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Mechanism of intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease: An observational study

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ABSTRACT

The aim of the present study was to investigate intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease (COPD). Male Sprague Dawley rats (n=40) were evenly randomized into control and COPD groups and the COPD model was established by regulated exposure to cigarette smoke for 6 months. Histopathological changes of the lung and intestinal tissues were detected by hematoxylin and eosin staining. Expression of the tight junction proteins occludin and zona occludens-1 (ZO-1) in the intestinal tissues were analyzed by western blotting, serum diamine oxidase (DAO) activity was detected by spectrophotometry, the urinary lactulose to mannitol ratio (L/M) was evaluated by high performance liquid chromatography, and intestinal tissue secretion of tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-8 were detected by ELISA. Lung histopathology revealed thinned alveolar walls, ruptured alveolar septa, enlarged and deformed alveoli, and the formation of bullae and emphysema due to alveolar fusion in the COPD group, while intestinal histopathology indicated clearly swollen intestines with darkened and gray mucosa, neutrophil infiltration of the intestinal mucosal and regional epithelial shedding. The occludin and ZO-1 expression levels were significantly lower in the COPD group compared with those in the corresponding control group (P<0.05), while the urinary L/M ratio was significantly higher (P<0.05). Furthermore, the serum DAO activity and secretion of TNF-α, IFN-γ and IL-8 in the intestinal tissues were significantly higher in the COPD group than in the control group (each P<0.05). Dysfunctional and structural changes were observed in the intestinal mucosal barrier in COPD model rats, which may be associated with the increased intestinal inflammatory responses.

No MeSH data available.


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Infiltration and accumulation of neutrophils together with epithelial structural damage in the intestinal mucosa of a rat from the chronic obstructive pulmonary disease group. Hematoxylin and eosin staining; high magnification (×100).
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f6-etm-0-0-3493: Infiltration and accumulation of neutrophils together with epithelial structural damage in the intestinal mucosa of a rat from the chronic obstructive pulmonary disease group. Hematoxylin and eosin staining; high magnification (×100).

Mentions: Gross observation indicated significant swelling of the gut in the rats of the COPD group compared with that in the normal rats, with darkened and gray mucosa in the former (Figs. 3 and 4). Under light microscopy, neutrophil infiltration of the intestinal mucosa, structural damage to the epithelium and pathological changes characterized by regional epithelial shedding and reduction in the number of intestinal villi were observed in the rats of the COPD group. By contrast, no evident pathological changes were observed in the intestinal mucosa of rats from the control group (Figs. 5 and 6).


Mechanism of intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease: An observational study
Infiltration and accumulation of neutrophils together with epithelial structural damage in the intestinal mucosa of a rat from the chronic obstructive pulmonary disease group. Hematoxylin and eosin staining; high magnification (×100).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4997986&req=5

f6-etm-0-0-3493: Infiltration and accumulation of neutrophils together with epithelial structural damage in the intestinal mucosa of a rat from the chronic obstructive pulmonary disease group. Hematoxylin and eosin staining; high magnification (×100).
Mentions: Gross observation indicated significant swelling of the gut in the rats of the COPD group compared with that in the normal rats, with darkened and gray mucosa in the former (Figs. 3 and 4). Under light microscopy, neutrophil infiltration of the intestinal mucosa, structural damage to the epithelium and pathological changes characterized by regional epithelial shedding and reduction in the number of intestinal villi were observed in the rats of the COPD group. By contrast, no evident pathological changes were observed in the intestinal mucosa of rats from the control group (Figs. 5 and 6).

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to investigate intestinal mucosal barrier dysfunction in a rat model of chronic obstructive pulmonary disease (COPD). Male Sprague Dawley rats (n=40) were evenly randomized into control and COPD groups and the COPD model was established by regulated exposure to cigarette smoke for 6 months. Histopathological changes of the lung and intestinal tissues were detected by hematoxylin and eosin staining. Expression of the tight junction proteins occludin and zona occludens-1 (ZO-1) in the intestinal tissues were analyzed by western blotting, serum diamine oxidase (DAO) activity was detected by spectrophotometry, the urinary lactulose to mannitol ratio (L/M) was evaluated by high performance liquid chromatography, and intestinal tissue secretion of tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-8 were detected by ELISA. Lung histopathology revealed thinned alveolar walls, ruptured alveolar septa, enlarged and deformed alveoli, and the formation of bullae and emphysema due to alveolar fusion in the COPD group, while intestinal histopathology indicated clearly swollen intestines with darkened and gray mucosa, neutrophil infiltration of the intestinal mucosal and regional epithelial shedding. The occludin and ZO-1 expression levels were significantly lower in the COPD group compared with those in the corresponding control group (P<0.05), while the urinary L/M ratio was significantly higher (P<0.05). Furthermore, the serum DAO activity and secretion of TNF-α, IFN-γ and IL-8 in the intestinal tissues were significantly higher in the COPD group than in the control group (each P<0.05). Dysfunctional and structural changes were observed in the intestinal mucosal barrier in COPD model rats, which may be associated with the increased intestinal inflammatory responses.

No MeSH data available.


Related in: MedlinePlus