Adherence of Pseudomonas aeruginosa to respiratory epithelium and the effect of leucocyte elastase

Plotkowski, Maria-Cristina; Beck, G; Tournier, Jean‐Marie; Bernardo-Filho, Mário; Marques, Elizabeth Andrade; Puchelle, Édith

doi:10.1099/00222615-30-4-285

Cited by 43 publications

(21 citation statements)

References 32 publications

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“…Thus, DNA-attached MPO might promote proinflammatory responses by catalyzing the production of hypochlorous acid and downstream-chlorinated amine compounds, as well as by enhancing neutrophil activation status and survival. The high local concentration of MPO on the biofilm and the augmented neutrophil Mac-1 expression, by increasing inflammation, might contribute to bacterial killing as well as to damage to the surrounding tissues, as previously proposed (61).…”

Section: Discussionsupporting

confidence: 60%

Extracellular DNA: A Major Proinflammatory Component of Pseudomonas aeruginosa Biofilms

Bass

Russo

Gabelloni

et al. 2010

The Journal of Immunology

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We previously demonstrated that extracellular bacterial DNA activates neutrophils through a CpG- and TLR9-independent mechanism. Biofilms are microbial communities enclosed in a polymeric matrix that play a critical role in the pathogenesis of many infectious diseases. Because extracellular DNA is a key component of biofilms of different bacterial species, the aim of this study was to determine whether it plays a role in the ability of biofilms to induce human neutrophil activation. We found that degradation of matrix extracellular DNA with DNase I markedly reduced the capacity of Pseudomonas aeruginosa biofilms to induce the release of the neutrophil proinflammatory cytokines IL-8 and IL-1β (>75%); reduced the upregulation of neutrophil activation markers CD18, CD11b, and CD66b (p < 0.001); reduced the number of bacteria phagocytosed per neutrophil contacting the biofilm; and reduced the production of neutrophil extracellular traps. Consistent with these findings, we found that biofilms formed by the lasI rhlI P. aeruginosa mutant strain, exhibiting a very low content of matrix extracellular DNA, displayed a lower capacity to stimulate the release of proinflammatory cytokines by neutrophils, which was not decreased further by DNase I treatment. Together, our findings support that matrix extracellular DNA is a major proinflammatory component of P. aeruginosa biofilms.

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Section: Discussionsupporting

confidence: 60%

Extracellular DNA: A Major Proinflammatory Component of Pseudomonas aeruginosa Biofilms

Bass

Russo

Gabelloni

et al. 2010

The Journal of Immunology

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“…Adherence of a nonmucoid strain of P. aeruginosa to the tracheal collagen layer was also found in rat trachea injured by brushing [43]. PLOTKOWSKI and co-workers [14,44,45] have also reported adherence of nonmucoid P. aeruginosa to type I collagen matrix [14], and to submucosal connective tissue obtained from the frog palate [44,45].…”

Section: Discussionmentioning

confidence: 93%

Interaction of Pseudomonas aeruginosa with human respiratory mucosa in vitro

Tsang

Rutman²,

Tanaka³

et al. 1994

Eur Respir J

100

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I In nt te er ra ac ct ti io on n o of f P Ps se eu ud do om mo on na as s a ae er ru ug gi in no os sa a w wi it th h h hu um ma an n r re es sp pi ir ra at to or ry y m mu uc co os sa a i in n v vi it tr ro o Transmission electron microscopy (TEM) showed that uninfected organ cultures had normal ultrastructure. TEM of infected organ cultures at 8 h showed significant epithelial damage: 43.9±10% of cells extruding from the epithelial surface, 17.7±3% of cells with loss of cilia, 32.9±10.2% of cells with mitochondrial damage, and 11.6±3% of cells with cytoplasmic blebbing. P. aeruginosa only infrequently adhered to normal epithelium, but adhered to areas of epithelial damage and to basement membrane. Scanning electron microscopy (SEM) of organ cultures up to 2 h found P. aeruginosa only infrequently associated with mucus. SEM at 4 h revealed P. aeruginosa predominantly associated with mucus and extruded damaged epithelial cells, but also occasionally associated with cilia, and very occasionally with unciliated cells. SEM also revealed loss of epithelial tight junctions in P. aeruginosa infected organ cultures, and P. aeruginosa were frequently seen in the gaps between epithelial cells. An extracellular matrix, possibly of bacterial origin, was seen bridging the space between bacteria and cell surface.We conclude that P. aeruginosa infection of this organ culture caused tissue damage and that P. aeruginosa preferentially adhered to mucus, damaged epithelium and basement membrane.

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“…In contrast, it has been clearly shown that injured repiratory epithelium is highly susceptible to P. aeruginosa adherence [26,27]. Desquamated cells [29], as well as the denuded extracellular matrix (ECM) [26,30], and in particular components of the ECM, including fibronectin [31] and laminin [32], either belonging to the basement membrane or secreted [30] in the extracellular milieu, represent preferential targets for P. aeruginosa attachment.…”

Section: Pseudomonas Aeruginosa Adherence To Respiratory Epitheliummentioning

confidence: 99%

Pseudomonas aeruginosa adherence to remodelling respiratory epithelium

Bentzmann¹,

Roger²,

Puchelle³

1996

Eur Respir J

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P Ps se eu ud do om mo on na as s a ae er ru ug gi in no os sa a a ad dh he er re en nc ce e t to o r re em mo od de el ll li in ng g r re es sp pi ir ra at to or ry y e ep pi it th he el li iu um m Normal respiratory epithelium is protected against bacteria via mucus and mucociliary clearance. Alteration of mucociliary clearance and of glycosylation of mucins in CF facilitates the access of bacteria to the underlying airway epithelial cells. Intact respiratory epithelium does not bind P. aeruginosa, whereas injured respiratory epithelium is highly susceptible to P. aeruginosa adherence. We found that the high affinity of respiratory epithelium, from CF and non-CF sources, for P. aeruginosa, during the wound repair process is related to the apical expression of asialo ganglioside M1 (aG M1 ). The affinity of repairing respiratory epithelium for P. aeruginosa is time-dependent, and is related to transient apical expression of aG M1 at the surface of repairing respiratory epithelial cells. CF respiratory epithelial cells apically express more aG M1 residues with relation to an increased affinity for P. aeruginosa than non-CF cells.High epithelial damage followed by repair represents a major cause of P. aeruginosa adherence to airway epithelium in cystic fibrosis. However, P. aerurignosa adherence and colonization are not restricted to cystic fibrosis disease and P. aeruginosa pneumonia may also occur in severely immunocompromised patients, suggesting that epithelial injury and decreased host-response favour the colonization of the airways by P. aeruginosa.

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Adherence of Pseudomonas aeruginosa to respiratory epithelium and the effect of leucocyte elastase

Cited by 43 publications

References 32 publications

Extracellular DNA: A Major Proinflammatory Component of Pseudomonas aeruginosa Biofilms

Extracellular DNA: A Major Proinflammatory Component of Pseudomonas aeruginosa Biofilms

Interaction of Pseudomonas aeruginosa with human respiratory mucosa in vitro

Pseudomonas aeruginosa adherence to remodelling respiratory epithelium

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