scholarly journals Phagocytosis and killing of Pseudomonas aeruginosa by mouse polymorphonuclear leukocytes in vitro promoted by antiserum to the slime glycolipoprotein.

1982 ◽  
Vol 37 (1) ◽  
pp. 378-381 ◽  
Author(s):  
O Bishop ◽  
T Orr ◽  
P F Bartell
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Polymorphonuclear Leukocytes

Pseudomonas aeruginosa tolerance to tobramycin, hydrogen peroxide and polymorphonuclear leukocytes is quorum-sensing dependent

Microbiology ◽  
2005 ◽  
Vol 151 (2) ◽  
pp. 373-383 ◽  
Author(s):  
Thomas Bjarnsholt ◽  
Peter Østrup Jensen ◽  
Mette Burmølle ◽  
Morten Hentzer ◽  
Janus A. J. Haagensen ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Polymorphonuclear Leukocytes ◽  
Present Report ◽  
Cell Communication ◽  
A Cell ◽  
Opportunistic Human Pathogen ◽  
Conventional Antibiotics

The opportunistic human pathogen Pseudomonas aeruginosa is the predominant micro-organism of chronic lung infections in cystic fibrosis (CF) patients. P. aeruginosa colonizes the CF lungs by forming biofilm structures in the alveoli. In the biofilm mode of growth the bacteria are highly tolerant to otherwise lethal doses of antibiotics and are protected from bactericidal activity of polymorphonuclear leukocytes (PMNs). P. aeruginosa controls the expression of many of its virulence factors by means of a cell–cell communication system termed quorum sensing (QS). In the present report it is demonstrated that biofilm bacteria in which QS is blocked either by mutation or by administration of QS inhibitory drugs are sensitive to treatment with tobramycin and H2O2, and are readily phagocytosed by PMNs, in contrast to bacteria with functional QS systems. In contrast to the wild-type, QS-deficient biofilms led to an immediate respiratory-burst activation of the PMNs in vitro. In vivo QS-deficient mutants provoked a higher degree of inflammation. It is suggested that quorum signals and QS-inhibitory drugs play direct and opposite roles in this process. Consequently, the faster and highly efficient clearance of QS-deficient bacteria in vivo is probably a two-sided phenomenon: down regulation of virulence and activation of the innate immune system. These data also suggest that a combination of the action of PMNs and QS inhibitors along with conventional antibiotics would eliminate the biofilm-forming bacteria before a chronic infection is established.

scholarly journals Polymorphonuclear Leukocytes Restrict Growth of Pseudomonas aeruginosa in the Lungs of Cystic Fibrosis Patients

2014 ◽  
Vol 82 (11) ◽  
pp. 4477-4486 ◽  
Author(s):  
Kasper N. Kragh ◽  
Morten Alhede ◽  
Peter Ø. Jensen ◽  
Claus Moser ◽  
Thomas Scheike ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Growth Rates ◽  
Polymorphonuclear Leukocytes ◽  
Growth Patterns ◽  
Tissue Samples ◽  
Content Type ◽  
Growth Physiology

ABSTRACTCystic fibrosis (CF) patients have increased susceptibility to chronic lung infections byPseudomonas aeruginosa, but the ecophysiology within the CF lung during infections is poorly understood. The aim of this study was to elucidate thein vivogrowth physiology ofP. aeruginosawithin lungs of chronically infected CF patients. A novel, quantitative peptide nucleic acid (PNA) fluorescencein situhybridization (PNA-FISH)-based method was used to estimate thein vivogrowth rates ofP. aeruginosadirectly in lung tissue samples from CF patients and the growth rates ofP. aeruginosain infected lungs in a mouse model. The growth rate ofP. aeruginosawithin CF lungs did not correlate with the dimensions of bacterial aggregates but showed an inverse correlation to the concentration of polymorphonuclear leukocytes (PMNs) surrounding the bacteria. A growth-limiting effect onP. aeruginosaby PMNs was also observedin vitro, where this limitation was alleviated in the presence of the alternative electron acceptor nitrate. The finding thatP. aeruginosagrowth patterns correlate with the number of surrounding PMNs points to a bacteriostatic effect by PMNs via their strong O2consumption, which slows the growth ofP. aeruginosain infected CF lungs. In support of this, the growth ofP. aeruginosawas significantly higher in the respiratory airways than in the conducting airways of mice. These results indicate a complex host-pathogen interaction in chronicP. aeruginosainfection of the CF lung whereby PMNs slow the growth of the bacteria and render them less susceptible to antibiotic treatment while enabling them to persist by anaerobic respiration.

scholarly journals Phenotypical Comparison of Pseudomonas Aeruginosa Isolated from Human and Veterinary Samples; Impact of Host Adaptation on Infection Pathogenesis

2021 ◽  
Author(s):  
Stefan J. Kaiser ◽  
Annalisa DeRosa ◽  
Christa Ewers ◽  
Frank Günther
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Water Samples ◽  
Biofilm Formation ◽  
Polymorphonuclear Leukocytes ◽  
Environmental Isolates ◽  
Antibiotic Resistant ◽  
Pet Owners ◽  
Zoonotic Risk ◽  
Genetically Determined

Abstract Purpose: Determinants of virulence in Pseudomonas aeruginosa vary strongly depending on its habitat. In this study, we analyzed these alterations depending on the host organism in isolates cultured from canine ears and compared it to clinical extended-spectrum antibiotic-resistant Pseudomonas aeruginosa isolates (XDR), clinical antibiotic-sensitive (non-XDR) from humans and environmental isolates (EI) analyzed during our first study in 2017. Methods: A total of 22 veterinary isolates cultured from canine ears (VET) were examined for spontaneous biofilm formation, stress response in biofilm formation induced by meropenem, in vitro fitness, susceptibility to human serum and polymorphonuclear leukocytes and the genetically determined virulence factors toxA, exoS, exoT, exoU, exoY, nan1, cif, lasA and lasB.Results: We observed significantly elevated spontaneous biofilm formation and serum susceptibility in VET isolates compared to EI and non-XDR isolates as well as significantly decreased in vitro fitness compared to XDR isolates. The VET isolates resembled most the XDR subgroup of isolates previously cultured from blood. Within the environmental isolates, we observed an increase of spontaneous biofilm formation and exoU presence in isolates cultured from community water samples over hospital water samples to pool samples.Conclusions: Considering the distinct differences in some features of the examined VET isolates, a higher degree of phenotypical adaption can be assumed. Increased biofilm formation seems to be a common and characteristic event in isolates adapted to a specific habitat. Therefore amplification of potentially more virulent Pseudomonas aeruginosa strains in domestic animals may lead to elevated zoonotic risk for example for pet owners.

scholarly journals Unmasking and redistribution of lysosomal sulfated glycoconjugates in phagocytic polymorphonuclear leukocytes.

1986 ◽  
Vol 34 (12) ◽  
pp. 1701-1707 ◽  
Author(s):  
R T Parmley ◽  
T Doran ◽  
R L Boyd ◽  
C Gilbert
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acid Phosphatase ◽  
Cell Surface ◽  
Human Neutrophil ◽  
Polymorphonuclear Leukocytes ◽  
Peritoneal Lavage ◽  
Thin Sections ◽  
Latex Beads ◽  
Primary Granules

Rabbit heterophil and human neutrophil primary granules contain sulfated glycosaminoglycans (GAGs) and acid phosphatase, which can be readily stained in immature but not mature lysosomes. To determine whether this loss of staining represents masking of reactive components or removal of these components, we examined rabbit heterophils to see if high-iron diamine (HID)-reactive sulfate and acid phosphatase staining reappears in phagocytic vacuoles. Rabbit heterophils, obtained by peritoneal lavage, were incubated in vitro with latex beads or Pseudomonas aeruginosa for 15-60 min. Pre-embedment HID staining was enhanced in thin sections of unosmicated specimens with thiocarbohydrazide and silver proteinate (TCH-SP). Phagocytosis of latex beads or bacteria was progressively more prominent with time. Primary granules that were degranulated or in the process of degranulating into phagocytic vacuoles demonstrated intense sulfate staining with large (13 +/- 7 nm) HID-TCH-SP stain deposits. Smaller (6 +/- 1 nm) HID-TCH-SP stain deposits were present in tertiary granules, which were less frequently observed degranulating into phagosomes. Acid phosphatase staining was most intense during early phagolysosome formation. HID-TCH-SP staining was also observed in extracellular degranulated lysosomal matrices and on the surface of many peritoneal heterophils. These results indicate that loss of sulfate staining in mature heterophil granules is the result of masking by intragranular substances rather than of removal, and that these components may be unmasked during phagocytosis and/or redistributed to the cell surface after exocytosis.

Revival of Krebs–Ringer balanced salt solution for the investigation of polymorphonuclear leukocytes and Pseudomonas aeruginosa biofilm interaction

2019 ◽  
Vol 77 (5) ◽  
Author(s):  
Thomas Bjarnsholt ◽  
Peter Østrup Jensen ◽  
Maria Alhede
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Salt Solution ◽  
Polymorphonuclear Leukocytes ◽  
Bacterial Infections ◽  
Treatment Strategies ◽  
Term Survival ◽  
Lactate Dehydrogenase Activity ◽  
Bacterial Aggregation ◽  
Novel Treatment Strategies

ABSTRACTTo study the interaction between aggregating bacteria and polymorphonuclear leukocytes (PMNs) in vitro, the chosen medium must favor both the isolated PMNs and the bacteria. To investigate the best-suited medium for the in vitro survival of isolated unactivated human PMNs, we compared three different mammalian cell media: Krebs–Ringer balanced salt solution (BSS), Hanks’ BSS (HBSS) and Roswell Park Memorial Institute (RPMI) 1640. The death of PMNs was estimated by the release of lactate dehydrogenase activity. Furthermore, two types of serum, human (HS) and fetal bovine (FBS), were compared at different concentrations (0%, 2%, 5%, 10%) and at three different time points (2, 4, 20 h). We show that Krebs–Ringer BSS prolonged the survival of PMNs compared to HBSS and RPMI 1640 and that the addition of 10% FBS significantly enhanced the long-term survival (20 h) compared to HS. Furthermore, we observed aggregation of Pseudomonas aeruginosa when grown in the presence of either a mixture of histones, histone H3, arginine or lysine. In this study, we show that the use of Krebs–Ringer BSS is highly relevant for the study of the interaction of bacteria and PMNs in relation to novel treatment strategies of biofilm infections due to the reproduction of bacterial aggregation as seen in chronic bacterial infections.

Defibrotide Inhibits Platelet Activation by Cathepsin G Released From Stimulated Polymorphonuclear Leukocytes

1992 ◽  
Vol 67 (06) ◽  
pp. 660-664 ◽  
Author(s):  
Virgilio Evangelista ◽  
Paola Piccardoni ◽  
Giovanni de Gaetano ◽  
Chiara Cerletti
Keyword(s):  
Platelet Activation ◽  
Polymorphonuclear Leukocytes ◽  
Direct Interaction ◽  
Cathepsin G ◽  
In Vivo Test ◽  
Cell Functions ◽  
Test Models ◽  
Antithrombotic Effects

SummaryDefibrotide is a polydeoxyribonucleotide with antithrombotic effects in experimental animal models. Most of the actions of this drug have been observed in in vivo test models but no effects have been reported in in vitro systems. In this paper we demonstrate that defibrotide interferes with polymorphonuclear leukocyte-induced human platelet activation in vitro. This effect was not related to any direct interaction with polymorphonuclear leukocytes or platelets, but was due to the inhibition of cathepsin G, the main biochemical mediator of this cell-cell cooperation. Since cathepsin G not only induces platelet activation but also affects some endothelial cell functions, the anticathepsin G activity of defibrotide could help to explain the antithrombotic effect of this drug.

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