Importance of lymph vessels in the transcapillary fluid balance in the gingiva studied in a transgenic mouse model.
Identifieur interne : 005844 ( Main/Exploration ); précédent : 005843; suivant : 005845Importance of lymph vessels in the transcapillary fluid balance in the gingiva studied in a transgenic mouse model.
Auteurs : Lilian Ephrem Mkonyi [Norvège] ; Athanasia Bletsa ; Inge Fristad ; Helge Wiig ; Ellen BerggreenSource :
- American journal of physiology. Heart and circulatory physiology [ 1522-1539 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Collagène (métabolisme), Facteurs temps, Femelle, Fragments Fc des immunoglobulines (génétique), Gencive (), Gingivite (immunologie), Gingivite (métabolisme), Immunoglobuline G (génétique), Lipopolysaccharides (immunologie), Liquide extracellulaire (métabolisme), Lymphoedème (génétique), Lymphoedème (immunologie), Lymphoedème (métabolisme), Modèles animaux de maladie humaine, Muqueuse de la bouche (), Mâle, Perméabilité capillaire, Porphyromonas gingivalis (immunologie), Pression, Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Régions promotrices (génétique), Souris, Souris de lignée C57BL, Souris transgéniques, Vaisseaux capillaires (immunologie), Vaisseaux capillaires (métabolisme), Vaisseaux lymphatiques (immunologie), Vaisseaux lymphatiques (métabolisme).
- MESH :
- génétique : Fragments Fc des immunoglobulines, Immunoglobuline G, Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire.
- immunologie : Gingivite, Lipopolysaccharides, Lymphoedème, Porphyromonas gingivalis, Vaisseaux capillaires, Vaisseaux lymphatiques.
- métabolisme : Collagène, Gingivite, Liquide extracellulaire, Lymphoedème, Vaisseaux capillaires, Vaisseaux lymphatiques.
- Animaux, Facteurs temps, Femelle, Gencive, Modèles animaux de maladie humaine, Muqueuse de la bouche, Mâle, Perméabilité capillaire, Pression, Régions promotrices (génétique), Souris, Souris de lignée C57BL, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Capillaries (immunology), Capillaries (metabolism), Capillary Permeability, Collagen (metabolism), Disease Models, Animal, Extracellular Fluid (metabolism), Female, Gingiva (blood supply), Gingivitis (immunology), Gingivitis (metabolism), Immunoglobulin Fc Fragments (genetics), Immunoglobulin G (genetics), Lipopolysaccharides (immunology), Lymphatic Vessels (immunology), Lymphatic Vessels (metabolism), Lymphedema (genetics), Lymphedema (immunology), Lymphedema (metabolism), Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mouth Mucosa (blood supply), Porphyromonas gingivalis (immunology), Pressure, Promoter Regions, Genetic, Time Factors, Vascular Endothelial Growth Factor Receptor-3 (genetics).
- MESH :
- chemical , genetics : Immunoglobulin Fc Fragments, Immunoglobulin G, Vascular Endothelial Growth Factor Receptor-3.
- chemical , immunology : Lipopolysaccharides.
- chemical , metabolism : Collagen.
- blood supply : Gingiva, Mouth Mucosa.
- genetics : Lymphedema.
- immunology : Capillaries, Gingivitis, Lymphatic Vessels, Lymphedema, Porphyromonas gingivalis.
- metabolism : Capillaries, Extracellular Fluid, Gingivitis, Lymphatic Vessels, Lymphedema.
- Animals, Capillary Permeability, Disease Models, Animal, Female, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Pressure, Promoter Regions, Genetic, Time Factors.
Abstract
The gingiva is frequently challenged by oral bacterial products leading to inflammatory responses such as increased fluid filtration and edema formation. The role of initial lymphatics for transcapillary fluid balance in the gingiva is unknown and was therefore investigated in genetically engineered K14-VEGF receptor 3-Ig (K14) lymphedema mice. The mutant mice demonstrated a total lack of lymphatics in the gingiva, whereas lymphatics were found in the submucosal parts of the alveolar mucosa, although they were almost completely absent in the mucosa. In wild-type (WT) mice, lymphatic vessels were detected in mucosal and submucosal parts of the alveolar mucosa. Interstitial fluid pressure (P(if)) measured with micropipettes was increased in the gingiva of K14 mice in the normal situation (P < 0.001) and after inflammation (P < 0.01) induced by lipopolysaccharide from the oral bacteria Porphyromonas gingivalis compared with WT littermates. Fluid volume expansion caused a >75% increase in interstitial fluid volume followed by a drop in P(if) after recovery in both strains. Continuous measurements during the expansion showed an increase in P(if) followed by a decline, suggesting that compliance is increased after the disruption of the extracellular matrix during edema formation. In the alveolar mucosa, no strain differences were observed in P(if) in the normal situation or after fluid volume expansion, suggesting that lymph vessels in the mucosa are not critical for tissue fluid regulation in any situation. Our study demonstrates an important role of gingival lymphatics in transcapillary fluid balance in the steady-state condition and during acute perturbations.
DOI: 10.1152/ajpheart.01199.2009
PubMed: 20472760
Affiliations:
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Heart and circulatory physiology</title><idno type="eISSN">1522-1539</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Capillaries (immunology)</term><term>Capillaries (metabolism)</term><term>Capillary Permeability</term><term>Collagen (metabolism)</term><term>Disease Models, Animal</term><term>Extracellular Fluid (metabolism)</term><term>Female</term><term>Gingiva (blood supply)</term><term>Gingivitis (immunology)</term><term>Gingivitis (metabolism)</term><term>Immunoglobulin Fc Fragments (genetics)</term><term>Immunoglobulin G (genetics)</term><term>Lipopolysaccharides (immunology)</term><term>Lymphatic Vessels (immunology)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphedema (genetics)</term><term>Lymphedema (immunology)</term><term>Lymphedema (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Mouth Mucosa (blood supply)</term><term>Porphyromonas gingivalis (immunology)</term><term>Pressure</term><term>Promoter Regions, Genetic</term><term>Time Factors</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Collagène (métabolisme)</term><term>Facteurs temps</term><term>Femelle</term><term>Fragments Fc des immunoglobulines (génétique)</term><term>Gencive ()</term><term>Gingivite (immunologie)</term><term>Gingivite (métabolisme)</term><term>Immunoglobuline G (génétique)</term><term>Lipopolysaccharides (immunologie)</term><term>Liquide extracellulaire (métabolisme)</term><term>Lymphoedème (génétique)</term><term>Lymphoedème (immunologie)</term><term>Lymphoedème (métabolisme)</term><term>Modèles animaux de maladie humaine</term><term>Muqueuse de la bouche ()</term><term>Mâle</term><term>Perméabilité capillaire</term><term>Porphyromonas gingivalis (immunologie)</term><term>Pression</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term><term>Régions promotrices (génétique)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term><term>Vaisseaux capillaires (immunologie)</term><term>Vaisseaux capillaires (métabolisme)</term><term>Vaisseaux lymphatiques (immunologie)</term><term>Vaisseaux lymphatiques (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Immunoglobulin Fc Fragments</term><term>Immunoglobulin G</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Lipopolysaccharides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Collagen</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Gingiva</term><term>Mouth Mucosa</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Fragments Fc des immunoglobulines</term><term>Immunoglobuline G</term><term>Lymphoedème</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Gingivite</term><term>Lipopolysaccharides</term><term>Lymphoedème</term><term>Porphyromonas gingivalis</term><term>Vaisseaux capillaires</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Capillaries</term><term>Gingivitis</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Porphyromonas gingivalis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Capillaries</term><term>Extracellular Fluid</term><term>Gingivitis</term><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Collagène</term><term>Gingivite</term><term>Liquide extracellulaire</term><term>Lymphoedème</term><term>Vaisseaux capillaires</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Capillary Permeability</term><term>Disease Models, Animal</term><term>Female</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Pressure</term><term>Promoter Regions, Genetic</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Facteurs temps</term><term>Femelle</term><term>Gencive</term><term>Modèles animaux de maladie humaine</term><term>Muqueuse de la bouche</term><term>Mâle</term><term>Perméabilité capillaire</term><term>Pression</term><term>Régions promotrices (génétique)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The gingiva is frequently challenged by oral bacterial products leading to inflammatory responses such as increased fluid filtration and edema formation. The role of initial lymphatics for transcapillary fluid balance in the gingiva is unknown and was therefore investigated in genetically engineered K14-VEGF receptor 3-Ig (K14) lymphedema mice. The mutant mice demonstrated a total lack of lymphatics in the gingiva, whereas lymphatics were found in the submucosal parts of the alveolar mucosa, although they were almost completely absent in the mucosa. In wild-type (WT) mice, lymphatic vessels were detected in mucosal and submucosal parts of the alveolar mucosa. Interstitial fluid pressure (P(if)) measured with micropipettes was increased in the gingiva of K14 mice in the normal situation (P < 0.001) and after inflammation (P < 0.01) induced by lipopolysaccharide from the oral bacteria Porphyromonas gingivalis compared with WT littermates. Fluid volume expansion caused a >75% increase in interstitial fluid volume followed by a drop in P(if) after recovery in both strains. Continuous measurements during the expansion showed an increase in P(if) followed by a decline, suggesting that compliance is increased after the disruption of the extracellular matrix during edema formation. In the alveolar mucosa, no strain differences were observed in P(if) in the normal situation or after fluid volume expansion, suggesting that lymph vessels in the mucosa are not critical for tissue fluid regulation in any situation. Our study demonstrates an important role of gingival lymphatics in transcapillary fluid balance in the steady-state condition and during acute perturbations.</div></front></TEI><affiliations><list><country><li>Norvège</li></country></list><tree><noCountry><name sortKey="Berggreen, Ellen" sort="Berggreen, Ellen" uniqKey="Berggreen E" first="Ellen" last="Berggreen">Ellen Berggreen</name><name sortKey="Bletsa, Athanasia" sort="Bletsa, Athanasia" uniqKey="Bletsa A" first="Athanasia" last="Bletsa">Athanasia Bletsa</name><name sortKey="Fristad, Inge" sort="Fristad, Inge" uniqKey="Fristad I" first="Inge" last="Fristad">Inge Fristad</name><name sortKey="Wiig, Helge" sort="Wiig, Helge" uniqKey="Wiig H" first="Helge" last="Wiig">Helge Wiig</name></noCountry><country name="Norvège"><noRegion><name sortKey="Mkonyi, Lilian Ephrem" sort="Mkonyi, Lilian Ephrem" uniqKey="Mkonyi L" first="Lilian Ephrem" last="Mkonyi">Lilian Ephrem Mkonyi</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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