Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis
Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-ind...
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| Other Authors: | , , , , , , , , , |
| Format: | article |
| Language: | Spanish |
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2010
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| Online Access: | http://repo.ulatina.edu.pa/handle/123456789/10 |
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| _version_ | 1869652464662216704 |
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| author | Barrera, Gabriela |
| author2 | Landoni, Verónica Martire-Greco, Daiana Chiarella, Paula Meiss, Roberto Gómez, Sonia A. Alves-Rosa, Fernanda Rearte, Barbara Isturiz, Martín Palermo, Marina S. Fernández, Gabriela C. |
| author2_role | author author author author author author author author author author |
| author_browse | Alves-Rosa, Fernanda Barrera, Gabriela Chiarella, Paula Fernández, Gabriela C. Gómez, Sonia A. Isturiz, Martín Landoni, Verónica Martire-Greco, Daiana Meiss, Roberto Palermo, Marina S. Rearte, Barbara |
| author_facet | Barrera, Gabriela Landoni, Verónica Martire-Greco, Daiana Chiarella, Paula Meiss, Roberto Gómez, Sonia A. Alves-Rosa, Fernanda Rearte, Barbara Isturiz, Martín Palermo, Marina S. Fernández, Gabriela C. |
| author_role | author |
| collection | Repositorio de la Universidad Latina de Panamá |
| dc.creator.none.fl_str_mv | Barrera, Gabriela Landoni, Verónica Martire-Greco, Daiana Chiarella, Paula Meiss, Roberto Gómez, Sonia A. Alves-Rosa, Fernanda Rearte, Barbara Isturiz, Martín Palermo, Marina S. Fernández, Gabriela C. |
| dc.date.none.fl_str_mv | 2010-12-13 2020-02-14T20:18:53Z 2020-02-14T20:18:53Z |
| dc.format.none.fl_str_mv | application/pdf |
| dc.identifier.none.fl_str_mv | 9781555819873 9781555819880 10.1128/IAI.01127-10 http://repo.ulatina.edu.pa/handle/123456789/10 |
| dc.language.none.fl_str_mv | spa |
| dc.publisher.none.fl_str_mv | Infection and Immunity |
| dc.rights.none.fl_str_mv | info:eu-repo/semantics/openAccess |
| dc.source.none.fl_str_mv | reponame:Repositorio de la Universidad Latina de Panamá instname:Universidad Latina de Panamá instacron:ULATINA |
| dc.title.none.fl_str_mv | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| dc.type.none.fl_str_mv | info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
| description | Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 CD11b ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis. |
| eu_rights_str_mv | openAccess |
| format | article |
| id | lrtest_66da4ea1b33a00f5ead76e76da36c0b4 |
| identifier_str_mv | 9781555819873 9781555819880 10.1128/IAI.01127-10 |
| instacron_str | ULATINA |
| institution | ULATINA |
| instname_str | Universidad Latina de Panamá |
| language | spa |
| network_acronym_str | lrtest |
| network_name_str | lr |
| oai_identifier_str | oai:repo.ulatina.edu.pa:123456789/10 |
| publishDate | 2010 |
| publishDateSort | 2010 |
| publisher.none.fl_str_mv | Infection and Immunity |
| reponame_str | Repositorio de la Universidad Latina de Panamá |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| spelling | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of SepsisBarrera, GabrielaLandoni, VerónicaMartire-Greco, DaianaChiarella, PaulaMeiss, RobertoGómez, Sonia A.Alves-Rosa, FernandaRearte, BarbaraIsturiz, MartínPalermo, Marina S.Fernández, Gabriela C.Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 CD11b ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis.Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 CD11b ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis.Infection and Immunity2020-02-14T20:18:53Z2020-02-14T20:18:53Z2010-12-13info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdf9781555819873978155581988010.1128/IAI.01127-10http://repo.ulatina.edu.pa/handle/123456789/10spainfo:eu-repo/semantics/openAccessreponame:Repositorio de la Universidad Latina de Panamáinstname:Universidad Latina de Panamáinstacron:ULATINAoai:repo.ulatina.edu.pa:123456789/102020-03-02T22:22:19Z |
| spellingShingle | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis Barrera, Gabriela |
| status_str | publishedVersion |
| title | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| title_full | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| title_fullStr | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| title_full_unstemmed | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| title_short | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| title_sort | Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis |
| url | http://repo.ulatina.edu.pa/handle/123456789/10 |