Intracellular growth in Acanthamoeba castellanii affects monocyte entry mechanisms and enhances virulence of Legionella pneumophila

Infect Immun. 1999 Sep;67(9):4427-34. doi: 10.1128/IAI.67.9.4427-4434.1999.

Abstract

Since Legionella pneumophila is an intracellular pathogen, entry into and replication within host cells are thought to be critical to its ability to cause disease. L. pneumophila grown in one of its environmental hosts, Acanthamoeba castellanii, is phenotypically different from L. pneumophila grown on standard laboratory medium (BCYE agar). Although amoeba-grown L. pneumophila displays enhanced entry into monocytes compared to BCYE-grown bacteria, the mechanisms of entry used and the effects on virulence have not been examined. To explore whether amoeba-grown L. pneumophila differs from BCYE-grown L. pneumophila in these characteristics, we examined entry into monocytes, replication in activated macrophages, and virulence in mice. Entry of amoeba-grown L. pneumophila into monocytes occurred more frequently by coiling phagocytosis, was less affected by complement opsonization, and was less sensitive to microtubule and microfilament inhibitors than was entry of BCYE-grown bacteria. In addition, amoeba-grown L. pneumophila displays increased replication in monocytes and is more virulent in A/J, C57BL/6 Beige, and C57BL/6 mice. These data demonstrate for the first time that the intra-amoebal growth environment affects the entry mechanisms and virulence of L. pneumophila.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acanthamoeba / microbiology*
  • Animals
  • Cell Line
  • Colchicine / pharmacology
  • Complement System Proteins / immunology
  • Cytochalasin D / pharmacology
  • Humans
  • Intracellular Fluid
  • Legionella pneumophila / growth & development*
  • Legionella pneumophila / immunology
  • Legionella pneumophila / pathogenicity*
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / microbiology*
  • Nocodazole / pharmacology
  • Phagocytosis
  • Virulence

Substances

  • Cytochalasin D
  • Complement System Proteins
  • Nocodazole
  • Colchicine