Human Immunity to Pseudomonas aeruginosa. I. In-Vitro Interaction of Bacteria, Polymorphonuclear Leukocytes, and Serum Factors

1972 ◽  
Vol 126 (3) ◽  
pp. 257-276 ◽  
Author(s):  
L. S. Young ◽  
D. Armstrong
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Polymorphonuclear Leukocytes ◽  
Serum Factors ◽  
Human Immunity ◽  
In Vitro Interaction

scholarly journals In vitro interaction of Bacteroides fragilis with polymorphonuclear leukocytes and serum factors.

1975 ◽  
Vol 11 (2) ◽  
pp. 337-342 ◽  
Author(s):  
D A Casciato ◽  
J E Rosenblatt ◽  
L S Goldberg ◽  
R Bluestone
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Bacteroides Fragilis ◽  
Serum Factors ◽  
In Vitro Interaction

scholarly journals TOXIC EFFECTS OF STREPTOCOCCAL M PROTEIN ON PLATELETS AND POLYMORPHONUCLEAR LEUKOCYTES IN HUMAN BLOOD

1971 ◽  
Vol 134 (2) ◽  
pp. 351-365 ◽  
Author(s):  
Edwin H. Beachey ◽  
Gene H. Stollerman
Keyword(s):  
Human Blood ◽  
Polymorphonuclear Leukocytes ◽  
Enzymatic Digestion ◽  
M Protein ◽  
Glass Capillary ◽  
Serum Factors ◽  
Streptococcal M Protein ◽  
Heat Stable ◽  
Extraction And Purification

Purified M protein isolated from Group A streptococci produced cytotoxic reactions in normal human blood in vitro. In the presence of M antigen, platelets aggregated, fused, and lysed. Polymorphonuclear leukocytes (PMN) surrounded the platelet aggregates, then became highly vacuolated and lysed. In addition, PMN progressively lost their capacity to phagocytose unrelated bacteria and to migrate in glass capillary pipettes. Platelet-PMN reactions were directly proportional to the type-specific precipitin reactivity of each M preparation and could be removed with homologous M antibody, only. Moreover, the reactivity of M protein was abolished by enzymatic digestion with trypsin, but not with lysozyme, strongly suggesting that cell-wall mucopeptide was not involved. Preliminary studies showed that platelet-PMN reactions require heat-stable and heat-labile serum factors, presumably antibody and complement. It is suggested that cytotoxic determinants are uncovered by the extraction and purification process and are intimately associated with the type-specific M determinant, possibly in a molecular complex.

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.

Evaluation of the in vitro interaction of fosfomycin and meropenem against metallo-β-lactamase–producing Pseudomonas aeruginosa using Etest and time-kill assay

2020 ◽  
pp. jim-2020-001573
Author(s):  
Sanjida Jahan ◽  
Heather Davis ◽  
Deborah S Ashcraft ◽  
George A Pankey
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Inhibitory Concentration ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Microdilution Method ◽  
Broth Microdilution Method ◽  
Time Kill ◽  
In Vitro Interaction ◽  
Antimicrobial Combinations

Pseudomonas aeruginosa is a nosocomial pathogen containing various resistance mechanisms. Among them, metallo-β-lactamase (MBL)–producing Pseudomonas are difficult to treat. Fosfomycin is an older antibiotic that has recently seen increased usage due to its activity against a broad spectrum of multidrug-resistant organisms. Our aim was to evaluate the combination of fosfomycin and meropenem against 20 MBL-producing P. aeruginosa (100% meropenem-resistant and 20% fosfomycin-resistant) using both an Etest minimal inhibitory concentration (MIC): MIC method and time-kill assay. MICs for fosfomycin and meropenem were determined by Etest and by broth microdilution method for the latter. The combination demonstrated synergy by Etest in 3/20 (15%) isolates and 5/20 (25%) isolates by time-kill assay. Results from the Etest method and time-kill assay were in agreement for 14/20 (70%) of isolates. No antagonism was found. Comparing both methods, Etest MIC: MIC method may be useful to rapidly evaluate other antimicrobial combinations.

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.

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