{"id":{"repo_id":"ubc","oai_identifier":"oai:circle.library.ubc.ca:2429/2035"},"canonical_url":"https://search.dev.ndltd.org/etd/ubc/oai:circle.library.ubc.ca:2429/2035","repository":{"repo_id":"ubc","name":"University of British Columbia","base_url":"http://circle.library.ubc.ca/oai/request"},"display":{"title":"Expression of leukocyte-endothelial adhesion molecules during acute inflammation in the lung","abstract":"Neutrophil (PMN)-endothelial cell adhesion is a critical step in the response of PMNsto inflammation. In the systemic circulation, the leukocyte adhesion molecule, L-selectin, facilitates PMN adhesion to inflamed endothelium while CD11/CD18 is required for PMN emigration into extravascular tissues. An inducible endothelial ligand for CD18 is intercellular adhesion molecule-1 (ICAM-1). In the pulmonary circulation, PMNs emigrate by either a CD 18-independent or CD 18-dependent mechanism. The objective of this thesis was to quantitate and compare the surface expression of L-selectin, CD 18, and ICAM-1 during CD18-independent and CD 18-dependent emigration. Rabbits and mice received airway instillates of Streptococcus pneumoniae or Escherichia coil endotoxin to induce CD 18-independent or CD18-dependent emigration, respectively. Ultra thin cryosections of frozen lung were immunogold labeled for L-selectin, CD 18, and ICAM-1. Gold particles on the plasma membranes were quantitated by transmission electron microscopy. In rabbits, CD 18-independent emigration was associated with L-selectin down modulation and CD18 up modulation on intravascular PMNs.A similar alteration of L-selectin and CD18 expression was observed during CD 18-dependent emigration but only after PMNs emigrated into the interstitium. Alterations in L-selectin and CD18 expression were only observed on PMNs within the inflammatory focus. In mice, capillary endothelial ICAM-1 expression was unchanged during CD 18-independent emigration. During CD 18-dependent emigration, ICAM-1 expression increased 4.2-fold and this increase bordered on statistical significance, suggesting that the mechanism of adhesion may be regulated by the expression of endothelial rather than PMN adhesion molecules. ICAM-1 was also constitutively expressed on alveolar Type I but not Type II pneumocytes, the precursors of Type I cells. During pneumonia, Type II but not Type I pneumocytes showed increasedICAM-1 expression, suggesting that ICAM-1 expression represents an early event in differentiation preceding proliferation. In vitro studies of unstimulated human PMNs showed that L-selectin was preferentially expressed on the PMN surface microvilli that mediate initial contact with endothelium. During transendothelial migration, L-selectin down modulation is temporally correlated with PMN-endothelial contact. These studies describe the ultrastructural localization of adhesion molecules in normal and inflamed lungs and increase our understanding of the correlation between expression and function of adhesion molecules.","abstract_html":"Neutrophil (PMN)-endothelial cell adhesion is a critical step in the response of PMNsto inflammation. In the systemic circulation, the leukocyte adhesion molecule, L-selectin, facilitates PMN adhesion to inflamed endothelium while CD11/CD18 is required for PMN emigration into extravascular tissues. An inducible endothelial ligand for CD18 is intercellular adhesion molecule-1 (ICAM-1). In the pulmonary circulation, PMNs emigrate by either a CD 18-independent or CD 18-dependent mechanism. The objective of this thesis was to quantitate and compare the surface expression of L-selectin, CD 18, and ICAM-1 during CD18-independent and CD 18-dependent emigration. Rabbits and mice received airway instillates of Streptococcus pneumoniae or Escherichia coil endotoxin to induce CD 18-independent or CD18-dependent emigration, respectively. Ultra thin cryosections of frozen lung were immunogold labeled for L-selectin, CD 18, and ICAM-1. Gold particles on the plasma membranes were quantitated by transmission electron microscopy. In rabbits, CD 18-independent emigration was associated with L-selectin down modulation and CD18 up modulation on intravascular PMNs.A similar alteration of L-selectin and CD18 expression was observed during CD 18-dependent emigration but only after PMNs emigrated into the interstitium. Alterations in L-selectin and CD18 expression were only observed on PMNs within the inflammatory focus. In mice, capillary endothelial ICAM-1 expression was unchanged during CD 18-independent emigration. During CD 18-dependent emigration, ICAM-1 expression increased 4.2-fold and this increase bordered on statistical significance, suggesting that the mechanism of adhesion may be regulated by the expression of endothelial rather than PMN adhesion molecules. ICAM-1 was also constitutively expressed on alveolar Type I but not Type II pneumocytes, the precursors of Type I cells. During pneumonia, Type II but not Type I pneumocytes showed increasedICAM-1 expression, suggesting that ICAM-1 expression represents an early event in differentiation preceding proliferation. In vitro studies of unstimulated human PMNs showed that L-selectin was preferentially expressed on the PMN surface microvilli that mediate initial contact with endothelium. During transendothelial migration, L-selectin down modulation is temporally correlated with PMN-endothelial contact. These studies describe the ultrastructural localization of adhesion molecules in normal and inflamed lungs and increase our understanding of the correlation between expression and function of adhesion molecules.","abstract_has_math":false,"creators":["Burns, Alan R."],"institution":"University of British Columbia","degree_name":"Doctor of Philosophy - PhD","degree_level":"doctoral","degree_discipline":"Pathology","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1993,"date_issued":"1993","date_published":"1993","updated_at":"2026-07-24T05:07:28Z","subjects":[],"languages":["eng"],"rights":["For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2429/2035","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Burns, Alan R."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["1993"]},{"key":"dc:publisher","label":"Institution","values":["University of British Columbia"]},{"key":"dc:type","label":"Dc Type","values":["Text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Pathology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy - PhD"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of British Columbia"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2429/2035","http://circle.library.ubc.ca/bitstream/2429/2035/1/ubc_1993_spring_phd_burns_alan.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Neutrophil (PMN)-endothelial cell adhesion is a critical step in the response of PMNsto inflammation. In the systemic circulation, the leukocyte adhesion molecule, L-selectin, facilitates PMN adhesion to inflamed endothelium while CD11/CD18 is required for PMN emigration into extravascular tissues. An inducible endothelial ligand for CD18 is intercellular adhesion molecule-1 (ICAM-1). In the pulmonary circulation, PMNs emigrate by either a CD 18-independent or CD 18-dependent mechanism. The objective of this thesis was to quantitate and compare the surface expression of L-selectin, CD 18, and ICAM-1 during CD18-independent and CD 18-dependent emigration. Rabbits and mice received airway instillates of Streptococcus pneumoniae or Escherichia coil endotoxin to induce CD 18-independent or CD18-dependent emigration, respectively. Ultra thin cryosections of frozen lung were immunogold labeled for L-selectin, CD 18, and ICAM-1. Gold particles on the plasma membranes were quantitated by transmission electron microscopy. In rabbits, CD 18-independent emigration was associated with L-selectin down modulation and CD18 up modulation on intravascular PMNs.A similar alteration of L-selectin and CD18 expression was observed during CD 18-dependent emigration but only after PMNs emigrated into the interstitium. Alterations in L-selectin and CD18 expression were only observed on PMNs within the inflammatory focus. In mice, capillary endothelial ICAM-1 expression was unchanged during CD 18-independent emigration. During CD 18-dependent emigration, ICAM-1 expression increased 4.2-fold and this increase bordered on statistical significance, suggesting that the mechanism of adhesion may be regulated by the expression of endothelial rather than PMN adhesion molecules. ICAM-1 was also constitutively expressed on alveolar Type I but not Type II pneumocytes, the precursors of Type I cells. During pneumonia, Type II but not Type I pneumocytes showed increasedICAM-1 expression, suggesting that ICAM-1 expression represents an early event in differentiation preceding proliferation. In vitro studies of unstimulated human PMNs showed that L-selectin was preferentially expressed on the PMN surface microvilli that mediate initial contact with endothelium. During transendothelial migration, L-selectin down modulation is temporally correlated with PMN-endothelial contact. These studies describe the ultrastructural localization of adhesion molecules in normal and inflamed lungs and increase our understanding of the correlation between expression and function of adhesion molecules."]},{"key":"dc:format","label":"Dc Format","values":["16441147","application/pdf"]},{"key":"dc:title","label":"Title","values":["Expression of leukocyte-endothelial adhesion molecules during acute inflammation in the lung"]}]}],"canonical_facts":{"dc:creator":["Burns, Alan R."],"dc:date":["1993"],"dc:description":["Neutrophil (PMN)-endothelial cell adhesion is a critical step in the response of PMNsto inflammation. In the systemic circulation, the leukocyte adhesion molecule, L-selectin, facilitates PMN adhesion to inflamed endothelium while CD11/CD18 is required for PMN emigration into extravascular tissues. An inducible endothelial ligand for CD18 is intercellular adhesion molecule-1 (ICAM-1). In the pulmonary circulation, PMNs emigrate by either a CD 18-independent or CD 18-dependent mechanism. The objective of this thesis was to quantitate and compare the surface expression of L-selectin, CD 18, and ICAM-1 during CD18-independent and CD 18-dependent emigration. Rabbits and mice received airway instillates of Streptococcus pneumoniae or Escherichia coil endotoxin to induce CD 18-independent or CD18-dependent emigration, respectively. Ultra thin cryosections of frozen lung were immunogold labeled for L-selectin, CD 18, and ICAM-1. Gold particles on the plasma membranes were quantitated by transmission electron microscopy. In rabbits, CD 18-independent emigration was associated with L-selectin down modulation and CD18 up modulation on intravascular PMNs.A similar alteration of L-selectin and CD18 expression was observed during CD 18-dependent emigration but only after PMNs emigrated into the interstitium. Alterations in L-selectin and CD18 expression were only observed on PMNs within the inflammatory focus. In mice, capillary endothelial ICAM-1 expression was unchanged during CD 18-independent emigration. During CD 18-dependent emigration, ICAM-1 expression increased 4.2-fold and this increase bordered on statistical significance, suggesting that the mechanism of adhesion may be regulated by the expression of endothelial rather than PMN adhesion molecules. ICAM-1 was also constitutively expressed on alveolar Type I but not Type II pneumocytes, the precursors of Type I cells. During pneumonia, Type II but not Type I pneumocytes showed increasedICAM-1 expression, suggesting that ICAM-1 expression represents an early event in differentiation preceding proliferation. In vitro studies of unstimulated human PMNs showed that L-selectin was preferentially expressed on the PMN surface microvilli that mediate initial contact with endothelium. During transendothelial migration, L-selectin down modulation is temporally correlated with PMN-endothelial contact. These studies describe the ultrastructural localization of adhesion molecules in normal and inflamed lungs and increase our understanding of the correlation between expression and function of adhesion molecules."],"dc:format":["16441147","application/pdf"],"dc:identifier":["http://hdl.handle.net/2429/2035","http://circle.library.ubc.ca/bitstream/2429/2035/1/ubc_1993_spring_phd_burns_alan.pdf"],"dc:language":["eng"],"dc:publisher":["University of British Columbia"],"dc:rights":["For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use."],"dc:title":["Expression of leukocyte-endothelial adhesion molecules during acute inflammation in the lung"],"dc:type":["Text"],"thesis:degree_discipline":["Pathology"],"thesis:degree_level":["doctoral"],"thesis:degree_name":["Doctor of Philosophy - PhD"],"thesis:institution_name":["University of British Columbia"]},"updated_at":"2026-07-24T05:07:28Z"}