Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023241 (Legionella)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The action of different preparations of interferon on Legionella strains has been studied in vivo and in vitro. The preparations of leukinferon at a concentration of 500 international units (I.U.) and reaferon at a concentration of 10,000 I.U. have been found to produce an inhibiting effect on Legionella strains in vitro, in a medium with carbon-yeast agar. Leukinferon at a concentration of 125 I.U. suppresses the growth of L. pneumophila also in a liquid medium. The preparation of leukinferon at a minimal concentration of 100 I.U. has been found to suppress the development of lethal infection in chick embryos infected with L. pneumophila strain Philadelphia 1.
 ...
PMID:[The action of interferon preparations on strains of Legionella of various serogroups and species]. 246 68

The present study was undertaken to define the effect of Legionella pneumophila protease on natural killer (NK) cell function in vitro. Lysis of target cells by human NK cells was determined using a 51Cr-release assay. The protease inhibited the NK cell cytolytic activity in a concentration- and time-dependent manner. The inhibitory effect of the protease was not affected by alpha interferon or interleukin 2. Legionella pneumophila protease partly inhibited the binding of effector cells to target cells as studied in a single cell agarose assay of monocyte-depleted cell populations. This effect of the protease on the binding of NK cells to target cells could interfere with the previously described enhanced NK cell activity induced by Legionella pneumophila. We could demonstrate in vitro inhibition of NK cell activity by Legionella pneumophila protease at very low concentrations, suggesting a possible relevance of this mechanism in the pathogenesis of Legionnaires' disease.
 ...
PMID:Inhibition of human natural killer cell activity by Legionella pneumophila protease. 251 1

Protective immunity of guinea pigs against Legionella pneumophila was studied by infecting the animals with a sublethal dose (about 2 x 10(4) CFU) of the organism. The bacteria multiplied in the liver, spleen, and lungs up to day 4 after the intraperitoneal infection. The live bacteria in these organs decreased quickly thereafter and were eliminated by day 7. A delayed-type skin reaction and lymphoproliferation of spleen cells to Formalin-killed L. pneumophila were detected from days 5 and 6, respectively, after infection. Peritoneal macrophages obtained from guinea pigs infected 6 days previously inhibited the intracellular growth of L. pneumophila. Antigen-stimulated spleen cell factor prepared from infected guinea pigs inhibited the intracellular growth of the organism in macrophages obtained from uninfected animals. Antigen-stimulated spleen cell factor prepared from spleen cells treated with anti-guinea pig T-cell monoclonal antibody did not inhibit growth. The activity of antigen-stimulated spleen cell factor was labile to pH 2 treatment, and the factor could not be absorbed by L. pneumophila antigen, suggesting that it contains gamma interferon. Our data show that T-cell-mediated immunity begins to work from an early period of infection with L. pneumophila in guinea pigs.
 ...
PMID:Macrophage-activating T-cell factor(s) produced in an early phase of Legionella pneumophila infection in guinea pigs. 280 31

L. pneumophila is a facultative intracellular opportunistic pathogen ubiquitously present in the environment. Much is now known concerning the ecological niche of this organism as well as many other characteristics of these bacteria, including physiology and biochemistry. However, much less is known about immune mechanisms responsible for host resistance vs susceptibility. Not only outer membrane protein rich fractions but also LPS-rich components are potent immunogens, both in experimental animals such as susceptible guinea pigs and more resistant rodent species like rats and mice. Immunity to these organisms can be readily observed by a variety of serologic techniques. Antibody titers increase rapidly after exposure of individuals to these bacteria either by infection or immunization. However, such antibody does not appear to play an important role in host resistance. Serum antibody plus complement is not lytic for the bacteria in vitro. Furthermore, antibody appears to promote the phagocytosis of the bacteria by monocytes and/or macrophages in culture but such phagocytosis does not result in killing of the bacteria, merely an enhanced uptake and subsequent replication of the organisms. Studies on cellular immunity have focused attention on the role of T lymphocytes, monocytes and macrophages. In addition, cutaneous hypersensitivity is readily induced by infection or immunization of experimental animals with Legionella or antigenic components. In vitro correlates of hypersensitivity is also readily evident after infection or immunization. Although lymphoid cells from guinea pigs only show evidence of responsiveness to Legionella antigens by the lymphocyte blastogenic reaction after animals have been sensitized, peripheral blood monocytes from man as well as splenocytes from mice show evidence of responsiveness to Legionella even before known infection or sensitization. However, higher blastogenic responses become evident after sensitization or infection. In addition, interleukins, such as interleukin 1 and 2, as well as interferon and tumor necrotizing factor, appear in response to Legionella antigens and seem to play a role in resistance mechanisms. Cellular replication of Legionella in monocytes from man as well as macrophages from susceptible animals seems related to susceptibility or resistance to these organisms. Further analyses of the nature and mechanism of humoral vs cellular immune responses to Legionella antigens will provide valuable information about immunity and resistance to these intracellular pathogens in susceptible individuals.
 ...
PMID:Legionella pneumophila immunity and immunomodulation: nature and mechanisms. 305 72

Legionella pneumophila has been shown to induce gamma interferon (IFN-gamma) both in vitro and in vivo during experimental infections of mice. With complement-mediated serologic depletion of murine splenocytes, the cellular sources of IFN-gamma following in vitro stimulation with L. pneumophila antigens were Thy-1.2+, Lyt-2-, L3T4-, and asialo-GM1+, which is consistent with the natural killer (NK) cell phenotype. Additionally, Percoll density discontinuous centrifugation demonstrated that maximal production of IFN coincided with high NK activity in fractions which were enriched for large granular lymphocytes. Furthermore, 18- to 24-h incubation of splenocytes with L. pneumophila whole-cell vaccine resulted in augmented NK cytotoxic activity against YAC-1 tumor target cells in a 51Cr release assay. The addition of macrophages to purified large granular lymphocyte populations augmented both IFN-gamma production and NK activity, suggesting that antigen is required for optimal responses. In an experimental infection model using an intratracheal inoculation route, NK activity was enhanced in the spleen, peripheral blood, and lung cells of infected mice, with maximal stimulation in the lung leukocytes at the site of infection. The results of the present study indicate that NK cells respond in vivo and in vitro to stimulation by L. pneumophila by producing IFN-gamma and by increased cytolytic activity.
 ...
PMID:Role of gamma interferon in induction of natural killer activity by Legionella pneumophila in vitro and in an experimental murine infection model. 312 79

Host defense mechanisms spaced along the respiratory tree and in the alveolar spaces effectively remove or contend with micro-organisms that enter the airways, so serious lung infections occur rarely in healthy people. Special circumstances, such as virgin exposure to a virulent microbe or a large innoculum of a pathogen, can result in illness, but usually routine surveillance host defenses are protective and suffice to keep colonizing airway flora in check. When pneumonia develops or recurrent sinopulmonary infection exists, however, some element of the normal defense apparatus may have failed or is inadequate. This review highlights several components of the apparatus, that is immunoglobulins IgG and IgA and the interaction of alveolar macrophages and lymphocytes, and examines deficiencies in their function that may result in infection. Along the conducting airways, poor mucociliary clearance and/or deficiencies in certain IgG subclass antibodies or destruction of IgA may predispose to sinopulmonary infections; these may be a manifestation of a hereditary disease. In pneumonia the alveolar macrophage is positioned as the central cell which must respond in several directions. This scavenger phagocyte first intercepts the microbe and either can kill or contain it or must call in some other phagocytic cell or inflammatory mediator(s) for assistance. Opsonic antibodies (IgG) and other nonimmune opsonins (complement and surfactant or fibronectin fragments) facilitate phagocytosis, but an absence of antibody may permit infection to develop with encapsulated bacteria (pneumococcus). Insufficient bone marrow reserves of PMNs or a paucity of chemotactic factors to attract them into the alveoli is a situation that may permit gram-negative bacilli and fungal organisms to flourish. Inability of immune T-lymphocytes to energize macrophages, through soluble cellular mediators that provide cell-mediated immunity and activation, makes containment of certain intracellular microbes impossible for these phagocytes (Legionella or mycobacteria). Likewise, concomitant infection of macrophages with viruses (human immunodeficiency virus, and cytomegalovirus or herpes viruses) plus an excessive T-lymphocyte suppressor cell influence may make P. carinii and common bacterial and fungal organisms difficult to contain in the lungs of AIDS patients. Consideration about what the lung host deficiency might be can make therapy more specific through immunization to develop special antibodies, replacement of certain immunoglobulins (IgG subclasses), or selective administration of cell mediators (gamma-interferon or interleukins).
 ...
PMID:Host defense impairments that may lead to respiratory infections. 331 80

Since 1980 a new epidemic form of disseminated mucocutaneous Kaposi's sarcoma (KS) with a progressive clinical course has been observed in populations at risk. Since 1982, 13 cases of AIDS-associated KS have been seen in our department; all of them were in young homosexual males with circulating HIV antibodies and a reduction in the ratio of T-helper to T-suppressor lymphocytes (0.05-1.3). Following systemic treatment with recombinant alpha A-interferon (rIFN-alpha A) over a period of 6 months (18 million IU/day for 3 months; later 18 million IU/3 X weekly) together with other concomitant measures (superficial X-ray radiation, argon laser radiation, surgical excision of isolated lesions) we registered complete remission of the remaining lesions in 2 cases, progression of the disease in 4 cases, and at least temporary stabilization of the disease in 7 cases. In 4 patients opportunistic infections occurred during rIFN treatment: Pneumocystis carinii pneumonia (PCP) with lethal outcome in 2 cases, atypical mycobacteriosis in 2 cases, and Legionella pneumoniae infection in 1 case. Two additional deaths were registered due to PCP appearing during the post-treatment period. Life-threatening virus infections were not observed during rIFN treatment. Out of 9 patients receiving prophylactic trimethoprim/sulfamethoxazole medication, only 1 developed allergic exanthema as a result of this drug combination. Occasionally, rIFN-induced leukopenia was seen and pronounced thrombocytopenia appeared in 1 patient during treatment. Overall, systemic rIFN therapy was well tolerated; its long-term administration in patients with AIDS-associated mucocutaneous KS seems to be well justified according to these preliminary observations.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Disseminated mucocutaneous Kaposi sarcoma in AIDS. Clinical and therapeutic experiences in 13 patients]. 361 Jun 36

Lipopolysaccharide isolated from Legionella pneumophila was found to be a potent antigen and inducer of antibody with strong adjuvant activity for related and unrelated antigens such as sheep erythrocytes by in vivo and in vitro systems. The LPS was also a potent stimulator of blastogenic responses by spleen cells from normal mice as well as from mice immunized with inactivated whole cells of Legionella. It strongly stimulated production of interferon and interleukin 1. These results indicate that the LPS of Legionella may be an important immune regulator in the host response.
 ...
PMID:Immunogenicity and adjuvanticity of lipopolysaccharide from Legionella pneumophila. 380 73

THC, the major psychoactive component of marijuana, has been shown both in humans and experimental animals to have immunomodulatory properties. For example, marijuana smokers may show impaired immunological functions, including deficiency of blood leukocyte blastogenesis to mitogens. Detailed studies with mice have shown that animals given THC can show marked immunomodulation, including suppression of antibody formation, deficient cytokine production, etc. However, recent studies have also shown that lymphoid cells evince enhanced production or release or IL1, but suppression of IL2 and interferon production. Such lymphoid cells treated in vitro with THC also show suppressed blastogenesis to antigens and mitogens, suppressed NK activity, etc. In contrast, it has recently been shown that THC can enhance production or release of pro-inflammatory cytokines. This includes release of these cytokines from macrophages, including augmented release of IL1, TNF alpha, and IL6 activity. Susceptibility of mice to infection with opportunistic organisms such as L. pneumophila has been found and this increased susceptibility can be modulated by THC. A toxic shock-like death to Legionella has been induced by THC treatment given one day before and one day after infection. Receptors to THC have been detected in the brain as well as in peripheral tissues, including lymphoid cells. Thus, immunomodulation induced by THC may be related to receptor effects as well as unrelated to such receptors. It is clear that THC and other cannabinoids are excellent tools for studying the mechanisms of immune modulation, especially altered susceptibility to microbial infection.
 ...
PMID:Marijuana, receptors and immunomodulation. 766 40

The major psychoactive component of marijuana, delta 9-tetrahydrocannabinol (THC), has been shown to suppress the functions of various immune cells. However, the relationship of these findings to THC-induced suppression of host resistance to infection has not been firmly established. In this report, we review the literature concerning THC's effects on cytokine production and resistance to infection with Legionella pneumophila (Lp). Recent reports have linked THC-induced immunomodulation with drug-induced modulation of the cytokine network. Specifically, THC in vivo suppresses interferon (IFN) production while in vitro modulates the production of tumor necrosis factor (TNF), interleukin-1 (IL-1), interleukin-2 (IL-2), and interleukin-2 receptor (IL-2R). These results suggested that THC treatment might alter host immunity by disrupting the cytokine network. Immunity and resistance to infection with Lp depends upon the activation of killer cells and the stimulation of the cytokine network. THC injection into rodents was observed to augment acute phase cytokine mobilization in response to a primary Lp infection; on the other hand, the drug suppressed the development of protective immunity and resistance to secondary Lp infection by causing a change in the profile of T helper cell cytokines produced by Th1 and Th2 cells. Thus, it appears that THC injection suppresses resistance to Lp infection by disrupting the cytokine network. Regarding the molecular mechanisms of these effects of THC, data is reviewed concerning the role of cannabinoid receptors (CR) in cells of the immune system. In summary, the literature to date supports the role of THC as an immunomodulator capable of suppressing resistance to infection through mechanisms involving alteration of the cytokine network. The role of CR receptors in these events has yet to be determined.
 ...
PMID:delta 9-Tetrahydrocannabinol, cytokines, and immunity to Legionella pneumophila. 777 82


<< Previous 1 2 3 4 5 6 7 Next >>