A549 lung epithelial cells grown as three-dimensional aggregates: alternative tissue culture model for Pseudomonas aeruginosa pathogenesis

Infect Immun. 2005 Feb;73(2):1129-40. doi: 10.1128/IAI.73.2.1129-1140.2005.

Abstract

A three-dimensional (3-D) lung aggregate model was developed from A549 human lung epithelial cells by using a rotating-wall vessel bioreactor to study the interactions between Pseudomonas aeruginosa and lung epithelial cells. The suitability of the 3-D aggregates as an infection model was examined by immunohistochemistry, adherence and invasion assays, scanning electron microscopy, and cytokine and mucoglycoprotein production. Immunohistochemical characterization of the 3-D A549 aggregates showed increased expression of epithelial cell-specific markers and decreased expression of cancer-specific markers compared to their monolayer counterparts. Immunohistochemistry of junctional markers on A549 3-D cells revealed that these cells formed tight junctions and polarity, in contrast to the cells grown as monolayers. Additionally, the 3-D aggregates stained positively for the production of mucoglycoprotein while the monolayers showed no indication of staining. Moreover, mucin-specific antibodies to MUC1 and MUC5A bound with greater affinity to 3-D aggregates than to the monolayers. P. aeruginosa attached to and penetrated A549 monolayers significantly more than the same cells grown as 3-D aggregates. Scanning electron microscopy of A549 cells grown as monolayers and 3-D aggregates infected with P. aeruginosa showed that monolayers detached from the surface of the culture plate postinfection, in contrast to the 3-D aggregates, which remained attached to the microcarrier beads. In response to infection, proinflammatory cytokine levels were elevated for the 3-D A549 aggregates compared to monolayer controls. These findings suggest that A549 lung cells grown as 3-D aggregates may represent a more physiologically relevant model to examine the interactions between P. aeruginosa and the lung epithelium during infection.

Publication types

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

MeSH terms

  • Antigens / metabolism
  • Antigens, Neoplasm
  • Biomarkers
  • Bioreactors
  • Cell Culture Techniques / methods
  • Collagen Type IV / metabolism
  • Epithelial Cells / metabolism
  • Epithelial Cells / microbiology*
  • Glycoproteins / metabolism
  • Humans
  • Interleukins / metabolism
  • Laminin / metabolism
  • Lung / metabolism
  • Lung / microbiology*
  • Models, Biological*
  • Mucin 5AC
  • Mucin-1
  • Mucins / metabolism
  • Pseudomonas Infections*
  • Pseudomonas aeruginosa
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Antigens
  • Antigens, Neoplasm
  • Biomarkers
  • Collagen Type IV
  • Glycoproteins
  • Interleukins
  • Laminin
  • MUC1 protein, human
  • MUC5AC protein, human
  • Mucin 5AC
  • Mucin-1
  • Mucins
  • Tumor Necrosis Factor-alpha