Gut microflora , an important part in maintaining the intestinal homeostasis , can participate in the development of intestinal mucosal immune system , promote the synthesis of secreted IgA ( sIgA) and interact with intestinal immune cells .Gut micro-flora also plays a significant role in the development of inflammatory bowel diseases , irritable bowel syndrome , pediatric allergic disea-ses and other disorders .This paper reviews the advances about the correlation of gut microflora and intestinal mucosal immunity .

Objective To compare the gastric mucosa damage induced by celecoxib and conventional NSAIDs——indomethacin. Methods NSAIDs induced gastric mucosal damage model in rats was obtained by pouring indomethacin, celecoxib respectively (n=8); After gastric damage induced by means of 100% ethanol, celecoxib were administered by gastric gavage (n=8). Gastric mucosal 6-keto-PGF 1? ,TXB 2 level and lesion index (LI) were measured. Morphological changes of gastric mucosa were assessed under light and scanning electronic microscopy. Results Indomethacin caused obvious gastric damage (LI:13.38?2.06) and a marked reduction of 6-keto-PGF 1? ,TXB 2 level was observed (P

The aim of the study was to demonstrate the influence of immersion and restraint stress on the ultrastructural changes in gastric acid barrier and parietal cells in rats. Twenty rats were randomly divided into control and stress groups. The gastric mucosal ulcer index was measured. The ultrastructural changes in parietal cells, epithelial cells, epithelial cell junctions, and basal lamina were observed by transmission electronic microscopy. Stress could induce gastric mucosal damage obviously. Parietal cells in a resting state in control group but became active in stress groups with plenty of mitochromosomes and secreting cysts. The cell membrane of epithelium on the luminal surface were were injured with the preservation of tight junction and basal lamina. The results indicated that the stress induced acid secretion of parietal cells, which destroys the luminal surface of the epithelium. It thus suggests the significance of epithelial cell membrane damage in the development of stress ulcer.

The aim of the study was to analyze the impact of stress on gastric mucosal hydrophobicity and the dontent of phospholipid in gastric glandular adherent mucus gel layer in rat. Forty rats were randomly divided into four groups, which were control group, 0.5, 1 and 2 h after water immersion restraint stress groups. The gastric mucosal contact angle and the content of phospholipid in mucosal surface scraping material (SSM) of glandualar stomach and gastric mucosal ulcer index were measured. The gastric mucosal contact angle in each group was (38.0?2.4)?、(26 8?1 8)?、(20 0?1 4)? and (14 4?3 3)? respectively. The content of phospholipid in SSM per gram of glandular stomach in each group were (46 76?4 73)、(32 49?9 45)、(25 51?5 78)、(18 14?7 91)、(36 76?4 73)?g respectively and the ulcer index was 0、2.8?1.0、6.0?1.6 and 11.4?3.1 respectively. The three parameters showed significant changes in stress conditions as compared with those in normal control ( P

To explore the significance of endothelin-1 converting enzyme (ECE-1)mRNA expression in the development and progression of stress ulcer in cold-restraint-stress(CRS) rats, a model was established by CRS-induced ulcers in rats. ET-1 contents in plasma and gastric mucosa of rats were measured by using radioimmunoassay(RIA)method, gastric mucosa blood flow(GMBF) in rats were determined by using laser-doppler flowmetry, ulcer index(UI) in rats was estimated according to"Guth standard", and the expression levels of ECE-1mRNA in gastric mucosa of normal and CRS rats were measured by using dot blot and reverse transcription-polymerase chain reaction(RT-PCR). The results indicated that compared with control values,the ET-1 contents in both plasma and gastric mucosa of CRS rats were increased significantly after stress (P

4 was found significantly higher in esomeprazole group than in rabeprazole group during first 4 hours (58.9% vs 32.1%), 24 hours on day 1 (73.7% vs 54.8%) and 24 hours on day 5 (84.2% vs 76.2%) (P 4 for at least 16 hours on day 1 and day 5 was higher in esomeprazole group than in rabeprazole group (day 1 63.9% vs 33.3%, day 5 88.9% vs 61.1%, P

Objective: To construct attenuated salmonella typhimurium haboring an eukaryotic co-expression plasmid encoding TIP30 and human IFN-? gene and observing its effect on the growth of adenoid cystic carcinoma. Methods: The TIP30 and human IFN-? genes were amplified by PCR and inserted into eukaryotic expression vector pCI-neofor the construction of expression plasmids pCI-TIP30 and pCI-IFN, respectively. A co-expression plasmid pCI-TIP30/IFN was constructed by linking TIP30 and human IFN-? gene using the sequence of internal ribosome binding sequence (IRES). Three recombinant expression plasmids were transformed into an attenuated AroA'autotrophic mutant of salmonella typhimurium SL7207, the resultant bacteria were used to infected murine macrophage in vitro and the expressed products were detected by Western blot and ELISA, respectively. Tumor growth was observed by oral administration of the recombinant salmonella typhimuriums to the nude mouse with adenoid cystic carcinoma. Results: Murine macrophage infected with recombinant salmonella transformed with both plasmids pCI-TIP30 and pCI-TIP30/IFN could express TIP30 protein, and murine macrophage infected with recombinant salmonella transformed with pCI-IFN or pCI-TIP30/IFN could secret human IFN-? in the culture supernatant. Attenuated salmonella typhimurium and three constructed recombinant salmonella typhimuriums all had evident inhibition onthe tumor growth in nude mouse with adenoid cystic carcinoma. Conclusion: The recombinant attenuated salmonella typhimuriums haboring plasmid pCI-TIP30, plasmidpCI-IFN and co-expressing plasmidp-CI-TIP30/IFN were successfully constructed, which could inhibit the growth of adenoid cystic carcinoma in nude mouse.

0. 05), but was higher than that of 1 h-stress group (P

Objective To analyze the etiology in pancreatic pseudocyst (PPC). Methods Medical records were reviewed and analyzed for 366 PPC patients who were admitted in Changhai hospitals from April 2000 to December 2009 in terms. Demographic data, etiology and primary disorders of PPC patients were recorded. Results The causes of 366 patients varied as follow: gallstones in 158 patients (43.2%);idiopathic in 79 (21.6%); alcohol in 50 (13.7%); trauma in 17 (4.6%); pancreatic tumor in 9 (2.5%);hyperlipidemia in 8 (2.2%); post-operative in 7 (1.9%), other in 38 (10.3%). Depending on Atlantes classification systerm the PPCs were classified into acute PPC in 204 patients (64.2%), chronic PPC in 98 patients (30.8%) and abscess in 16 patients (5.0%). The 4 most common causes of acute PPC were gallstones, idiopathic, alcohol and trauma; the 3 most common causes of chronic PPC were gallstones,idiopathic, alcohol. Conclusions Gallstones is the main etiologic cause of the PPCs in China, followed by idiopathic and alcohol, which is significantly different with that in Western countries.

Objective To observe the changes of zymophagy during experimental acute pancreatitis (AP) induced by caerulein.Methods Pancreatic acinar cell line AR42J cells were cultured in 6-well plates till 90％ confluent and then divided into AP group and control group.Caerulein (1 × 10-8 mol/L) was added into AP group to establish AP cell model,and 1640 cell culture medium was added into control group.After caerulein treated for one,four,six,eight,12 and 24 hours,cells and cell culture supernatant were collected.The levels of cytokine interleukin (IL)-1,tumor necrosis factor (TNF)α,trypsinogen activation (TAP) and amylase were measured with enzyme-linked immunosorbent assay (ELISA) method.The expression of LC3 and Beclin1 at mRNA of each group were detected by reverse transcription-polymerase chain reaction (RT-PCR).The LC3B protein level of each group were detected by Western blotting.The changes of autophagosome and zymophagosome were observed by transmission electron microscopy.The difference between AP group and control group was analyzed by analysis of variance.Results The level of IL-1,TNFα,amylase and TAP in cell culture supernatant of control group was (18.83±7.10) pg/mL,(14.20±3.79) pg/mL,(10.03±2.85) U/L and (39.48±8.62) pg/mL,respectively.Those of AP group significantly increased at first hour ((62.13±11.25) pg/mL,F=3.32,P＜0.01 ; (30.98±7.11) pg/mL,F=3.05,P＜0.05; (25.06±6.82) U/L,F=2.90,P＜0.05 and (128.51± 18.30) pg/mL),F=2.62,P＜0.01,at fourth or sixth hour reached peak (IL-1 at fourth hour:(71.96± 15.82) pg/mL,F=7.25,P＜0.01;TNFα at sixth hour:(39.92±8.94) pg/mL,F=4.93,P＜0.05; amylase at fourth hour:(28.83 ± 8.31) U/L,F=2.06,P＜0.05; TAP at fourth hour:(146.29± 29.36) pg/mL,F=0.14,P＜0.01) and then gradually decreased.At fourth and sixth hour,the expression of LC3 at mRNA level in AP group was 3.18±0.82,1.71±0.14,respectively,while the expression of Beclin-1 rnRNA at first,fourth hour was 2.44±0.34 and 4.13±0.30,all of them were significantly increased compared with those of control group (0.21±0.04 and 0.30±0.08,LC3 mRNA F=0.79、0.06; Beclin mRNA F=2.31、0.36,all P＜ 0.05).There were no significant differences at other time points.The numbers of autophagosome and zymophagosome of AP group were significantly higher than those of control group under transmission electron microscopy.Conclusion Zymophagy occurred during AP cell model induced by caerulein,which suggested that zymophagy might involve in the mechanism of AP.