Legionnaires disease: historical perspective.

Winn, W C

doi:10.1128/cmr.1.1.60-81.1988

Cited by 60 publications

(93 citation statements)

References 122 publications

(155 reference statements)

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“…The infection is transmitted by inhaling aerosols from contaminated water sources. Chest X-rays of patients with Legionnaires' disease commonly show pneumonia (Winn, 1988). An abundant inflammatory exudate can microscopically be observed in the alveoli, respiratory bronchioles and terminal bronchioles of the lung.…”

Section: Introductionmentioning

confidence: 99%

Collagen binding protein Mip enables Legionella pneumophila to transmigrate through a barrier of NCI-H292 lung epithelial cells and extracellular matrix

et al. 2007

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SummaryGuinea pigs are highly susceptible to Legionella pneumophila infection and therefore have been the preferred animal model for studies of legionellosis. In this study guinea pig infections revealed that the Legionella virulence factor Mip (macrophage infectivity potentiator) contributes to the bacterial dissemination within the lung tissue and the spread of Legionella to the spleen. Histopathology of infected animals, binding assays with components of the extracellular matrix (ECM), bacterial transmigration experiments across an artificial lung epithelium barrier, inhibitor studies and ECM degradation assays were used to elucidate the underlying mechanism of the in vivo observation. The Mip protein, which belongs to the enzyme family of FK506-binding proteins (FKBP), was shown to bind to the ECM protein collagen (type I, II, III, IV, V, VI). Transwell assays with L. pneumophila and recombinant Escherichia coli HB101 strains revealed that Mip enables these bacteria to transmigrate across a barrier of NCI-H292 lung epithelial cells and ECM (NCI-H292/ECM barrier). Mipspecific monoclonal antibodies and the immunosuppressants rapamycin and FK506, which inhibit the peptidyl prolyl cis/trans isomerase (PPIase) activity of Mip, were able to inhibit this transmigration. By using protease inhibitors we found that the penetration of the NCI-H292/ECM barrier additionally requires a serine protease activity. Degradation assays with 35 Slabelled ECM proteins supported the finding of a concerted action of Mip and a serine protease. The described synergism between the activity of the collagen binding Mip protein and the serine protease activity represents an entirely new mechanism for bacterial penetration of the lung epithelial barrier and has implications for other prokaryotic and eukaryotic pathogens.

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Section: Introductionmentioning

confidence: 99%

Collagen binding protein Mip enables Legionella pneumophila to transmigrate through a barrier of NCI-H292 lung epithelial cells and extracellular matrix

et al. 2007

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“…According to a retrospective study by the Center for Disease Control (CDC) involving case reports during the year 1992 from four U.S. counties located in California, Oregon, Minnesota, and Connecticut, as many as 14% of deaths occurred in people 1 -49 years old without an underlying medical condition may have been due to infectious causes (Perkins et al, 1996). This observation takes on added significance because in the latter quarter of the last century, a number of new infectious agents and diseases have been identified, including, among others, Legionnaires' disease (Winn, 1988), Lyme's disease (Burgdorfer, 2001), the human immunodeficiency virus (HIV) (Montagnier, 2002), the hepatitis C virus (HCV) (Purcell, 1993), and, more recently, the hantavirus responsible for a new pulmonary syndrome (Hawes and Seabolt, 2003) and the Nipah virus outbreak in South East Asia (Lam and Chua, 2002).…”

Section: Emerging Diseases and Sarsmentioning

confidence: 99%

The Search for a Practical Approach to Emerging Diseases: The Case of Severe Acute Respiratory Syndrome (SARS)

Selmi

Ansari

Invernizzi

et al. 2002

Journal of Immunology Research

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“…Dade and co-workers in 1977 [57], the causative agent of pneumonic illness called Legionnaires' disease, is a Gram-negative monopolar flagellated bacterium, shown to be a facultativc intracellular pathogen [88]. Among other species of the genus Legionella which have been described in the meantime, human pathogens are also found.…”

Section: Legionella Pneumophila First Described By Mc-mentioning

confidence: 99%

“…The natural habitat of Icgionellac is fresh water. They can easily be isolated from domestic water systems, as well as from ponds and rivers [88]. Rowbotham [73] discovered that in the natural environmental habitats legionellae replicate intraccllularly in free-living protozoa, especially in amoebae.…”

Section: Legionella Pneumophila First Described By Mc-mentioning

confidence: 99%

“…useful to address epidemiological questions. Some L. pneumophila isolates harbor plasmids [56] which do not seem to play a role in pathogenicity, since plasmid-free derivatives are fully virulent [88]. Additionally it could be shown that transfer of the conjugative plasmid pCH1 (120 kb in size) to plasmid-less avirulent or virulent strains did not alter the intracellular growth characteristics of these strains in U 937 macrophage-like cells or amoebae [59].…”

Section: Analysis Of the L Pneumophila Genomementioning

confidence: 99%

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Genetic approaches to study Legionella pneumophila pathogenicity

Ott

1994

FEMS Microbiology Reviews

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Legionella pneumophila is an intracellular pathogen replicating in human macrophages during the course of infection of the lungs. Infection by legionellae often leads to severe pneumonia, termed Legionnaires' disease. Genetic approaches to identify the factors responsible for L. pneumophila pathogenicity started with the construction of genomic libraries in Escherichia coli. Various L. pneumophila-specific genes were cloned in E. coli K-12 by identification using functional assays, antibody screening and hybridization ('reverse genetics'). By disrupting the genes via allelic exchange, mutants have been created to assess the influence of the factors on pathogenicity. Among the cloned genes, only for the gene product of the mip gene, encoding a 24-kDa surface-associated protein (macrophage infectivity potentiator) unequivocal evidence for its contribution to pathogenicity could be provided. Two hemolytic factors that have been cloned do not seem to play a role in L. pneumophila pathogenicity. Genetic systems for transposon mutagenesis of the L. pneumophila genome (Tn5, Tn903dIIlacZ, MudphoA), including Tn phoA shuttle mutagenesis, have been established and specifically adapted to identify mutants which displayed an impaired capability to multiply inside macrophages and with a reduced in vivo virulence. Furthermore, by complementation of avirulent mutants, genetic loci could be identified which restored the virulence.

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Legionnaires disease: historical perspective.

Cited by 60 publications

References 122 publications

Collagen binding protein Mip enables Legionella pneumophila to transmigrate through a barrier of NCI-H292 lung epithelial cells and extracellular matrix

Collagen binding protein Mip enables Legionella pneumophila to transmigrate through a barrier of NCI-H292 lung epithelial cells and extracellular matrix

The Search for a Practical Approach to Emerging Diseases: The Case of Severe Acute Respiratory Syndrome (SARS)

Genetic approaches to study Legionella pneumophila pathogenicity

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