Pseudomonas aeruginosa Strains with Lipopolysaccharide Defects Exhibit Reduced Intracellular Viability after Invasion of Corneal Epithelial Cells

Pseudomonas aeruginosa Induces Membrane Blebs in Epithelial Cells, Which Are Utilized as a Niche for Intracellular Replication and Motility

“…We have previously shown that P. aeruginosa can invade epithelial cells (24,25) and can replicate inside cells after invasion, requiring a complete LPS core (16). The data presented in this study show that the survival and replication of P. aeruginosa within corneal and other epithelial cells are modulated by the ExsA-regulated T3SS.…”

“…Invasion also involves numerous host cell intracellular signaling proteins, including Src-family tyrosine kinases (15,17,18,34), calcium-calmodulin (17), MEK-ERK (19), Akt (36,37), and the actin cytoskeleton (35,43,44,57). However, little is known of the intracellular fate of P. aeruginosa after internalization or of the bacterial or host cell factors involved in intracellular survival/replication, with the exception that a complete LPS core is required (16,69). Here we tested the hypothesis that intracellular survival and replication of invasive P. aeruginosa in epithelial cells also requires an intact T3SS.…”

Surfactant Protein D Is Present in Human Tear Fluid and the Cornea and Inhibits Epithelial Cell Invasion byPseudomonas aeruginosa

“…SP-D can bind to both LPS rough and smooth strains of P. aeruginosa and enhances their phagocytosis by monocytes (5). Since the LPS core is a ligand for internalization of P. aeruginosa by epithelial cells (41) and is used for survival within those cells after invasion (8), the mechanism by which SP-D inhibits epithelial cell invasion could involve LPS interactions. SP-D has been shown to have opposite effects on P. aeruginosa internalization by macrophages and epithelial cells.…”

“…In this study, we hypothesized that SP-D was present in human tear fluid and contributed to tear fluid protection of corneal epithelial cells against P. aeruginosa invasion. This hypothesis was based upon previously published data showing (i) the presence of SP-D in the human lacrimal gland (37) and in the lacrimal gland and tear film of C57BL/6 mice (1) and (ii) that SP-D can interact with gram-negative bacteria via the core region of the bacterial lipopolysaccharide (LPS) (26); the LPS core is involved in P. aeruginosa invasion of and survival within corneal epithelial cells (8,41).…”

Mesophilic Aeromonas UDP-glucose pyrophosphorylase (GalU) mutants show two types of lipopolysaccharide structures and reduced virulence

“…Besides its function as a substrate for glucosyltransferases resulting in glucosylated surface structures, UDP-glucose plays a well-established biochemical role as a glycosyl donor in the enzymic biosynthesis of carbohydrates (Csonka & Epstein, 1996;Stimson et al, 1995). The galU gene was found to be important for pathogenesis of infections due to a number of Gram-negative pathogens, including Actinobacillus pleuropneumoniae (Rioux et al, 1999), Escherichia coli (Komeda et al, 1977), Klebsiella pneumoniae (Chang et al, 1996), Pseudomonas aeruginosa (Evans et al, 2002;Priebe et al, 2004), Shigella flexneri (Sandlin et al, 1995) and Vibrio cholerae (Nesper et al, 2001). The phenotypes of the K. pneumoniae and V. cholerae galU mutants were dominated by abnormal capsule synthesis rather than LPS O-antigen abnormalities, and several of the galU mutants also had defects in other surface proteins, such as IscA for S. flexneri (Sandlin et al 1995) and flagella for E. coli (Komeda et al, 1977).…”