PURPOSE: Small intestinal function returns first after surgery, and then the function of the stomach returns to normal after postoperative ileus (POI). The aim of this study was to investigate inflammatory responses in the muscle coat of stomach and small intestine in guinea pig POI model. MATERIALS AND METHODS: The distance of charcoal migration from pylorus to the distal intestine was measured. Hematoxylin and eosin (H&E) and immunohistochemical stain for calprotectin were done from the histologic sections of stomach, jejunum and ileum obtained at 3 and 6 hour after operation. Data were compared between sham operation and POI groups. RESULTS: The distance of charcoal migration was significantly reduced in the 3 and 6 hour POI groups compared with sham operated groups (p<0.05). On H&E staining, the degree of inflammation was significantly higher in the stomach of 3 hour POI groups compared with jejunum and ileum of POI groups or sham operated groups (p<0.05). Calprotectin positive cells were significantly increased in the muscle coat of stomach of 3 hour POI groups compared with jejunum and ileum of POI groups or sham operated groups (p<0.05). There was strong association between the degree of inflammation and calprotectin positive cells in stomach. CONCLUSION: Postoperative ileus induced by cecal manipulation significantly increased the degree of inflammation and calprotectin positive cells in the muscle coat of stomach as a remote organ. The relevance of degree of inflammation and the recovery time of ileus should be pursued in the future research.
Animals ; Charcoal ; Guinea Pigs ; Ileus/*immunology ; Male ; Muscle, Smooth/*immunology ; Stomach/*immunology

Atherosclerosis is a chronic progressive vascular disease. It starts early in life, has a long asymptomatic phase, and a progression accelerated by various cardiovascular risk factors. The endothelium is an active inner layer of the blood vessel. It generates many factors that regulate vascular tone, the adhesion of circulating blood cells, smooth muscle proliferation, and inflammation, which are the key mechanisms of atherosclerosis and can contribute to the development of cardiovascular events. There is growing evidence that functional impairment of the endothelium is one of the first recognizable signs of development of atherosclerosis and is present long before the occurrence of atherosclerotic cardiovascular disease. Therefore, understanding the endothelium's central role provides not only insights into pathophysiology, but also a possible clinical opportunity to detect early disease, stratify cardiovascular risk, and assess response to treatments. In the present review, we will discuss the clinical implications of endothelial function as well as the therapeutic issues for endothelial dysfunction in cardiovascular disease as primary and secondary endothelial therapy.
Animals ; Atherosclerosis/*drug therapy/*immunology ; Cytokines/*immunology ; Endothelium, Vascular/*immunology ; Humans ; *Models, Immunological ; Muscle, Smooth, Vascular/*immunology

Antibodies, Antinuclear ; blood ; Autoantibodies ; blood ; Autoimmunity ; Biomarkers ; blood ; Hepatitis C ; blood ; immunology ; Humans ; Mitochondria ; immunology ; Muscle, Smooth ; immunology ; Retrospective Studies

BACKGROUND/AIMS: Exclusion of liver disease from other causes such as autoimmune hepatitis is necessary for diagnosis of nonalcoholic fatty liver disease (NAFLD). However, there has been no study on the prevalence and significance of autoantibodies in the patients with clinically suspected NAFLD in Korea, where hepatitis B is endemic and autoimmune hepatitis is relatively uncommon. METHODS: We prospectively tested for anti-nuclear antibody (ANA), anti-smooth muscle antibody (ASMA), and anti-mitochondrial antibody (AMA) in 135 serially enrolled patients with suspected NAFLD. We compared the clinical characteristics and biochemical indices of the ANA-positive or ASMA-positive group with those of the autoantibody-negative group. RESULTS: Sixteen patients (11.8%) had serum autoantibodies; there was ANA in 8 patients (5.9%), ASMA in 7 (5.1%), and AMA in 2 (1.5%). Both ANA and AMA were positive in one patient. The ANA-positive or ASMA-positive group showed an older age (49.5+/-13.0 vs. 42.0+/-10.9 years, respectively, P=0.018) and higher levels of serum globulin (3.1+/-0.4 vs. 2.9+/-0.4 g/dL, respectively, P=0.037), compared with the autoantibody-negative group. Two cases with positive ANA or ASMA fulfilled the diagnostic criteria for probable autoimmune hepatitis and two cases with positive AMA were suspected as primary biliary cirrhosis. CONCLUSIONS: These findings suggest that autoantibodies could be found in some patients with suspected NAFLD in Korea, AMA-positivity or ASMA-positivity could be associated with old age and high serum globulin, and some of the autoantibody-positive cases could be diagnosed as autoimmune hepatitis or primary biliary cirrhosis. Further studies are necessary to clarify the clinical significance of autoantibody positivity in those patients.
Adult ; Aged ; Antibodies, Antinuclear/analysis ; Autoantibodies/*blood ; English Abstract ; Fatty Liver/*immunology ; Female ; Humans ; Male ; Middle Aged ; Muscle, Smooth/immunology

The objective of this study is to investigate whether BCG infection before, during or after sensitization suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley (SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle (TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage (BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats. Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen sensitization.
Animal ; Asthma/immunology* ; BCG Vaccine/immunology* ; Disease Models, Animal ; Disease Models, Animal ; Eosinophils/immunology ; Leukocyte Count ; Lung/immunology* ; Male ; Muscle, Smooth, Vascular/immunology ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Vaccination

The objective of this study is to investigate whether BCG infection before, during or after sensitization suppresses allergen-induced airway hyperresponsiveness and eosinophilic inflammation in allergic asthma rats, and to determine the required dose of BCG to induce such an inhibition. Eighty-seven Sprague-Dawley (SD) rats were sensitized and provoked with ovalbumin (OA). A pretreatment of 6 x 10(4) or 6 x 10(5) colony forming units (CFUs) of BCG or saline was done at four different times: 3 days before sensitization, at sensitization, 3 days before provocation, or at provocation. The assessment of tracheal smooth muscle (TSM) responsiveness to electrical field stimulation or acetylcholine (ACh) and bronchoalveolar lavage (BAL) were performed 1 day after OA provocation. Doses of 6 x 10(4) CFUs inhibited TSM sensitivity of rats infected 3 days before sensitization or at sensitization, but not 3 days before provocation or at provocation. However, doses of 6 x 10(5) CFUs significantly inhibited not only the airway eosinophilia of rats infected 3 days before sensitization or at sensitization, but also the TSM sensitivity of rats infected 3 days before provocation or at provocation. In conclusion, BCG infection suppresses the development of sensitivity of airway smooth muscle and airway eosinophilic inflammation in allergic asthma rats. Furthermore, a relatively high dose of BCG infection inhibits airway sensitivity, even after allergen sensitization.
Animal ; Asthma/immunology* ; BCG Vaccine/immunology* ; Disease Models, Animal ; Disease Models, Animal ; Eosinophils/immunology ; Leukocyte Count ; Lung/immunology* ; Male ; Muscle, Smooth, Vascular/immunology ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Vaccination

OBJECTIVETo observe the effects of interleukin-8 monoclonal antibody on smooth muscle cell proliferation and balloon inflation-induced abdominal aorta stenosis in rabbits.

METHODSThirty-six New Zealand white rabbits were randomly assigned to balloon inflation group (group A, n = 12), interleukin-8 monoclonal antibody pre-treated rabbits (2 mg/kg for 3 days before balloon inflation, group B, n = 12) and sham-operated control group (group C, n = 12). Peripheral blood was collected before experiment and at 4 h, 1, 3, 7, 14, and 28 days post balloon inflation or sham operation and the levels of IL-8 were measured by enzyme linked immunosorbent assay (ELISA). The ratio of positive and negative masculine cells in the high power microscopic field was determined in proliferating cell nuclear antigen (PCNA) stained slide. Histopathologic examination was performed in abdominal aorta and luminal area, intima and tunica media area were measured.

RESULTSPlasma interleukin-8 began to rise at 4 h and peaked at 1 day and remained increased up to 28 days after balloon inflation in rabbits of group A, plasma interleukin-8 level in group A was significantly higher than in group B and C at 4 h and thereafter post operation. The ratio of positive and negative masculine cells was significantly increased in group A compared to group C and was significantly lower in group B than in group A. Abdominal aorta stenosis, luminal area, intima and tunica media area were significantly reduced in group B than in group A. Correlation analysis indicated that there were positive relations between plasma IL-8 level and intima thickness, area of intima and tunica media, respectively (r = 0.894, 0.783, 0.801, 0.912, all P < 0.01).

CONCLUSIONSPlasma IL-8 level is increased in this abdominal aorta stenosis model and is positively correlated to the severity of abdominal aorta stenosis. IL-8 monoclonal antibody could significantly reduce abdominal aorta stenosis in this abdominal aorta stenosis model.

Animals ; Antibodies, Monoclonal ; pharmacology ; therapeutic use ; Aorta, Abdominal ; pathology ; Aortic Coarctation ; drug therapy ; pathology ; Cell Proliferation ; drug effects ; Interleukin-8 ; immunology ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; drug effects ; Rabbits

OBJECTIVETo investigate the clinical significance of liver function and autoantibodies in patients with acute or chronic drug-induced liver injury.

METHODS51 patients with drug-induced liver injury were divided into acute drug induced liver injury group and chronic drug induced liver injury group, liver function and autoantibodies were compared between these two groups.

RESULTSThere was no significant difference (P more than 0.05) in alanine aminotransferase [(412.1+/-387.5) U/L and (376.0+/-319.7) U/L], aspartate aminotransferase [(352.5+/-457.9) U/L and (198.8+/-142.7) U/L], total bilirubin [(109.7+/-104.80)micromol/L and(102.4+/-135.7)micromol/L], direct bilirubin [(66.4+/-73.3)micromol/L and (61.2+/-72.1)micromol/L], alkaline phosphatase [(133.4+/-50.1) U/L and (147.4+/-97.3) U/L], gamma-glutamyltransferase [(139.9+/-134.1) U/L and (180.6+/-227.9) U/L], and albumin [(41.3+/-4.9) g/L and (39.8+/-5.3)g/L] between these two groups, however, the level of globulin [(25.1+/-5.3) g/L and (28.6+/-5.1) g/L] was significantly different between these two groups (P less than 0.05). The titers of Anti-nuclear antibody (ANA) and smooth muscle antibody (SMA) were less than or equal to 1:320 in patients with acute drug induced liver injury. The titers of ANA, antimitochondrial antibody (AMA), and SMA were more than or equal to 1:320 in most of the patients with chronic drug induced liver injury.

CONCLUSIONLiver function has no value in the diagnosis of acute or chronic drug induced liver injury. High titer autoantibodies are found in patients with chronic drug induced liver injury.

Acute Disease ; Adult ; Antibodies, Antinuclear ; blood ; Autoantibodies ; blood ; Chemical and Drug Induced Liver Injury ; blood ; diagnosis ; immunology ; Diagnosis, Differential ; Drug-Related Side Effects and Adverse Reactions ; Female ; Humans ; Liver ; pathology ; physiopathology ; Liver Function Tests ; Male ; Microsomes ; immunology ; Middle Aged ; Muscle, Smooth ; immunology

BACKGROUNDAutoantibodies against angiotensin AT1 receptor have been discovered in patients with preeclampsia or malignant hypertension. Some studies have demonstrated that the autoantibodies are involved in the immunopathogenesis of hypertension and have an agonist effect similar to angiotensin II.

METHODSAutoantibodies against AT1 receptor were purified from sera of patients with primary hypertension by affinity chromatography. Proliferation of cultured rat vascular smooth muscle cells was detected by bromodeoxyuridine incorporation and activation of signalling molecules detected by Western blotting and electrophoretic mobility shift assay.

RESULTSThe AT1-RAb caused a significant proliferation similar to the Ang II during first 24 hours. The levels of nuclear factor-kappaB (NF-kappaB), phosphorylated JAK2, phosphorylated STAT1 (pSTAT1) and phosphorylated STAT3 (pSTAT3) molecules were increased in response to the autoantibodies. In contrast, the activations of NF-kappaB and JAK-STAT were blocked by losartan, pyrrolidinedithiocarbamate (a specific inhibitor of NF-kappaB) and AG490 (a specific inhibitor of the JAK2 tyrosine kinase). The expressions of NF-kappaB, pSTAT1 and pSTAT3 reached peak levels at different times. Moreover, the relative densities of electrophoretic bands showed that activation of pSTAT3 was more significant than STAT1 induced by AT1-RAb.

CONCLUSIONSThese results suggest that the autoantibodies against AT1 receptor have an agonist effect similar to Ang II in proliferation of VSMCs and the NF-kappaB and JAK-STAT proteins play essential roles. The effect is different from Ang II in that STAT3 is the main downstream activating molecule in JAK-STAT signalling pathway.

Animals ; Autoantibodies ; immunology ; Cell Proliferation ; Humans ; Hypertension ; immunology ; Janus Kinase 2 ; physiology ; Muscle, Smooth, Vascular ; cytology ; NF-kappa B ; physiology ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 ; immunology ; STAT3 Transcription Factor ; physiology ; Signal Transduction ; physiology

Actins ; immunology ; Adolescent ; Adult ; Aged ; Antibodies, Antineutrophil Cytoplasmic ; blood ; Antibodies, Antinuclear ; blood ; Autoantibodies ; blood ; Child ; Child, Preschool ; Female ; Hepatitis, Autoimmune ; diagnosis ; immunology ; Humans ; Male ; Middle Aged ; Muscle, Smooth ; immunology