OBJECTIVE: To explore the efficacy of prophylactic oral lipopolysaccharide (LPS) in sepsis induced by cecal ligation and puncture (CLP). MATERIAL: Male Balb/c mice. LPS serotype O55: B5 TREATMENT: Mice were treated every 4 days for a total of 5 times with 50 mug of LPS by intraperitoneal (IP) or oral (O) routes. Treatment was stopped one week prior to CLP. Control (C) groups received the vehicle orally, and sham (S) groups were used as reference. METHODS: Histopathology was performed to determine inflammation in liver and lung. Serum cytokines were measured by ELISA, and TNFalpha tissue expression by RTPCR. Antibodies against LPS were measured by ELISA. RESULTS: Administration of LPS by the oral route significantly increased survival (p<0.05) of mice in association with a reduction of Kupffer cells in liver, pulmonary edema in lung, shorter or delayed TNFalpha expression in target organs, a trend to decreased IFN gamma and increased IL-10 serum levels, and a notable increase in the production of specific IgM anti-LPS antibodies. CONCLUSIONS: LPS by oral route protected against CLP. The underlying mechanisms could be the modulation of the proinflammatory response and an increased production of IgM anti-LPS antibodies.
OBJECTIVE: To explore the efficacy of prophylactic oral lipopolysaccharide (LPS) in sepsis induced by cecal ligation and puncture (CLP). MATERIAL: Male Balb/c mice. LPS serotype O55: B5 TREATMENT: Mice were treated every 4 days for a total of 5 times with 50 mug of LPS by intraperitoneal (IP) or oral (O) routes. Treatment was stopped one week prior to CLP. Control (C) groups received the vehicle orally, and sham (S) groups were used as reference. METHODS: Histopathology was performed to determine inflammation in liver and lung. Serum cytokines were measured by ELISA, and TNFalpha tissue expression by RTPCR. Antibodies against LPS were measured by ELISA. RESULTS: Administration of LPS by the oral route significantly increased survival (p<0.05) of mice in association with a reduction of Kupffer cells in liver, pulmonary edema in lung, shorter or delayed TNFalpha expression in target organs, a trend to decreased IFN gamma and increased IL-10 serum levels, and a notable increase in the production of specific IgM anti-LPS antibodies. CONCLUSIONS:LPS by oral route protected against CLP. The underlying mechanisms could be the modulation of the proinflammatory response and an increased production of IgM anti-LPS antibodies.
Authors: R Márquez-Velasco; A X Martínez-Velázquez; L M Amezcua-Guerra; F Flores-Guzmán; A Díaz-Quiñonez; F Massó; J Paniagua-Solís; R Bojalil Journal: Inflamm Res Date: 2011-07-02 Impact factor: 4.575
Authors: Mariana Patlán; Fausto Sánchez-Muñoz; Luis M Amezcua-Guerra; Adriana Granados; Araceli Páez; Felipe Massó; Ana M Mejía; Angeles Soster; Rafael Bojalil; Lenin Pavón; Luis A Jiménez-Zamudio; Ricardo Márquez-Velasco Journal: Biol Res Date: 2017-12-21 Impact factor: 5.612