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)

We investigated the difference in natural resistance to Legionella pneumophila infection between aged (18-20-month-old) and young (3-month-old) mice of ddY strain. Aged mice were more susceptible to the bacterial infection than young mice; 50% lethal doses of L. pneumophila for aged and young mice were 2.2 x 10(7) and 8.5 x 10(7) colony forming units (CFU), respectively, after intraperitoneal injection of the bacteria. The bacterial burden in the livers was larger in aged than young mice after a challenge with a sublethal dose of L. pneumophila. However, peritoneal macrophages of aged mice paradoxically had a greater capacity to kill intracellular L. pneumophila than those of young mice. Interferon-gamma (IFN-gamma) production from naive spleen cells was compared after an in vitro stimulation with formalin-killed L. pneumophila. Spleen cells of aged mice produced significantly less IFN-gamma than those of young mice. When anti-murine IFN-gamma monoclonal antibody was administered before the bacterial infection, the subsequent bacterial burden in the livers significantly increased in young but not in aged mice. These data suggest that, in aged mice, IFN-gamma production is depressed at an early phase of L. pneumophila infection and it renders aged mice more susceptible to the infection.
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PMID:Decreased capacity of aged mice to produce interferon-gamma in Legionella pneumophila infection. 856 84

Legionella pneumophila, the causative agent of Legionnaires' disease and Pontiac fever, replicates within and eventually kills human macrophages. In this study, we show that L. pneumophila is cytotoxic to HL-60 cells, a macrophage-like cell line. We demonstrate that cell death mediated by L. pneumophila occurred at least in part through apoptosis, as shown by changes in nuclear morphology, an increase in the proportion of fragmented host cell DNA, and the typical ladder pattern of DNA fragmentation indicative of apoptosis. We further sought to determine whether potential virulence factors like the metalloprotease and the macrophage infectivity potentiator of L. pneumophila are involved in the induction of apoptosis. None of these factors are essential for the induction of apoptosis in HL-60 cells but may be involved in other cytotoxic mechanisms that lead to accidental cell death (necrosis). The ability of L. pneumophila to promote cell death may be important for the initiation of infection, bacterial survival, and escape from the host immune response. Alternatively, the triggering of apoptosis in response to bacterial infection may have evolved as a means of the host immune system to reduce or inhibit bacterial replication.
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PMID:Evidence for apoptosis of human macrophage-like HL-60 cells by Legionella pneumophila infection. 894 24

In this retrospective study we aimed to assess the diagnostic yield of bronchoalveolar lavage (BAL) in kidney transplant patients who were suspected of having severe respiratory infection or in whom empirical antibiotic treatment had failed. All BAL procedures performed on kidney transplanted patients suspected of having respiratory infections between January 1, 1988 and July 31, 1996 were analyzed. BAL was carried out in the standard way and samples were sent for cytologic and bacteriologic study. Thirty-three patients with a mean age of 48.5 years were enrolled. All had been receiving immunosuppressive treatment and the mean time following transplantation was 320 days. Thirty-one had received antibiotic treatment before BAL. BAL was positive for 21 of the 33 patients (64%). Twenty-two pathogens were identified: 6 Pneumocystis carinii, 4 Cytomegalovirus, 3 Mycobacterium tuberculosis, 2 Aspergillus fumigatus, 2 Herpes simplex type I, 1 Streptococcus pneumoniae, 1 Staphylococcus aureus, 1 Streptococcus mitis, 1 Legionella pneumophila, 1 Legionella longbeachae. BAL was negative for 12 patients, of whom 8 were tentatively diagnosed of bacterial infection, 3 of acute pulmonary edema and one of pulmonary infarction. Based on the results, therapy was changed for 20 patients (61%), 19 (58%) because an unsuspected pathogen was identified and 1 because treatment could be simplified. The diagnostic yield of BAL is high (64%) in kidney transplant patients suspected of respiratory infection and is useful for managing such cases, as evidenced by the fact that a high proportion (19/33) of our patients were infected by pathogens not covered by empirical treatment.
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PMID:[Usefulness of bronchoalveolar lavage in the renal transplant patient with suspected respiratory infection]. 980 76

Even though cigarette smoking has been shown to suppress immune responses in the lungs, little is known about the effect of cigarette smoke components on respiratory infections. In the present study, the effects of cigarette smoke condensate (CSC) on bacterial replication in alveolar macrophages and the immune responses of macrophages to infection were examined. Furthermore, a possible immunotherapeutic effect of epigallocatechin gallate (EGCg), a major form of tea catechins, on the CSC-induced suppression of antimicrobial activity and immune responses of alveolar macrophages was also determined. The treatment of murine alveolar macrophage cell line (MH-S) cells with CSC significantly enhanced the replication of Legionella pneumophila in macrophages and selectively down-regulated the production of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) induced by bacterial infection. The treatment of macrophages with EGCg not only overcame the CSC-induced suppression of antimicrobial activity but also strengthened the resistance of macrophages to infection. EGCg also markedly up-regulated the CSC-suppressed IL-6 and TNF-alpha production by macrophages in response to infection. The results of exogenous TNF-alpha treatment and neutralization treatment with anti-TNF-alpha and anti-gamma-interferon (IFN-gamma) antibodies and the determination of IFN-gamma mRNA levels indicate that CSC-suppressed macrophages can be activated by EGCg to inhibit L. pneumophila growth by up-regulation of TNF-alpha and IFN-gamma production. Thus, this study revealed that CSC selectively alters the immune responses of macrophages to L. pneumophila infection and leads to an enhancement of bacterial replication in macrophages. In addition, the tea catechin EGCg can diminish such suppressive effects of CSC on alveolar macrophages.
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PMID:Epigallocatechin gallate, a potential immunomodulatory agent of tea components, diminishes cigarette smoke condensate-induced suppression of anti-Legionella pneumophila activity and cytokine responses of alveolar macrophages. 1209 87

The use of human recombinant CuZn superoxide dismutase (rhSOD) in addition to exogenous surfactant has been studied as a therapeutic strategy to prevent acute and chronic lung injury in premature infants with blood monocytes (MO). However, scavenging of superoxide by rhSOD may compromise bacterial killing by phagocytes. In the present study, we investigated the interaction of exogenous surfactant and rhSOD with the antibacterial activity of human blood MO. MO were preincubated in the presence or absence of: (1) modified natural surfactant (Curosurf); 1 mg/ml); (2) rhSOD (2,500 U/ml) and (3) bovine catalase (25,000 U/ml). Bacteria (Legionella pneumophila or Escherichia coli) were then added and incubated for 6 h. Viable bacteria were determined by counting colony-forming units. The ability of the MO to generate superoxide anions (O2-) in response to bacterial infection was also investigated. The antibacterial capacity of MO was not impaired by the presence of rhSOD either alone or combined with Curosurf. In some instances, bactericidal activity was even potentiated by the addition of rhSOD. Exposure of MO to catalase interfered with the increased bacterial killing of MO and rhSOD, suggesting that hydrogen peroxide (H2O2) production was critically important in the process of bacterial killing. Both bacterial species were also found to induce the generation of intra- and extracellular O2- by MO. Data indicate that rhSOD potentiates the killing of bacteria by human MO. The mechanism of action appears to be related to the ability of bacteria to induce the generation of O2-, which in turn is converted to H2O2 in the presence of rhSOD. This has important implications in the development of therapeutic intervention strategies using antioxidant therapy in premature infants with respiratory distress syndrome.
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PMID:Effects of exogenous surfactant and recombinant human copper-zinc superoxide dismutase on oxygen-dependent antimicrobial defenses. 1216 31

Legionella pneumophila is a gram-negative microorganism that causes a severe pneumonia known as "legionnaires disease." Toll-like receptor 4 (TLR4) transduces the lipopolysaccharide signal and is therefore considered to play a role in host defense against gram-negative bacterial infection. To determine the role of TLR4 in L. pneumophila pneumonia, C3H/HeJ mice, which display a nonfunctional gene encoding TLR4 (TLR4), and wild-type (wt) C3H/HeN mice were intranasally inoculated with L. pneumophila serogroup 1. Infection proceeded in an identical way in TLR4 mutant and wt mice, as reflected by similar bacterial outgrowth in the lungs. In addition, the inflammatory responses to L. pneumophila infection-as assessed by histopathologic analysis, cell influx in bronchoalveolar lavage fluid, myeloperoxidase activity in lungs, and lung cytokine concentrations-were indistinguishable in TLR4 mutant and wt mice. These data suggest that, in this mouse model, TLR4 does not play a role in resistance to L. pneumophila.
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PMID:Toll-like receptor 4 is not involved in host defense against pulmonary Legionella pneumophila infection in a mouse model. 1219 88

The current authors present the case of a 68-yr-old female patient who developed severe respiratory failure after medication with ciprofloxacin for acute urinary tract infection. A chronic subdural haematoma was surgical evacuated. Postoperatively, an acute urinary tract infection was treated with ciprofloxacin. Six days later, C-reactive protein was rising and the patient was suffering from intermittent high fever, dyspnoea and severe hypoxaemia. The high-resolution-computed tomography (HRCT) showed an interstitial lung disease in the anterior upper lobe on the left side as well as in the lingula. Assuming a bacterial infection amoxyl/clavulanic acid was started which did not improve the clinical symptoms. Bronchoalveolar lavage revealed a marked lymphocytosis (87%). Analysis for typical bacterial infections, Tuberculosis, Mycoplasma, Chlamydia and Legionella spp. were all negative. Another HRCT scan was made because of worsening of symptoms and this showed rapidly progressive infiltrates in most lobes. An open lingular biopsy showed an interstitial lymphoplasmocytotic infiltrate with some eosinophilic granulocytes and a few scattered giant cell granulomas, consistent with hypersensitivity pneumonitis. The patient's symptoms rapidly improved with systemic corticosteroid therapy and another HRCT scan revealed complete remission of pulmonary infiltrates. Ciprofloxacin can induce interstitial pneumonitis with acute respiratory failure. This is an important fact considering that ciprofloxacin is a widely used antibiotic agent in treatment of urinary tract infection.
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PMID:Ciprofloxacin-induced acute interstitial pneumonitis. 1473 49

Legionnaires' disease is an acute bacterial infection, generally sustained by Legionella pneumophila, which involves primarily the lower respiratory tract, although it is often associated with multi-systemic extrapulmonary manifestations. Afflicted patients may sometimes have gastrointestinal symptoms, liver function abnormalities, renal failure or central nervous system complications, while cutaneous manifestations are very uncommon and may include erythematous, maculopapular or petechial skin lesions. Pathogenesis of skin involvement in the setting of Legionnaires' disease is still uncertain, but may involve toxic or immunological mechanisms. Two exceptional cases of Legionella pneumonia complicated by diffuse, macular rash in two adult women are described, in association with severe peripheral polyneuropathy and flaccid quadriplegia in one case.
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PMID:Legionnaires' disease associated with macular rash: two cases. 1619 57

The gram-negative plant-pathogenic bacterium Xanthomonas campestris pv. vesicatoria is the causative agent of bacterial spot disease in pepper and tomato plants, which leads to economically important yield losses. This pathosystem has become a well-established model for studying bacterial infection strategies. Here, we present the whole-genome sequence of the pepper-pathogenic Xanthomonas campestris pv. vesicatoria strain 85-10, which comprises a 5.17-Mb circular chromosome and four plasmids. The genome has a high G+C content (64.75%) and signatures of extensive genome plasticity. Whole-genome comparisons revealed a gene order similar to both Xanthomonas axonopodis pv. citri and Xanthomonas campestris pv. campestris and a structure completely different from Xanthomonas oryzae pv. oryzae. A total of 548 coding sequences (12.2%) are unique to X. campestris pv. vesicatoria. In addition to a type III secretion system, which is essential for pathogenicity, the genome of strain 85-10 encodes all other types of protein secretion systems described so far in gram-negative bacteria. Remarkably, one of the putative type IV secretion systems encoded on the largest plasmid is similar to the Icm/Dot systems of the human pathogens Legionella pneumophila and Coxiella burnetii. Comparisons with other completely sequenced plant pathogens predicted six novel type III effector proteins and several other virulence factors, including adhesins, cell wall-degrading enzymes, and extracellular polysaccharides.
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PMID:Insights into genome plasticity and pathogenicity of the plant pathogenic bacterium Xanthomonas campestris pv. vesicatoria revealed by the complete genome sequence. 1623 9

An important aspect of Legionnaires' disease is the growth of the causative agent, Legionella pneumophila, within infected host cells. Many proteins including stress proteins of L. pneumophila were strongly induced in a wild type strain that had been used to infect U937 human macrophage-like cells. In contrast, the expression of the proteins was much weaker within a protozoan host, Acanthamoeba polyphaga. The results suggested that active bacterial protein synthesis is required more within macrophages than within protozoa for adaptation of L. pneumophila to intracellular environments. The synthesis of these proteins was not observed in intracellular growth-deficient strains after infection in either type of host cells. The inability of protein synthesis in these strains is correlated with their inability of intracellular growth. Furthermore, on U937 infection, the synthesis of beta-galactosidase encoded in an inducible reporter construct immediately ceased in the in intracellular growth-deficient strains after infection, while the wild type strain was able to synthesize it during the course of infection. These results suggested that the intracellular growth of Legionella pneumophila within macrophages requires active protein synthesis from an earlier stage of bacterial infection.
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PMID:Differences in protein synthesis between wild type and intracellular growth-deficient strains of Legionella pneumophila in U937 and Acanthamoeba polyphaga. 1648 72


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