<i>Pseudomonas aeruginosa</i>flagellar motility activates the phagocyte PI3K/Akt pathway to induce phagocytic engulfment

Lovewell, Rustin R.; Hayes, Sandra M.; O’Toole, George A.; Berwin, Brent

doi:10.1152/ajplung.00319.2013

Cited by 46 publications

(44 citation statements)

References 37 publications

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“…PA strains isolated from CF patients with chronic infections are often non-motile, lacking flagellin and pilin, whilst environmental isolates and isolates obtained during early colonization are motile (Luzar et al, 1985). These non-motile strains are also resistant to phagocytosis by macrophages (Lovewell et al, 2014; Luzar et al, 1985). In contrast, non-CF mucus has been shown in vitro to inhibit adhesion and the subsequent loss of motility (Yeung et al, 2012).…”

Section: Respiratory Tract Mucusmentioning

confidence: 99%

The Interaction between Respiratory Pathogens and Mucus

Zanin

Baviskar

Webster

et al. 2016

Cell Host & Microbe

245

228

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Summary The interaction between respiratory pathogens and their hosts is complex and incompletely understood. This is particularly true when pathogens encounter the mucus layer covering the respiratory tract. The mucus layer provides an essential first host barrier to inhaled pathogens that can prevent pathogen invasion and subsequent infection. Respiratory mucus has numerous functions and interactions, both with the host and with pathogens. This review summarizes the current understanding of respiratory mucus and its interactions with the respiratory pathogens Pseudomonas aeruginosa, respiratory syncytial virus and influenza viruses, with particular focus on influenza virus transmissibility and host-range specificity. Based on current findings we propose that respiratory mucus represents an understudied host-restriction factor for influenza virus.

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Section: Respiratory Tract Mucusmentioning

confidence: 99%

The Interaction between Respiratory Pathogens and Mucus

Zanin

Baviskar

Webster

et al. 2016

Cell Host & Microbe

245

228

View full text Add to dashboard Cite

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“…Bacterial motility is a key phenomenon essential for adhesion and colonization, ultimately 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 advantage [34][35][36][37] . Recently, Hamblett et al 38 using a large set of CF isolates of P. aeruginosa showed that pulmonary exacerbation correlated well with reduced twitching motility of the bacterium.…”

Section: Cf Strains Have Decreased Motility and Adhesion Compared To mentioning

confidence: 99%

Pseudomonas aeruginosa Cell Membrane Protein Expression from Phenotypically Diverse Cystic Fibrosis Isolates Demonstrates Host-Specific Adaptations

et al. 2016

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Pseudomonas aeruginosa is a Gram-negative, nosocomial, highly adaptable opportunistic pathogen especially prevalent in immuno-compromised cystic fibrosis (CF) patients. The bacterial cell surface proteins are important contributors to virulence, yet the membrane subproteomes of phenotypically diverse P. aeruginosa strains are poorly characterized. We carried out mass spectrometry (MS)-based proteome analysis of the membrane proteins of three novel P. aeruginosa strains isolated from the sputum of CF patients and compared protein expression to the widely used laboratory strain, PAO1. Microbes were grown in planktonic growth condition using minimal M9 media, and a defined synthetic lung nutrient mimicking medium (SCFM) limited passaging. Two-dimensional LC-MS/MS using iTRAQ labeling enabled quantitative comparisons among 3171 and 2442 proteins from the minimal M9 medium and in the SCFM, respectively. The CF isolates showed marked differences in membrane protein expression in comparison with PAO1 including up-regulation of drug resistance proteins (MexY, MexB, MexC) and down-regulation of chemotaxis and aerotaxis proteins (PA1561, PctA, PctB) and motility and adhesion proteins (FliK, FlgE, FliD, PilJ). Phenotypic analysis using adhesion, motility, and drug susceptibility assays confirmed the proteomics findings. These results provide evidence of host-specific microevolution of P. aeruginosa in the CF lung and shed light on the adaptation strategies used by CF pathogens.

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“…Previous data demonstrated that the PI3K/Akt pathway, which is an important mammalian intracellular signaling pathway for phagocytosis of many bacteria by host cells, is activated in response to motile bacteria but not by non-motile bacteria [32, 37]. Relative Akt activation was quantitatively measured by FACS analysis following intracellular staining for phosphorylated Akt (phospho-Akt).…”

Section: Resultsmentioning

confidence: 99%

“…The phenotypic assay for swimming motility was performed as previously described in 0.3% LB agar plates [21, 32]. Images were collected at 48-h post inoculation to monitor the formation of bacterial halos to assess the relative swimming motilities of the bacterial strains.…”

Section: Methodsmentioning

confidence: 99%

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The effect of loss of O-antigen ligase on phagocytic susceptibility of motile and non-motile Pseudomonas aeruginosa

Demirdjian

Schutz

Wargo

et al. 2017

Molecular Immunology

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The bacterial pathogen Pseudomonas aeruginosa undergoes adaptation and selection over the course of chronic respiratory tract infections which results in repeatedly-observed phenotypic changes that are proposed to enable its persistence. Two of the clinically significant P. aeruginosa phenotypic changes are loss of flagellar motility and modifications to LPS structure, including loss of O-antigen expression. The effect of loss of O-antigen, frequently described as conversion from smooth to rough LPS, and the combined effect of loss of motility and O-antigen on phagocytic susceptibility by immune cells remain unknown. To address this, we generated genetic deletion mutants of waaL, which encodes the O-antigen ligase responsible for linking O-antigen to lipid A-core oligosaccharide, in both motile and non-motile P. aeruginosa strains. With the use of these bacterial strains we provide the first demonstration that, despite a progressive selection for P. aeruginosa with rough LPS during chronic pulmonary infections, loss of the LPS O-antigen does not confer phagocytic resistance in vitro. However, use of the waaLmotABmotCD mutant revealed that loss of motility confers resistance to phagocytosis regardless of the smooth or rough LPS phenotype. These findings reveal how the O-antigen of P. aeruginosa can influence bacterial clearance during infection and expand our current knowledge about the impact of bacterial phenotypic changes during chronic infection.

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Pseudomonas aeruginosaflagellar motility activates the phagocyte PI3K/Akt pathway to induce phagocytic engulfment

Abstract: Lovewell RR, Hayes SM, O'Toole GA, Berwin B. Pseudomonas aeruginosa flagellar motility activates the phagocyte PI3K/Akt pathway to induce phagocytic engulfment.

Cited by 46 publications

References 37 publications

The Interaction between Respiratory Pathogens and Mucus

The Interaction between Respiratory Pathogens and Mucus

Pseudomonas aeruginosa Cell Membrane Protein Expression from Phenotypically Diverse Cystic Fibrosis Isolates Demonstrates Host-Specific Adaptations

The effect of loss of O-antigen ligase on phagocytic susceptibility of motile and non-motile Pseudomonas aeruginosa

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