SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation

Detalhes bibliográficos
Autor(a) principal: Oliveira, Tales Lyra [UNIFESP]
Data de Publicação: 2016
Outros Autores: Candeia-Medeiros, Navylla, Cavalcante-Araujo, Polliane M., Melo, Igor Santana, Favaro-Pipi, Elaine, Fatima, Luciana Alves [UNIFESP], Rocha, Antonio Augusto [UNIFESP], Goulart, Luiz Ricardo, Machado, Ubiratan Fabres [UNIFESP], Campos, Ruy R. [UNIFESP], Sabino-Silva, Robinson
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: https://repositorio.unifesp.br/handle/11600/57962
http://dx.doi.org/10.1038/srep21752
Resumo: High glucose concentration in the airway surface liquid (ASL) is an important feature of diabetes that predisposes to respiratory infections. We investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacterial proliferation. Non-diabetic and diabetic rats were intranasally treated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration and bacterial proliferation (methicillin-resistant Sthaphylococcus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry. BAL glucose concentration and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) the BAL glucose concentration; whereas phlorizin increased the BAL glucose concentration (100%). These regulations were accompanied by parallel changes of in vitro MRSA and P. aeruginosa proliferation in BAL (r = 0.9651 and r = 0.9613, respectively, Pearson correlation). The same regulations were observed in in vivo P. aeruginosa proliferation. In summary, the results indicate a relationship among SGLT1 activity, ASL glucose concentration and pulmonary bacterial proliferation. Besides, the study highlights that, in situations of pulmonary infection risk, such as in diabetic subjects, increased SGLT1 activity may prevent bacterial proliferation whereas decreased SGLT1 activity can exacerbate it.
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spelling Oliveira, Tales Lyra [UNIFESP]Candeia-Medeiros, NavyllaCavalcante-Araujo, Polliane M.Melo, Igor SantanaFavaro-Pipi, ElaineFatima, Luciana Alves [UNIFESP]Rocha, Antonio Augusto [UNIFESP]Goulart, Luiz RicardoMachado, Ubiratan Fabres [UNIFESP]Campos, Ruy R. [UNIFESP]Sabino-Silva, Robinson2020-08-21T17:00:22Z2020-08-21T17:00:22Z2016Scientific Reports. London, v. 6, p. -, 2016.2045-2322https://repositorio.unifesp.br/handle/11600/57962http://dx.doi.org/10.1038/srep21752WOS000370631800001.pdf10.1038/srep21752WOS:000370631800001High glucose concentration in the airway surface liquid (ASL) is an important feature of diabetes that predisposes to respiratory infections. We investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacterial proliferation. Non-diabetic and diabetic rats were intranasally treated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration and bacterial proliferation (methicillin-resistant Sthaphylococcus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry. BAL glucose concentration and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) the BAL glucose concentration; whereas phlorizin increased the BAL glucose concentration (100%). These regulations were accompanied by parallel changes of in vitro MRSA and P. aeruginosa proliferation in BAL (r = 0.9651 and r = 0.9613, respectively, Pearson correlation). The same regulations were observed in in vivo P. aeruginosa proliferation. In summary, the results indicate a relationship among SGLT1 activity, ASL glucose concentration and pulmonary bacterial proliferation. Besides, the study highlights that, in situations of pulmonary infection risk, such as in diabetic subjects, increased SGLT1 activity may prevent bacterial proliferation whereas decreased SGLT1 activity can exacerbate it.CAPESFederal University of UberlandiaFAPEMIGFAPEALFAPESPFAPEAL fellowshipUniv Fed Alagoas, Inst Biol Sci & Hlth, Alagoas, BrazilUniv Fed Sao Paulo, Dept Physiol, Sao Paulo, BrazilUniv Fed Uberlandia, Natl Reference Ctr Leprosy & Sanit Dermatol, Uberlandia, MG, BrazilUniv Sao Paulo, Inst Biomed Sci, Dept Physiol, Sao Paulo, BrazilUniv Fed Uberlandia, Inst Genet & Biochem, Uberlandia, MG, BrazilUniv Calif Davis, Dept Med Microbiol & Immunol, Davis, CA USAUniv Fed Uberlandia, Inst Biomed Sci, Dept Physiol, Uberlandia, MG, BrazilUniv Fed Sao Paulo, Dept Physiol, Sao Paulo, BrazilFAPESP: 201/04831-1Web of Science-engNature Publishing GroupScientific ReportsSGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferationinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleLondon6info:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000370631800001.pdfapplication/pdf1763617${dspace.ui.url}/bitstream/11600/57962/1/WOS000370631800001.pdf66d847b07993b23b2e71793ebb538becMD51open accessTEXTWOS000370631800001.pdf.txtWOS000370631800001.pdf.txtExtracted texttext/plain45217${dspace.ui.url}/bitstream/11600/57962/2/WOS000370631800001.pdf.txteabe006b1cb12f738af7d6951018030bMD52open accessTHUMBNAILWOS000370631800001.pdf.jpgWOS000370631800001.pdf.jpgIM Thumbnailimage/jpeg7418${dspace.ui.url}/bitstream/11600/57962/4/WOS000370631800001.pdf.jpge0225f05e218bf2b7c6f22e34482ace4MD54open access11600/579622022-07-31 19:28:03.849open accessoai:repositorio.unifesp.br:11600/57962Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-07-31T22:28:03Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
title SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
spellingShingle SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
Oliveira, Tales Lyra [UNIFESP]
title_short SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
title_full SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
title_fullStr SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
title_full_unstemmed SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
title_sort SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation
author Oliveira, Tales Lyra [UNIFESP]
author_facet Oliveira, Tales Lyra [UNIFESP]
Candeia-Medeiros, Navylla
Cavalcante-Araujo, Polliane M.
Melo, Igor Santana
Favaro-Pipi, Elaine
Fatima, Luciana Alves [UNIFESP]
Rocha, Antonio Augusto [UNIFESP]
Goulart, Luiz Ricardo
Machado, Ubiratan Fabres [UNIFESP]
Campos, Ruy R. [UNIFESP]
Sabino-Silva, Robinson
author_role author
author2 Candeia-Medeiros, Navylla
Cavalcante-Araujo, Polliane M.
Melo, Igor Santana
Favaro-Pipi, Elaine
Fatima, Luciana Alves [UNIFESP]
Rocha, Antonio Augusto [UNIFESP]
Goulart, Luiz Ricardo
Machado, Ubiratan Fabres [UNIFESP]
Campos, Ruy R. [UNIFESP]
Sabino-Silva, Robinson
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Oliveira, Tales Lyra [UNIFESP]
Candeia-Medeiros, Navylla
Cavalcante-Araujo, Polliane M.
Melo, Igor Santana
Favaro-Pipi, Elaine
Fatima, Luciana Alves [UNIFESP]
Rocha, Antonio Augusto [UNIFESP]
Goulart, Luiz Ricardo
Machado, Ubiratan Fabres [UNIFESP]
Campos, Ruy R. [UNIFESP]
Sabino-Silva, Robinson
description High glucose concentration in the airway surface liquid (ASL) is an important feature of diabetes that predisposes to respiratory infections. We investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacterial proliferation. Non-diabetic and diabetic rats were intranasally treated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration and bacterial proliferation (methicillin-resistant Sthaphylococcus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry. BAL glucose concentration and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) the BAL glucose concentration; whereas phlorizin increased the BAL glucose concentration (100%). These regulations were accompanied by parallel changes of in vitro MRSA and P. aeruginosa proliferation in BAL (r = 0.9651 and r = 0.9613, respectively, Pearson correlation). The same regulations were observed in in vivo P. aeruginosa proliferation. In summary, the results indicate a relationship among SGLT1 activity, ASL glucose concentration and pulmonary bacterial proliferation. Besides, the study highlights that, in situations of pulmonary infection risk, such as in diabetic subjects, increased SGLT1 activity may prevent bacterial proliferation whereas decreased SGLT1 activity can exacerbate it.
publishDate 2016
dc.date.issued.fl_str_mv 2016
dc.date.accessioned.fl_str_mv 2020-08-21T17:00:22Z
dc.date.available.fl_str_mv 2020-08-21T17:00:22Z
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dc.identifier.citation.fl_str_mv Scientific Reports. London, v. 6, p. -, 2016.
dc.identifier.uri.fl_str_mv https://repositorio.unifesp.br/handle/11600/57962
http://dx.doi.org/10.1038/srep21752
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dc.identifier.doi.none.fl_str_mv 10.1038/srep21752
dc.identifier.wos.none.fl_str_mv WOS:000370631800001
identifier_str_mv Scientific Reports. London, v. 6, p. -, 2016.
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