Intestinal d-Galactose Transport in an Endotoxemia Model in the Rabbit

Amador, P.; García-Herrera, J.; Marca, M.C.; Osada, Jesús; Acı́n, Sergio; Navarro, María Á.; Salvador, María Luisa Esteban; Lostao, M. P.; Rodríguez-Yoldi, Ma. Jesus

doi:10.1007/s00232-007-9012-5

Cited by 34 publications

(20 citation statements)

References 49 publications

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“…In this way, we reported an inhibitory effect of LPS on D-fructose uptake across the small intestine of rabbit in vitro and in vivo [12,13] and on D-galactose intestinal absorption in vivo [14].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Amador¹,

Marca

García-Herrera³

et al. 2008

Cell Physiol Biochem

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Background/Aims: Previous studies from our laboratory have revealed impaired intestinal absorption of D-galactose in lipopolysaccharide-treated rabbits. The aim of the present work was to examine the effect of LPS on D-galactose intestinal absorption in vitro. Methods: D-galactose intestinal transport was assessed employing three techniques: sugar uptake in rings of everted jejunum, transepithelial flux in Ussing-type chambers and transport assays in brush border membrane vesicles. The level of expression of the Na⁺/D-galactose cotransporter (SGLT1) was analyzed by Western blot. Results: LPS decreased the mucosal D-galactose transport in rabbit jejunum but a preexposition to the endotoxin was required. LPS affected the Na⁺-dependent transport system by increasing the apparent Km value without affecting the Vmax. It also decreased the Na⁺, K⁺-ATPase activity. However, it did not inhibit neither the uptake of D-galactose by brush border membrane vesicles nor modified the SGLT1 protein levels in the brush border, suggesting an indirect endotoxin effect. This inhibitory effect, was reduced by selective inhibitors of Ca²⁺-calmodulin (W13), protein kinase C (GF 109203X), p38 mitogen-activated protein kinase (SB 203580), c-Jun N-terminal kinase (SP 600125) and mitogen extracellular kinase (U 0126). Conclusion: LPS inhibits the mucosal Na⁺-dependent D-galactose intestinal absorption and the Na⁺, K⁺-ATPase activity when it is added to the tissue. Intracellular processes related to protein kinases seem to be implicated in the endotoxin effect.

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Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Amador¹,

Marca

García-Herrera³

et al. 2008

Cell Physiol Biochem

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“…Early weaning causes bacterial imbalances in the intestinal populations, favoring Escherichia coli growth and subsequent release of lipopolysaccharide (LPS) from the cell wall of these bacteria (Amador et al ., 2007). The LPS is considered an important pathogenic agent and a potent stimulator of innate immunity and inflammation (Zhenfeng et al ., 2008).…”

Section: Introductionmentioning

confidence: 99%

Escherichia coli lipopolysaccharide affects intestinal mucin secretion in weaned pigs

Zapata

Rodríguez²,

Ramírez³

et al. 2015

Rev Colomb Cienc Pecu

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El lipopolisacárido de Escherichia coli afecta la secreción de mucinas intestinales en cerdos destetados O lipopolissacárido de Escherichia coli afecta a secreção de mucina intestinal em porcos desmamadosSummary Background: to the best of our knowledge, the effects of lipopolysaccharide (LPS) from Escherichia coli on goblet cells and intestinal mucin secretion of weaned pigs has not been reported, and it is unknown whether these effects could trigger enteritis. Objective: to determine the effect of E . coli LPS on intestinal mucin secretion in weaning piglets. Methods: fifty-two piglets weaned at 21 days of age were fed a basal diet supplemented with four LPS levels (0.0, 0.3, 0.5, and 1.0 µg/mg) during 10 days. Piglets were slaughtered on days 1, 5, 7, and 10 post-weaning and samples of small and large intestine were taken for histochemical staining to determine goblet cell population and type of mucins produced (acidic, sulphated, non-sulphated, or neutral). Results: acidic mucin was reduced on day 5 post-weaning independently of the dietary LPS level supplied to piglets. Recovery of acidic mucins was observed during days 7 and 10 post-weaning. Neutral mucins increased on day 5 and decreased on days 7 and 10 post-weaning. High LPS levels decreased goblet cells population and secretion of all types of mucins. This effect was remarkably high for diet two (D2: 0.5 mg LPS/mg food). Conclusions: early weaning (21 d) and LPS addition to the diet affect mucin secretion and intestinal epithelium integrity by modifying goblet cell populations and their balance between acidic and neutral mucin secretion. These findings explain some abnormalities related with post-weaning diarrhea syndrome and help to explain its pathophysiology.

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“…Debido a lo anterior, el destete favorece la desaparición de la población microbiana de lactobacilos (Gram positivas) predominante en estómago e intestino, y el aumento de la población de bacterias Gram negativas (principalmente E. coli), la cual libera desde sus paredes productos proinflamatorios como el lipopolisacárido (LPS) (7).…”

Section: Introductionunclassified

Lesiones en órganos de cerdos posdestete, inducidas por el lipopolisacárido de E. coli

Gutiérrez

2013

Rev MVZ Córdoba

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RESUMENObjetivo. Evaluar el efecto de la ingestión de varios niveles de Lipopolisacárido (LPS) de E. coli sobre las manifestaciones clínicas y lesiones en órganos de cerdos recién destetados. Materiales y métodos. El trabajo de campo se realizó en el Centro San Pablo, perteneciente a la Universidad Nacional de Colombia. El estudio se realizó con 52 cerdos destetados (6.5±0.5 kg) a los 21 días de edad. Los animales fueron alimentados durante 10 días con una dieta basal compuesta de leche y algunos de sus derivados, adicionada con cuatro niveles de LPS (0, 0.3, 0.5 y 1.0 µg/ml de alimento). Los cerdos se sacrificaron escalonadamente los días 1, 5, 7 y 10 posdestete y se tomaron muestras de intestino delgado, estómago, hígado, páncreas, corazón, pulmón, riñón y bazo. El monitoreo clínico y paraclínico se realizó diariamente durante la investigación. Para determinar la ganancia de peso, los animales fueron pesados el día del destete y el día del sacrificio. Resultados. Hubo diferencia (p<0.01) en las variables peso de los órganos y ganancia de peso, donde los animales que consumieron el mayor nivel de LPS presentaron los menores valores, llegando a su mínimo nivel el día 10 posdestete. Las variables presentación de: lesiones macroscópicas, diarreas, y temperatura rectal, aumentaron con el nivel de inclusión de LPS en la dieta, llegando a su máximo nivel el día 10 posdestete (p<0.01). Conclusiones. El LPS de E. coli provoca la inhibición del crecimiento corporal y de los órganos en estudio y una alta incidencia de diarreas. ORIGINAL 3535 ABSTRACTObjective: To evaluate the effects of the intake of several levels of lipopolysaccharides (LPS) from E. coli on clinical manifestations and injuries in organs of newly weaned pigs. Materials and methods. The experiment was conducted at the San Pablo Production Center of the Universidad Nacional de Colombia. 52 weaned pigs at 21 days of age were used. The animals were fed a basal diet composed of milk and some of its derivatives, and an addition of four LPS levels (0, 0.3, 0.5 and 1.0 µg / mg of feed) during 10 days. The pigs were sequentially sacrificed on days 1, 5, 7, and 10 after weaning, and samples of the small intestine, stomach, liver, pancreas, heart, lungs, kidney and spleen were extracted. Clinical and laboratory monitoring was performed daily during the investigation. To determine weight gain, the animals were weighed on weaning day, and on slaughter day. Results: There were statistical differences (p<0.01) in organ weights and weight gain, where animals that consumed the highest levels of LPS showed the lowest values, reaching the lowest level on day 10 post-weaning. The variables: macroscopic lesions, diarrhea, and rectal temperature increased with the increase in LPS levels in the diet, reaching their peaks on day 10 post-weaning (p<0.01). Conclusions: E. coli LPS causes inhibition of the studied body and organ growth parameters, and a high incidence of post-weaning diarrhea.

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Intestinal d-Galactose Transport in an Endotoxemia Model in the Rabbit

Cited by 34 publications

References 49 publications

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Lipopolysaccharide Induces Inhibition of Galactose Intestinal Transport in Rabbits <i>in vitro</i>

Escherichia coli lipopolysaccharide affects intestinal mucin secretion in weaned pigs

Lesiones en órganos de cerdos posdestete, inducidas por el lipopolisacárido de E. coli

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