Some bacterial parameters influencing the neutrophil oxidative burst response to Pseudomonas aeruginosa biofilms

Abstract

Persistence of bacteria in spite of a normal host immune system and relevant antibiotic treatment is a key problem in many chronic infections, such as the bronchopulmonary P. aeruginosa infection in cystic fibrosis patients. The capability of bacteria to establish themselves in microcolonies or biofilms is an important protective mechanism of the microorganisms. We examined the human PMN oxidative burst response to P. aeruginosa in biofilm and in planktonic form. The PMN chemiluminescence response to P. aeruginosa in biofilms was reduced to 30.5–47.5% (p<0.04) and the superoxide response to 85.9% (p<0.02) of the response to equivalent numbers of planktonic bacteria. Mechanical disruption of the biofilms before the assays elicited a significantly increased response in the chemiluminescence experiments and to nonopsonized biofilms in the superoxide anion experiments. We conclude that biofilm bacteria, although able to stimulate the PMN, result in a reduced, suboptimal response leading to lack of efficient eradication of the bacteria in the chronic infection.

Pseudomonas aeruginosa alginate is refractory to Th1 immune response and impedes host immune clearance in a mouse model of acute lung infection

“…This supports in vitro studies that demonstrated that alginate protected bacteria from phagocytosis, opsonization, antibodies, complement and PMN infiltration (Laharrague et al, 1984;Oliver & Weir, 1985;Eftekhar & Speert, 1988;Krieg et al, 1988;Stiver et al, 1988;Jensen et al, 1990;Pedersen et al, 1990;Mathee et al, 1999). Conversion of bacteria to the nontractable, alginate-producing phenotype is partly due to PMN infiltration (Mathee et al, 1999).…”

“…Overproduction of alginate could be an important contributory factor for Alg þ PAOmucA22 persistence and virulence. This study supports previous inferences that alginate is a virulence factor that contributes to bacterial adherence and persistence (Marcus & Baker, 1985;Ramphal & Pier, 1985;Doig et al, 1987), formation of microcolony and biofilm growth (Høiby, 1975;Lam et al, 1980;, inhibition of PMN chemotaxis (Stiver et al, 1988;Pedersen et al, 1990), suppression of lymphocyte and PMN function (Pedersen et al, 1990;Mai et al, 1993), formation of a physical barrier to the immune system and antibiotics (Nichols et al, 1989;Evans et al, 1991;Hoyle & Costerton, 1991;Mathee et al, 1994) and resistance to opsonic killing by PMNs and macrophages (Meshulam et al, 1984;Cabral et al, 1987;Jensen et al, 1990;.…”

Biofilm formation by Pseudomonas fluorescens WCS365: a role for LapD

“…Each individual bacterium first undergoes reversible attachment, which involves contact of the pole of the cell with the surface -this interaction is relatively weak and can be easily disrupted. Eventually the cell attaches by its long axis, so-called irreversible attachment, in which the bacterium is very firmly attached to the surface, resulting in the formation of a monolayer of cells (Fletcher, 1996;Hinsa et al, 2003;Jensen et al, 1992;Lawrence et al, 1987;Marshall, 1979;van Loosdrecht et al, 1990;Zobell, 1943). Subsequent steps result in the formation of microcolonies leading to the development of a 'mature' biofilm (Davey & O'Toole, 2000;Reisner et al, 2005;Webb et al, 2003).…”

Conversion of Pseudomonas aeruginosa to mucoidy in cystic fibrosis: environmental stress and regulation of bacterial virulence by alternative sigma factors

“…This ligand inaccessibility is further compounded by the generation of a functional "opsonin-receptor mismatch" due to the action of inflammatory products such as neutrophil elastase (76). Furthermore, P. aeruginosa biofilms elicit lower oxidative bursts in neutrophils then do the free-floating, plank-tonic bacteria (38). In a chemostat model of aged biofilm, the sessile organism could not be eradicated by the same doses of antibiotics that killed the planktonic form (1), suggestive of the role in antibiotic resistance in vivo.…”