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

Female AKR/J mice were challenged with the Washington strain of Legionnaires' disease (LD) bacteria. Nonimmunized mice inoculate intraperitoneally with 2 x 10(8) colony forming units became ill within 4 h and died within 24 h. Progressive histopathologic changes initiated as early as 2 h after inoculation involved the lymphoid organs, the crypts of the small intestine, and the liver. Necrosis with minimal inflammatory cell reaction was the primary lesion. Immunization with a soluble LD bacterial antigen failed to prevent illness but protected against death and development of abnormal histologic changes.
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PMID:Immunologic protection against the Legionnaires' disease bacterium in the AKR/J mouse. 43 55

We have tried to characterize the blastogenic responses of murine spleen lymphoid cells from BALB/c mice immunized with Legionella pneumophila serogroup (SG) 1 (Philadelphia 1 strain) and non-treated mice. Lymphoid cells from immunized mice showed stronger blastogenic responses following stimulation with concanavalin A or formalin-treated L. pneumophila SG1 whole cell antigen than those showed by lymphoid cells from non-treated mice. These cells from immunized mice also responded strongly when stimulated in vitro with other SGs of L. pneumophila, while these responded weakly when stimulated with other species of Legionella. Serum antibody titers of immunized mice against each SG of L. pneumophila were examined and the cross reactions were also recognized. However, the relatedness of serum antibody titers and the blastogenic responses against each serogroup of L. pneumophila was small. The epitopes recognized by the cellular immunity might be different in part from those recognized by serum antibodies, and investigations should be made on what the cellular immunity recognizes and how it works.
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PMID:[Mechanism of acquired resistance against Legionella--blastogenic responses of murine spleen lymphoid cells following the stimulation with Legionella antigens]. 143 59

The reliability of bronchoscopy with transbronchial biopsies for the diagnosis of acute graft rejection has recently been questioned. We present our experience with 59 transbronchial and bronchial biopsies and two open-lung biopsies from 12 patients that underwent lung transplantation. The diagnosis of acute rejection was established in 14 biopsies based on the absence of infection and presence of one or more of the following features: perivascular lymphoid infiltrates, usually associated with endothelial swelling; bronchial "acute on chronic" inflammation; and/or angiitis. Problems and potential pitfalls in the diagnosis of acute graft rejection in lung transplant patients are discussed. The biopsies were also sensitive for the diagnosis of cytomegalovirus pneumonitis and fungal infections but were not helpful for the diagnosis of bacterial pneumonias. Indeed, one patient died with Legionella sp. pneumonia diagnosed only on open-lung biopsy after two negative transbronchial biopsies. The significance of other histologic changes, such as nonspecific interstitial pneumonitis, diffuse alveolar damage, acute alveolitis, goblet cell hyperplasia of the bronchial mucosa, and pulmonary infarction, is discussed.
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PMID:Lung transplantation: the pathologic diagnosis of pulmonary complications. 164 51

The acquired immunodeficiency syndrome (AIDS) is a devastating new disease caused by the human immunodeficiency virus (HIV). This retrovirus causes profound immunoincompetence in its infected hosts, who are thereafter susceptible to develop myriad severe and relapsing protozoal, fungal, bacterial, viral, and arthropodal opportunistic infections, as well as unusual malignancies. The more than 50,000 patients who have developed AIDS in the United States have produced a sudden unexpected deluge of diagnostic dilemmas that are stressing laboratories of pathology everywhere. This paper describes the gross and microscopic pathology of the numerous complications in patients infected by HIV: (a) the prodromal AIDS-related complex with persistent generalized lymphadenopathy, (b) lymphoid infiltration of salivary gland and lung, including the complex of lymphoid interstitial pneumonitis-pulmonary lymphoid hyperplasia, (c) extranodal non-Hodgkin's lymphomas, (d) multifocal mucocutaneous and visceral Kaposi's sarcoma, (e) small cell undifferentiated (oat cell) carcinomas, (f) protozoal infections caused by Pneumocystis carinii, Toxoplasma gondii, Acanthamoeba, Cryptosporidium species (sp.), and Isospora belli, (g) the causes of chronic enteritis, (h) mycotic infections caused by Candida sp., Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, and Sporothrix schenckii, (i) bacterial infections caused by Mycobacterium avium-intracellulare, M. tuberculosis, M. kansasii, Nocardia sp., Listeria monocytogenes, Legionella sp., Treponema pallidum, and others, (j) viral infections caused by cytomegalovirus, herpes simplex and zoster, polyomavirus (progressive multifocal leukoencephalopathy), hepatitis B, molluscum contagiosum, and papillomavirus, (k) oral hairy leukoplakia, (l) subacute encephalopathy, and (m) Norwegian scabies.
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PMID:The pathology of AIDS. 283 78

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.
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PMID:Legionella pneumophila immunity and immunomodulation: nature and mechanisms. 305 72

The lymphocyte blastogenic transformation assay was adapted to study responsiveness of lymphoid cells from animals and humans to Legionella pneumophila antigens in vitro. Spleen cells from guinea pigs after active immunization with Legionella vaccine, but not from normal animals, responded by blast cell transformation when stimulated in vitro with killed Legionella whole-cell vaccine, sonic extracts thereof, or a purified somatic antigen. The response was dose dependent. Similar lymphocyte blastogenesis occurred with spleen cells from mice sensitized to Legionella by sublethal infection with the bacteria. In addition, blastogenesis occurred with peripheral blood leukocytes from human volunteers tested in vitro with whole-cell vaccine, sonic extracts, or purified somatic antigen. Maximum responsiveness generally occurred 4 to 5 days after stimulation of human peripheral blood leukocytes, but a day or two earlier with spleen cells from normal or sensitized mice. Guinea pig spleen cells generally showed peak responses at the same time as human peripheral blood leukocytes after stimulation in vitro. Blastogenic responses with purified antigen were comparable to those with the whole-cell vaccine or sonic extract. Such antigens from Legionella provide a useful material for inducing responses in vitro as a correlate of cellular immunity to these bacteria.
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PMID:Lymphoid cell blastogenesis as an in vitro indicator of cellular immunity to Legionella pneumophila antigens. 647 97

Cell-free sonic extracts prepared from Legionella pneumophila serogroup 1 were found to enhance the uptake of [3H]thymidine by normal mouse spleen cell cultures in vitro and also stimulate an enhanced antibody response to sheep erythrocytes, both in immunized and nonimmunized cultures. Increased background antibody responses to other erythrocyte species also occurred, indicating that the Legionella antigen was a polyclonal B cell activator. A purified cell wall component with physicochemical properties relatively similar to endotoxin, but without toxicity for mice, was found to have mitogenic activity for normal mouse spleen cells and immunostimulatory properties for anti-erythrocyte antibody response. Heating the sonicate or the purified somatic antigen for 10 min diminished immunoenhancing activity but had little effect on mitogenic properties. These results point to the complex effects of Legionella-derived antigens on normal lymphoid cell function and indicate that antigens derived from Legionella have marked immunomodulatory properties.
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PMID:Legionella pneumophila-induced immunostimulation and blastogenesis of normal mouse spleen cells in vitro. 663 14

An agarose microdroplet technique was utilized to assess the cellular immunity of guinea pig lymphoid cells to Legionella pneumophila antigen in vitro. Both direct and indirect migration inhibition procedures were shown to be capable of detecting sensitization of guinea pigs to L. pneumophila antigens. Animals injected with adjuvant alone or unrelated antigens did not yield spleen cells responsive to L. pneumophila, indicating the specificity of the response. Migration inhibition factor induction by Legionella antigen in vitro correlated well with skin test responses in vivo. The positive reaction detected by migration inhibition occurred at times similar to that of skin reactivity but later than that of the earliest serum antibody titers. The assay appears to be useful for monitoring sensitization to Legionella and may be applicable to the study of cell-mediated immunity to this bacterium in infected individuals.
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PMID:Agar microdroplet assay for delayed hypersensitivity to Legionella pneumophila serogroup 1. 686 1

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.
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PMID:Marijuana, receptors and immunomodulation. 766 40

The primary polyphenol in green tea extract is the catechin epigallocatechin gallate (EGCG). Various studies have shown significant suppressive effects of catechin on mammalian cells, either tumor or normal cells, including lymphoid cells. Previous studies from this laboratory reported that EGCG has marked suppressive activity on murine macrophages infected with the intracellular bacterium Legionella pneumophila (Lp), an effect mediated by enhanced production of both tumor necrosis factor-alpha (TNF-alpha) and gamma-interferon (IFN-gamma). In the present study, primary murine bone marrow (BM)-derived dendritic cells (DCs), a phagocytic monocytic cell essential for innate immunity to intracellular microorganisms, such as Lp, were stimulated in vitro with the microbial stimulant lipopolysaccharide (LPS) from gram-negative bacteria, the cell wall component from gram-positive bacteria muramyldipeptide (MDP) or infected with Lp. Production of the T helper cell (Th1)-activating cytokine, interleukin-12 (IL-12) and the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha),produced mainly by phagocytic cells and important for antimicrobial immunity, was determined in cell culture supernatants by enzyme-linked immunosorbent assay (ELISA). Treatment of the cells with EGCG inhibited, in a dose-dependent manner, production of IL-12. In contrast, enhanced production of TNF-alpha occurred in a dose-dependent manner in the DC cultures stimulated with either soluble bacterial product or infected with Lp. Thus, the results of this study show that the EGCG catechin has a marked effect in modulating production of these immunoregulatory cytokines in stimulated DCs, which are important for antimicrobial immunity, especially innate immunity. Further studies are necessary to characterize the physiologic function of the effect of EGCG on TNF-alpha and IL-12 during Lp infection, and the mechanisms involved.
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PMID:Epigallocatechin gallate modulates cytokine production by bone marrow-derived dendritic cells stimulated with lipopolysaccharide or muramyldipeptide, or infected with Legionella pneumophila. 1617 32


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