Host-parasite interactions between Bordetella pertussis and human polymorphonuclear leukocytes.

Persistent Link:
http://hdl.handle.net/10150/185641
Title:
Host-parasite interactions between Bordetella pertussis and human polymorphonuclear leukocytes.
Author:
Steed, Lisa Lovett.
Issue Date:
1991
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Little is known regarding the interaction of Bordetella pertussis with polymorphonuclear leukocytes (PMNL) or the role PMNL play as an initial line of defense against B. pertussis infection. An in vitro system was developed to establish optimum conditions for the study of phagocytosis and killing of three virulent strains of B. pertussis and a series of derivative mutants using strictly human PMNL and sera. Optimum phagocytosis of B. pertussis occurred by opsonization with human anti-B. pertussis antibody (HAPA), while autologous normal sera (NS) did not induce significant phagocytosis. An antiserum made in rabbits against an avirulent strain was required as an opsonin for significant phagocytosis of several avirulent strains. Over 50% of all B. pertussis strains and mutants tested survived PMNL bactericidal activities while Escherichia coli controls were readily killed. Therefore, if internalized, B. pertussis has an innate ability to survive within human PMNL. No one virulence factor appears to be superior to another in determining survivability. Electron microscopic studies using acid phosphatase as a lysosomal marker demonstrated that virulent B. pertussis strains are capable of surviving intracellularly within PMNL phagosomes and that such survival is due to inhibition of phagosome-lysosome fusion. PMNL respiratory burst activity is unaffected by internalized B. pertussis. This strongly suggests that inhibition of phagosome-lysosome fusion is the key mechanism of B. pertussis intracellular survival within PMNL.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Dissertations, Academic; Immunology; Microbiology.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Microbiology and Immunology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Friedman, Richard L.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleHost-parasite interactions between Bordetella pertussis and human polymorphonuclear leukocytes.en_US
dc.creatorSteed, Lisa Lovett.en_US
dc.contributor.authorSteed, Lisa Lovett.en_US
dc.date.issued1991en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractLittle is known regarding the interaction of Bordetella pertussis with polymorphonuclear leukocytes (PMNL) or the role PMNL play as an initial line of defense against B. pertussis infection. An in vitro system was developed to establish optimum conditions for the study of phagocytosis and killing of three virulent strains of B. pertussis and a series of derivative mutants using strictly human PMNL and sera. Optimum phagocytosis of B. pertussis occurred by opsonization with human anti-B. pertussis antibody (HAPA), while autologous normal sera (NS) did not induce significant phagocytosis. An antiserum made in rabbits against an avirulent strain was required as an opsonin for significant phagocytosis of several avirulent strains. Over 50% of all B. pertussis strains and mutants tested survived PMNL bactericidal activities while Escherichia coli controls were readily killed. Therefore, if internalized, B. pertussis has an innate ability to survive within human PMNL. No one virulence factor appears to be superior to another in determining survivability. Electron microscopic studies using acid phosphatase as a lysosomal marker demonstrated that virulent B. pertussis strains are capable of surviving intracellularly within PMNL phagosomes and that such survival is due to inhibition of phagosome-lysosome fusion. PMNL respiratory burst activity is unaffected by internalized B. pertussis. This strongly suggests that inhibition of phagosome-lysosome fusion is the key mechanism of B. pertussis intracellular survival within PMNL.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectDissertations, Academicen_US
dc.subjectImmunologyen_US
dc.subjectMicrobiology.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineMicrobiology and Immunologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorFriedman, Richard L.en_US
dc.contributor.committeememberRyan, Kenneth J.en_US
dc.contributor.committeememberSonger, J. Glennen_US
dc.contributor.committeememberGalgiani, John N.en_US
dc.contributor.committeememberYocum, Daviden_US
dc.identifier.proquest9208039en_US
dc.identifier.oclc711883597en_US
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