Legionella Pneumophila Immunity and Immunomodulation: Nature and Mechanisms

Friedman, Herman; Klein, Thomas; Widen, Raymond; Newton, Catherine; Blanchard, Didier; Yamamoto, Y

doi:10.1007/978-1-4757-5421-6_32

Cited by 13 publications

(6 citation statements)

References 11 publications

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“…In other infective models, such as Cryptococcus neoformans , MBL has been shown to increase binding of cryptococcal mannoprotein to human peripheral blood mononuclear cells and enhance production of TNF [32]. There are few data to support complement killing of L. pneumophila [33]. MBL‐mediated opsonophagocytosis via non‐complement receptors may be shown to increase intracellular killing potentially through the efficient delivery of L. pneumophila to lysosomes.…”

Section: Discussionmentioning

confidence: 99%

Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease

Eisen

Stubbs

Spilsbury

et al. 2007

Clinical and Experimental Immunology

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SummaryInnate immune system deficiency may predispose to severe infections such as Legionnaires' disease. We have investigated the role of mannose-binding lectin (MBL) deficiency in the Melbourne Aquarium Legionnaires' disease outbreak. Serum samples from patients and controls that were exposed but shown to be uninfected from the Melbourne Aquarium Legionnaires' disease outbreak were tested for MBL function (C4 deposition) and level (mannanbinding). MBL function was lower in Legionnaires' disease cases than in ageand sex-matched uninfected, exposed controls. The frequency of MBL deficiency with C4 deposition < 0·2 U/ml was significantly higher in Legionnaires' disease cases than in controls. This also applied to Legionnaires' disease cases requiring hospital care. There was no difference in MBL mannan-binding levels between Legionnaires' disease patients and controls. There was no significant interval change in MBL function or level after a mean of 46 days. MBL complement activation functional deficiency appears to predispose to Legionnaires' disease.

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Section: Discussionmentioning

confidence: 99%

Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease

Eisen

Stubbs

Spilsbury

et al. 2007

Clinical and Experimental Immunology

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“…Legionella pneumophila, the causative agent of Legionnaires' disease, is a facultative intracellular pathogen of mononuclear phagocytic cells (MPCs), primarily alveolar macrophages (27,32,35,36,47,51). Susceptibility to replicative L. pneumophila lung infections is determined, in large part, by the permissiveness of host MPCs to growth of the bacteria (2,13,19,32,49,50). In the susceptible host, resistance to L. pneumophila is mediated by the induction of cellular immunity and the production of cytokines, including gamma interferon (IFN-␥) (6,28,29,36,37,43,49).…”

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confidence: 99%

In vivo regulation of replicative Legionella pneumophila lung infection by endogenous tumor necrosis factor alpha and nitric oxide

et al. 1995

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The in vivo role of endogenous tumor necrosis factor alpha (TNF-␣) and reactive nitrogen intermediates (RNIs) in modulation of growth of Legionella pneumophila in the lung was assessed using a murine model of replicative L. pneumophila lung infection. Intratracheal inoculation of mice with L. pneumophila resulted in induction of endogenous TNF-␣, which preceded clearance of L. pneumophila from the lung. Inhibition of endogenous TNF-␣ activity, via in vivo administration of TNF-␣ neutralizing antibody, or inhibition of endogenous RNIs, via administration of the nitric oxide (NO) synthetase inhibitor N-monomethyl-L-arginine (NMMA), resulted in enhanced growth of L. pneumophila in the lung at >3 days postinfection (when compared with untreated L. pneumophila-infected mice). Because of the similar kinetics of enhanced pulmonary growth of L. pneumophila in mice treated in vivo with either anti-TNF-␣ antibody or NMMA, the immunomodulatory effect of NO on endogenous TNF-␣ activity in the lung was assessed. Administration of NMMA to L. pneumophila-infected mice resulted in a significant decrease in endogenous TNF-␣ activity in the lung during replicative L. pneumophila infections in vivo. However, administration of exogenous TNF-␣ to NMMA-treated mice failed to significantly enhance clearance of L. pneumophila from the lung. Results of these studies indicate that both endogenous NO and TNF-␣ facilitate resolution of replicative L. pneumophila lung infections and that regulation of L. pneumophila replication by TNF-␣ is mediated, at least in part, by NO.

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“…12,13 Interestingly, the presence of lymphoblasts in the setting of Legionella infection is frequently observed in the blood of both patients and experimental animals. [14][15][16] Furthermore, a lymphocyte blastogenic response has been shown to occur even earlier than the production of measurable antibodies in 13 patients with acute legionellosis and has been suggested to be potentially useful to diagnosis. 17 The main immunophenotypical BAL findings at presentation included an increase of both activated T-lymphocytes (both HLA-DR þ and CD25 þ cells) and, in 2 out of 3 patients, of g=d T-lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Lymphocyte activation with lymphokines production is thought to be a key factor for the host resistance to Legionella infection and occurs in the blood in the first 2 weeks of infection as part of the cell-mediated immune response orchestrated by the host against the organism. 14,18 The T-lymphocytes bearing the g=d receptor, on the other hand, are important in the host defence against intracellular pathogens, as members of the Legionellaceae family are. 19,20 In 14 patients with Pontiac fever, a mild and transient form of intracellular bacterial disease caused by Legionella micdadei, Kroca and coworkers noticed an initial depletion of circulatory g=d T-cells, followed by a pronounced and long-lasting expansion.…”

Section: Discussionmentioning

confidence: 99%

Bronchoalveolar lavage findings in severe community-acquired pneumonia due to Legionella pneumophila serogroup 1

Trisolini

Agli

Cancellieri³

et al. 2004

Respiratory Medicine

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Legionella Pneumophila Immunity and Immunomodulation: Nature and Mechanisms

Cited by 13 publications

References 11 publications

Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease

Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease

In vivo regulation of replicative Legionella pneumophila lung infection by endogenous tumor necrosis factor alpha and nitric oxide

Bronchoalveolar lavage findings in severe community-acquired pneumonia due to Legionella pneumophila serogroup 1

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