Legionella as a Cause of Severe Pneumonia

Vergis, Emanuel N.; Akbaş, Efsun; Yu, Victor L.

doi:10.1055/s-2000-9934

Cited by 15 publications

(16 citation statements)

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“…(11,12), while most pneumonia patients due to L. Pneumophila need to be treated in the ICU (13,14). The clinical symptoms of atypical pathogen CAP can be misleading, for the patients might have atypical symptoms like muscle pain, weakness, dry cough and so on (15).…”

Section: Clinical Diagnosis Of Capmentioning

confidence: 99%

Atypical pathogen infection in community-acquired pneumonia

Fei

2016

BST

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Section: Clinical Diagnosis Of Capmentioning

confidence: 99%

Atypical pathogen infection in community-acquired pneumonia

Fei

2016

BST

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“…Legionella bacteria are facultative intracellular parasites of amoeba replicating in natural and man-made aquatic environments (1). Infection of humans is observed after inhalation of contaminated water aerosol droplets.…”

mentioning

confidence: 99%

“…T he Gram-negative Legionella pneumophila is the causative agent of Legionnaires' disease, a severe communityacquired pneumonia, and the second most commonly detected pathogen in pneumonia that is admitted to intensive care units in industrialized countries (1,2). Legionella bacteria are facultative intracellular parasites of amoeba replicating in natural and man-made aquatic environments (1).…”

mentioning

confidence: 99%

Histone Acetylation and Flagellin Are Essential for Legionella pneumophila-Induced Cytokine Expression

Schmeck

Lorenz

N′Guessan

et al. 2008

The Journal of Immunology

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Legionella pneumophila causes severe pneumonia. Acetylation of histones is thought to be an important regulator of gene transcription, but its impact on L. pneumophila-induced expression of proinflammatory cytokines is unknown. L. pneumophila strain 130b induced the expression of the important chemoattractant IL-8 and genome-wide histone modifications in human lung epithelial A549 cells. We analyzed the IL-8-promoter and found that histone H4 was acetylated and H3 was phosphorylated at Ser10 and acetylated at Lys14, followed by transcription factor NF-κB. Recruitment of RNA polymerase II to the IL-8 promoter corresponded with increases in gene transcription. Histone modification and IL-8 release were dependent on p38 kinase and NF-κB pathways. Legionella-induced IL-8 expression was decreased by histone acetylase (HAT) inhibitor anacardic acid and enhanced by histone deacetylase (HDAC) inhibitor trichostatin A. After Legionella infection, HATs p300 and CREB-binding protein were time-dependently recruited to the IL-8 promoter, whereas HDAC1 and HDAC5 first decreased and later reappeared at the promoter. Legionella specifically induced expression of HDAC5 but not of other HDACs in lung epithelial cells, but knockdown of HDAC1 or 5 did not alter IL-8 release. Furthermore, Legionella-induced cytokine release, promoter-specific histone modifications, and RNA polymerase II recruitment were reduced in infection with flagellin-deletion mutants. Legionella-induced histone modification as well as HAT-/HDAC-dependent IL-8 release could also be shown in primary lung epithelial cells. In summary, histone acetylation seems to be important for the regulation of proinflammatory gene expression in L. pneumophila infected lung epithelial cells. These pathways may contribute to the host response in Legionnaires’ disease.

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“…3 Increasing in incidence in the United States, Legionnaires' disease is one of the leading causes of community-acquired pneumonia and requires a higher public health priority. [4][5][6][7][8] An earlier study by Brzozowski et al 9 on diagnostic testing practices for infectious diseases supports the findings of Garrison et al 1 Brzozowski and colleagues (R.L.B. is a coauthor) conducted a survey of hospital microbiology laboratories in Georgia to assess diagnostic testing practices in 2006 for selected infectious diseases, including Legionella.…”

Section: Legionella Hospital Laboratory Testing Practices In Georgiamentioning

confidence: 72%