Summary： The present study aimed to examine the effect of intedeukin （IL）-4 on neutrophil chemo- taxis in airway inflammation in asthmatic rats and the possible mechanism. Male Wistar rats were intranasally instill...Summary： The present study aimed to examine the effect of intedeukin （IL）-4 on neutrophil chemo- taxis in airway inflammation in asthmatic rats and the possible mechanism. Male Wistar rats were intranasally instilled with recombinant rat （rr） IL-4 （rrlL-4） at different doses [2, 4 or 8μ g/animal, dis- solved in 200 μL normal saline （NS）] or rrlL-4 at 4 μg/animal （dissolved in 200 μL NS）. NS （200 μL） and LPS （6 mg/kg/animal, dissolved in 200 IxL NS） were intranasally given respectively in the negative and positive control groups. Moreover, the asthmatic lung inflammation was induced in rats which were then intranasally treated with rrlL-4 （4 μg/animal） or LPS （6 mg/kg/animal）. The normal rats treated with different doses of rrlL-4 and those asthmatic rats were sacrificed 6 h later. And animals instilled with rrlL-4 at 4 μg were sacrificed 6, 12 or 24 h later. The bronchoalveolar lavage fluid （BALF） and lungs were harvested for detection of leukocyte counts by Wright-Giemsa staining and lung histopa- thology by haematoxylin-eosin （HE） staining. The levels of cytokine-induced neutrophil chemoattrac- tant （CINC）-I and intercellular adhesion molecule （ICAM）-I in BALF were determined by ELISA. Real-time PCR was used to measure the mRNA expression of C1NCs （CINC-1, CINC-2u, CINC-2a, CINC-3） and ICAM-1 in lung tissues. The results showed that the intranasal instillation of IL-4 did not induce a recruitment of neutrophils in BALF in rats. However, IL-4 could increase the CINC-1 level in BALF in a dose-dependent manner at 6 h. But the mRNA expression levels of CINC-1, C1NC-2a, CINC-2, CINC-3 were not significantly increased in lungs of IL-4-treated rats relative to NS negative control group. Moreover, IL-4 was found to augment the mRNA expression oflCAM-1 in lungs and the ICAM-1 level in BALF at 6 h. However, the increase in CINC-1 and ICAM-1 levels in BALF of IL-4-treated asthmatic rats was not significantly different from that in untreated asthmatic rats. These findings indicate that IL-4 does not directly recruit neutrophils in the rat lungs, but it may contribute to airway neutrophilia through up-regulation of CINC-1 and ICAM-1.展开更多
BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most...BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most common causes of gastrointestinal dysfunction, and the pathogenesis is closely related to endotoxemia and intestinal barrier injury. Bifidobacterium is one of the main probiotics in the human body that is involved in digestion, absorption, metabolism, nutrition, and immunity.Bifidobacterium plays an important role in maintaining the intestinal mucosal barrier integrity. This study investigated the protective mechanism of Bifidobacterium during ileal injury in rats.AIM To investigate the effects of Bifidobacterium on cytokine-induced neutrophil chemoattractant(CINC) and insulin-like growth factor 1(IGF-1) in the ileum of rats with endotoxin injury.METHODS Preweaning rats were randomly divided into three groups: Control(group C),model(group E) and treatment(group T). Group E was intraperitoneally injected with lipopolysaccharide(LPS) to create an animal model of intestinal injury.Group T was intragastrically administered Bifidobacterium suspension 7 d before LPS. Group C was intraperitoneally injected with normal saline. The rats were killed at 2, 6 or 12 h after LPS or physiological saline injection to collect ilealtissue samples. The expression of ileal CINC mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR), and expression of ileal IGF-1 protein and mRNA was detected by immunohistochemistry and RT-PCR,respectively.RESULTS The ileum of rats in Group C did not express CINC mRNA, ileums from Group E expressed high levels, which was then significantly decreased in Group T(F =23.947, P < 0.05). There was no significant difference in CINC mRNA expression at different times(F = 0.665, P > 0.05). There was a high level of IGF-1 brown granules in ileal crypts and epithelial cells in Group C, sparse staining in Group E, and dark, dense brown staining in Group T. There was a significant difference between Groups C and E and Groups E and T(P < 0.05). There was no significant difference in IGF-1 protein expression at different times(F = 1.269, P > 0.05). IGF-1 mRNA expression was significantly different among the three groups(P < 0.05),though not at different times(F = 0.086, P > 0.05).CONCLUSION Expression of CINC mRNA increased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium reduced CINC m RNA expression. IGF-1 protein and mRNA expression decreased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium prevented the decrease in IGF-1 expression. Bifidobacterium may increase IGF-1 expression and enhance intestinal immune barrier function in rats with endotoxin injury.展开更多
基金supported by a grant from the National Natural Science Foundation of China(No.30770945)
文摘Summary： The present study aimed to examine the effect of intedeukin （IL）-4 on neutrophil chemo- taxis in airway inflammation in asthmatic rats and the possible mechanism. Male Wistar rats were intranasally instilled with recombinant rat （rr） IL-4 （rrlL-4） at different doses [2, 4 or 8μ g/animal, dis- solved in 200 μL normal saline （NS）] or rrlL-4 at 4 μg/animal （dissolved in 200 μL NS）. NS （200 μL） and LPS （6 mg/kg/animal, dissolved in 200 IxL NS） were intranasally given respectively in the negative and positive control groups. Moreover, the asthmatic lung inflammation was induced in rats which were then intranasally treated with rrlL-4 （4 μg/animal） or LPS （6 mg/kg/animal）. The normal rats treated with different doses of rrlL-4 and those asthmatic rats were sacrificed 6 h later. And animals instilled with rrlL-4 at 4 μg were sacrificed 6, 12 or 24 h later. The bronchoalveolar lavage fluid （BALF） and lungs were harvested for detection of leukocyte counts by Wright-Giemsa staining and lung histopa- thology by haematoxylin-eosin （HE） staining. The levels of cytokine-induced neutrophil chemoattrac- tant （CINC）-I and intercellular adhesion molecule （ICAM）-I in BALF were determined by ELISA. Real-time PCR was used to measure the mRNA expression of C1NCs （CINC-1, CINC-2u, CINC-2a, CINC-3） and ICAM-1 in lung tissues. The results showed that the intranasal instillation of IL-4 did not induce a recruitment of neutrophils in BALF in rats. However, IL-4 could increase the CINC-1 level in BALF in a dose-dependent manner at 6 h. But the mRNA expression levels of CINC-1, C1NC-2a, CINC-2, CINC-3 were not significantly increased in lungs of IL-4-treated rats relative to NS negative control group. Moreover, IL-4 was found to augment the mRNA expression oflCAM-1 in lungs and the ICAM-1 level in BALF at 6 h. However, the increase in CINC-1 and ICAM-1 levels in BALF of IL-4-treated asthmatic rats was not significantly different from that in untreated asthmatic rats. These findings indicate that IL-4 does not directly recruit neutrophils in the rat lungs, but it may contribute to airway neutrophilia through up-regulation of CINC-1 and ICAM-1.
基金Supported by the Education Department of Heilongjiang Province,China,No.11521124
文摘BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most common causes of gastrointestinal dysfunction, and the pathogenesis is closely related to endotoxemia and intestinal barrier injury. Bifidobacterium is one of the main probiotics in the human body that is involved in digestion, absorption, metabolism, nutrition, and immunity.Bifidobacterium plays an important role in maintaining the intestinal mucosal barrier integrity. This study investigated the protective mechanism of Bifidobacterium during ileal injury in rats.AIM To investigate the effects of Bifidobacterium on cytokine-induced neutrophil chemoattractant(CINC) and insulin-like growth factor 1(IGF-1) in the ileum of rats with endotoxin injury.METHODS Preweaning rats were randomly divided into three groups: Control(group C),model(group E) and treatment(group T). Group E was intraperitoneally injected with lipopolysaccharide(LPS) to create an animal model of intestinal injury.Group T was intragastrically administered Bifidobacterium suspension 7 d before LPS. Group C was intraperitoneally injected with normal saline. The rats were killed at 2, 6 or 12 h after LPS or physiological saline injection to collect ilealtissue samples. The expression of ileal CINC mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR), and expression of ileal IGF-1 protein and mRNA was detected by immunohistochemistry and RT-PCR,respectively.RESULTS The ileum of rats in Group C did not express CINC mRNA, ileums from Group E expressed high levels, which was then significantly decreased in Group T(F =23.947, P < 0.05). There was no significant difference in CINC mRNA expression at different times(F = 0.665, P > 0.05). There was a high level of IGF-1 brown granules in ileal crypts and epithelial cells in Group C, sparse staining in Group E, and dark, dense brown staining in Group T. There was a significant difference between Groups C and E and Groups E and T(P < 0.05). There was no significant difference in IGF-1 protein expression at different times(F = 1.269, P > 0.05). IGF-1 mRNA expression was significantly different among the three groups(P < 0.05),though not at different times(F = 0.086, P > 0.05).CONCLUSION Expression of CINC mRNA increased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium reduced CINC m RNA expression. IGF-1 protein and mRNA expression decreased in the ileum of preweaning rats with endotoxin injury, and exogenous administration of Bifidobacterium prevented the decrease in IGF-1 expression. Bifidobacterium may increase IGF-1 expression and enhance intestinal immune barrier function in rats with endotoxin injury.
