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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific immunity developed by mice against protozoan (Toxoplasma gondii and Besnoitia jellisoni) and bacterial (Listeria monocytogenes) infections was compared with nonspecific protection conferred by prior infections. The results indicated that homologous immunity protected mice from more than 10-5 LD50 of T. gondii or B. jellisoni, but from only 10-2 LD50 of L. monocytogenes. Heterospecific protection among these organisms was for 10-0.4 minus 10-1.2 LD50. In studies in hamsters specific immunity to protozoan (T. gondii and B. jellisoni) and viral (equine Herpesvirus type 1 and Oriboca virus) infections was compared with nonspecific protection conferred by prior infections with several heterospecific agents: T. gondii; B. jellison; equine Herpesvirus type 1; Oriboca, Ossa, vesicular stomatitis, yellow fever, and Newcastle disease viruses; L. monocytogenes; and the bacillus Calmette-Guerin strain of Mycobacterium tuberculosis. The results indicated that homologous immunity in hamsters was effective against 10-6 minus 10-7 LD50 of T. gondii, B. jellisoni, equine Herpesvirus type 1, or Oriboca virus. Prior infection with Newcastle disease virus protected (probably by interferon induction) against 10-3 LD50 of equine Herpesvirus type 1. Heterospecific protection among other agents was for less than 10 LD50. This insignificant heterospecific protection in infections in which cellular immunity plays a role suggests that both the induction phase and the expression phase are specific.
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PMID:Specific immunity and nonspecific resistance to infection: listeria, protozoa, and viruses in mice and hamsters,. 16 41

Female C57B1/10 mice injected intravenously (i.v.) with nonviable Mycobacterium tuberculosis Jamaica cells associated with oil-droplet emulsions (WCV) were highly resistant to the i.v. injection of encephalomyocarditis virus (EMCV). Resistance to infection (87% survival) was detected from 1 week to at least 12 weeks after injection of WCV. Mice vaccinated i.v. also were resistant to intraperitoneal, subcutaneous, or intramuscular virus challenge, but were not resistant to intracranial challenge. Mice vaccinated intraperitoneally also were resistant to virus infection, whereas WCV administered intramuscularly or subcutaneously did not protect mice from virus injected by any route. Less than 50% of WCV mice that survived virus challenge possessed serum anti-EMCV-neutralizing antibody (less than 1:10), and none had detectable (less than 1:10) serum interferon. Interferon was not detected in sera of WCV mice from 4 to 144 h after i.v. injection of EMCV. Studies concerning the effects of WCV on EMCV infection suggest that mice may be protected by mechanisms that inhibit early viral replication and spread of virus to the central nervous system.
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PMID:Enhanced resistance against encephalomyocarditis virus infection in mice, induced by a nonviable Mycobacterium tuberculosis oil-droplet vaccine. 20 33

Mice infected with Mycobacterium tuberculosis BCG were more resistant than normal mice to ectromelia virus infection. It is suggested that enhanced interferon production in peritoneal exudate cells and spleen cells of BCG-infected mice plays an important role in this resistance.
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PMID:Effect of Mycobacterium tuberculosis BCG infection on the resistance of mice to ectromelia virus infection: participation of interferon in enhanced resistance. 20 73

Contrary to the results of an earlier study in which polyinosinic-polycytidylic acid [poly(I:C)] administered intraperitoneally to mice had no effect on multiplication of Mycobacterium leprae in the mouse footpad, the local administration of poly(I:C) every 12 h for 15 doses during logarithmic multiplication was found both to inhibit bacterial multiplication and to produce high tissue levels of interferon (IF). Local administration of poly(I) alone inhibited multiplication of M. leprae to almost as great a degree without at the same time producing a measurable IF titer in the footpad tissues. Mouse IF and "mock" IF both inhibited bacterial multiplication to the same degree, but administration of only the former resulted in a measurable IF titer. Polyadenylic-polyuridylic acid administered locally neither inhibited multiplication nor induced IF; fetal calf serum, administered in the same concentration as found in the preparations of IF and mock IF, was modestly inhibitory, without inducing IF. Thus, the local administration of poly(I:C) appears to have inhibited multiplication of M. leprae independently of IF induction.
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PMID:Inhibition of multiplication of Mycobacterium leprae by polyinosinic-polycytidylic acid. 31 45

Mice with delayed hypersensitivity induced by infection with Mycobacterium bovis strain BCG were desensitized by a single large dose of specific antigen (old tuberculin, OT) or a nonspecific interferon stimulus (bacterial lipopolysaccharide, LPS). Subsequent challenge of the desensitized animals revealed only a homologous hyporeactivity, that is, mice desensitized with OT showed decreased type II and migration inhibitory factor (MIF) responses to the specific antigen, which were unaffected by desensitization with LPS. Conversely, mice desensitized with LPS showed a decreased type I interferon and MIF response to LPS, which was unaffected by desensitization with OT. These results suggest that type I interferon and its accompanying low-titered MIF activity are produced by cell populations different from those that produce type II interferon and its accompanying high-titered MIF activity.
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PMID:Type I and II interferons and migration inhibitory factor: production in Mycobacterium bovis BCG-infected mice desensitized with old tuberculin or lipopolysaccharide. 34 89

Antigen-specific type II interferon was produced in vitro by harvesting supernatants of spleen cell cultures from Swiss-Webster mice sensitized with Mycobacterium bovis strain BCG and challenged with old tuberculin. Treatment of C3H mouse spleen cell cultures with appropriate anti-Ia, anti-IgG, anti-Thy-1 or anti-Ly-2,3 sera resulted in a significant decrease in production of type II interferon. Removal of nylon wool adherent cells or cells with histamine receptors by column chromatography similarly caused reduced production of type II interferon. Recombination of spleen cell cultures treated with anti-Ia and anti-Thy-1 sera or of cells treated with anti-IgG and anti-Thy-1 resulted in restored production of type II interferon. Interferon production was also restored by combination of cells passed through histamine columns with anti-Ia treated cells, or those passed through nylon wool columns with anti-Thy-1 treated cells. Anti-Ly-1 serum treatment had no effect on interferon production. Removal of plastic-adherent cells or cells that had phagocytosed carbonyl iron also decreased interferon production, suggesting that macrophages were also involved in type II interferon production. Recombination of non-adherent spleen cells with anti-Ia and anti-Thy-1 sera treated spleen cells, however, did not restore interferon production, suggesting that other cells in addition to macrophages are depleted by the adherence procedure. These findings indicate that type II interferon is produced by suppressor or cytotoxic (Ly-2,3+) T lymphocytes in co-operation with one or two additional cell types: (i) B lymphocytes, and (ii) macrophages.
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PMID:In vitro production and cellular origin of murine type II interferon. 37 63

Migration inhibitory factor (MIF) and type II interferon were released into the circulation after mice had been sensitized i.v. with a bacillus of Calmette and Guerin (BCG) cell-wall-in-oil vaccine and then challenged four weeks later with 50 mg old tuberculin. At least two components of BCG, protein (PPD) and lipid (P-3), have been identified which are essential for the type of sensitization in which mediators are released after appropriate challenge. The route of sensitization had a marked effect on the development of delayed footpad reactions, release of lymphokines, and resistance to infection with virulent tubercle bacilli. Sensitization by the subcutaneous route tended to induce more pronounced delayed footpad reactions, whereas the i.v. route of sensitization was associated with maximum release of mediators. A close correlation existed between the conditions of sensitization that resulted in maximum production of lymphokines (MIF and Type II interferon) and those that caused protection against aerosol challenge with a virulent strain of Mycobacterium tuberculosis.
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PMID:Migration inhibitory factor and type II interferon in the circulation of mice sensitized with mycobacterial components. 109 Jun 52

Delayed-type hypersensitivity (DTH) is the standard measure of T-cell responsiveness to infectious organisms. For leprosy, the Mitsuda reaction, a local immune response to cutaneous challenge with Mycobacterium leprae, is considered to represent a measure of DTH against the pathogen. We analyzed the diversity of the T-cell receptor beta-chain repertoire in Mitsuda reactions to determine the breadth of the mycobacterial antigens involved. The polymerase chain reaction was used to compare V beta usage in the Mitsuda reaction T-cell lines established and unstimulated peripheral blood. These molecular analyses revealed a skewed T-cell receptor V beta gene usage in the Mitsuda reaction and in T-cell lines from lesions. To examine the reactivity of T cells from these lesions, T-cell lines were tested against the available native and recombinant antigens of M. leprae. T-cell lines derived from Mitsuda reactions responded more strongly to the 10-kDa M. leprae antigen, a homolog of GroES in Escherichia coli, than to other M. leprae proteins. T-cell lines were also shown to proliferate strongly in response to the 17- and 3-kDa proteins. The pattern of the lymphokine mRNA of these cells was reminiscent of the pattern of murine TH1 cells, positive for interleukin-2 and gamma interferon and weakly positive for interleukin-4. These data indicate that a limited array of T cells, perhaps recognizing stress proteins, secrete a type 1 lymphokine profile in the DTH response to mycobacteria.
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PMID:Limited T-cell receptor beta-chain diversity of a T-helper cell type 1-like response to Mycobacterium leprae. 132 60

Mycobacterium tuberculosis- or group A streptococcus-activated gamma/delta T cells from normal healthy individuals were negatively sorted and restimulated in vitro from 48 h. Significant amounts of gamma interferon were detected after restimulation with M. tuberculosis, group A streptococci, or Listeria monocytogenes. In contrast, interleukin 4 was undetectable in the culture supernatants. Our findings provide indirect evidence for the involvement of gamma/delta T cells in immunity against tubercle bacilli and probably other bacteria.
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PMID:Gamma interferon and interleukin 2, but not interleukin 4, are detectable in gamma/delta T-cell cultures after activation with bacteria. 153 13

Both recombinant interferon alpha and deoxycoformycin (dCF) are effective in the treatment of hairy cell leukaemia. In an attempt to reduce the complications from dCF therapy, a pilot study of the Eastern Cooperative Oncology Group (ECOG) first treated patients with interferon to improve peripheral blood cell counts before dCF treatment began. Thirty-four patients were treated for 3 months with recombinant interferon alpha-2a (rIFN alpha-2a), 3 x 10(6) IU subcutaneously three times a week for 3 months, and then by dCF, 4 mg/m2 intravenously every 2 weeks for a maximum of 12 months. The overall response rate was 94% (32/34); 76% of patients (26/34) had complete response (CR) (90% confidence interval, 62-88%) and 18% (6/34) partial response. One patient was found to have a Mycobacterium avium infection while receiving rIFN alpha-2a. Without specific antimycobacterial therapy and with continued administration of rIFN alpha-2a and dCF, the infection resolved and he achieved CR. Three patients had culture-negative febrile episodes during the dCF phase of treatment. Non-disseminated herpes zoster developed in four patients, but three of the episodes occurred only after treatment was discontinued. Sequential administration of rIFN alpha-2a and dCF resulted in fewer infections (P = 0.027) than in ECOG's previous study of dCF used alone. Two patients died, one of combined hairy cell leukaemia and non-Hodgkin's lymphoma of intermediate histologic type 17 months after entry into the study and the other of cardiac arrest 20 months after entry. Thirty-two patients were alive with a median follow-up of 21 months (range 13-31 months). This combination produces durable CRs with a low incidence of infection.
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PMID:Sequential administration of recombinant interferon alpha and deoxycoformycin in the treatment of hairy cell leukaemia. 158 Dec 31


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