Icm/dot-independent entry of Legionella pneumophila into amoeba and macrophage hosts

Purnima Bandyopadhyay, Huifang Xiao, Hope A. Coleman, Alexa Price-Whelan, Howard M. Steinman

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Legionella pneumophila, the causative agent of Legionnaires' disease, expresses a type IVB secretion apparatus that translocates bacterial proteins into amoeba and macrophage hosts. When stationary-phase cultures are used to infect hosts, the type IVB apparatus encoded by the icm/dot genes is required for entry, delay of phagosome-lysosome fusion, and intracellular multiplication within host cells. Null mutants with mutations in icm/dot genes are defective in these phenotypes. Here a new model is described in which hosts are infected with stationary-phase cultures that have been incubated overnight in pH 6.5 buffer. This model is called Ers treatment because it enhances the resistance to acid, hydrogen peroxide, and antibiotic stress beyond that of stationary-phase cultures. Following Ers treatment entry into amoeba and macrophage hosts does not require dotA, which is essential for Legionella virulence phenotypes when hosts are infected with stationary-phase cultures, dotB, icmF, icmV, or icmX. Defective host entry is also suppressed for null mutants with mutations in the KatA and KatB catalase-peroxidase enzymes, which are required for proper intracellular growth in amoeba and macrophage hosts. Ers treatment-induced suppression of defective entry is not associated with increased bacterial adhesion to host cells or with morphological changes in the bacterial envelope but is dependent on protein expression during Ers treatment. By using proteomic analysis, Ers treatment was shown to induce a protein predicted to contain eight tetratricopeptide repeats, a motif previously implicated in enhanced entry of L. pneumophila. Characterization of Ers treatment-dependent changes in expression is proposed as an avenue for identifying icm/dot-independent factors that function in the entry of Legionella into amoeba and macrophage hosts.

Original languageEnglish (US)
Pages (from-to)4541-4551
Number of pages11
JournalInfection and Immunity
Volume72
Issue number8
DOIs
StatePublished - Aug 2004

Fingerprint

Legionella pneumophila
Amoeba
Macrophages
Legionella
Bacterial Adhesion
Phenotype
Legionnaires' Disease
Phagosomes
Mutation
Bacterial Proteins
Lysosomes
Proteomics
Catalase
Hydrogen Peroxide
Peroxidase
Genes
Virulence
Buffers
Proteins
Anti-Bacterial Agents

ASJC Scopus subject areas

  • Immunology

Cite this

Icm/dot-independent entry of Legionella pneumophila into amoeba and macrophage hosts. / Bandyopadhyay, Purnima; Xiao, Huifang; Coleman, Hope A.; Price-Whelan, Alexa; Steinman, Howard M.

In: Infection and Immunity, Vol. 72, No. 8, 08.2004, p. 4541-4551.

Research output: Contribution to journalArticle

Bandyopadhyay, Purnima ; Xiao, Huifang ; Coleman, Hope A. ; Price-Whelan, Alexa ; Steinman, Howard M. / Icm/dot-independent entry of Legionella pneumophila into amoeba and macrophage hosts. In: Infection and Immunity. 2004 ; Vol. 72, No. 8. pp. 4541-4551.
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