture of meningocephalitis 1.5 years later. Benign-looking lymphohistiocytic infiltrates with varying degrees of hemophagocytosis were present in the bone marrow, pleural effusion, cerebrospinal fluid (CSF), liver, and brain. Clinical and laboratory evidence of immunologic dysregulation during the disease could be demonstrated. Frequent and intense viral and bacterial infectious diseases were encountered. The laboratory examination most consistently found was the absence of natural killer (NK) cell activity against K562 target cells. The impaired activity of NK cells persisted during all stages of the disease including remission, although NK cell numbers, determined morphologically and immunophenotypically (by Leu-11, Leu-7), were normal. Natural killer activity could not be restored by interferon. Moreover, the interferon system appeared to be intact. Impaired monokin interleukin 1 (IL-I) production by peripheral blood monocytes was found and could not be restored by indomethacin. Lymphopenia, a mild decrease in T4 numbers, and subsequently, decreased proliferative response to mitogens was noted. Elevated immunoglobulin levels were found during exacerbations and viral episodes, at times accompanied by the presence of auto-antibodies. The exaggerated fatal lymphohistiocytic response typical for FHLH could be attributed to a underlying genetic pathologic dysregulation of the various immunological response pathways.
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PMID:Immunologic dysregulation in a patient with familial hemophagocytic lymphohistiocytosis. 244 62

Infectious disease is typically accompanied by changes in the number and types of circulating leukocytes. To examine the effects of infectious challenge on the distribution of rabbit WBC, rabbits were inoculated IV with Streptococcus pyogenes, Escherichia coli, or Candida albicans. Blood was collected prior to and every 6 to 12 hours after inoculation for 48 hours. Infectious challenge did not substantially alter total WBC counts, but did cause neutrophilia and lymphopenia for 6 to 48 hours after inoculation. Similar patterns of leukocyte distribution were observed in rabbits with naturally developing clinical problems. Thus, high total WBC counts may not be a common characteristic of acute infectious conditions in rabbits, but differential distributions of various leukocyte populations can provide useful markers of disease in this species.
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PMID:Hematologic effects of exposure to three infective agents in rabbits. 252 33


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