POSTHEMORRHAGIC SHOCK MESENTERIC LYMPH IMPAIRS SPLENIC DENDRITIC CELL FUNCTION IN MICE.

ABSTRACT: Dendritic cell (DC)-mediated immune dysfunction is involved in the process of severe hemorrhagic shock that leads to sepsis. Although post-hemorrhagic shock mesenteric lymph (PHSML) induces immune organs injuries and apoptosis, whether PHSML exerts adverse effects on splenic DCs remains unknown. In this study, we established a hemorrhagic shock model (40 ± 2 mm Hg for 60 min) followed by fluid resuscitation with the shed blood and equal Ringer's solution and drained the PHSML after resuscitation. At 3 h after resuscitation, we harvested the splenic tissue to isolate DCs using anti-CD11c immunomagnetic beads and then detected the necrotic and apoptotic rates in splenocytes and splenic DCs. We also detected the levels of TNF-α, IL-10, and IL-12 in the culture supernatants and surface marker expressions of MHC-II, CD80, and CD86 of splenic DCs following LPS stimulation for 24 h. Second, we purified the DCs from splenocytes of normal mice to investigate the effects of PHSML treatment on cytokine production and surface marker expression following LPS stimulation. The results showed that PHSML drainage attenuated LPS-induced cell death of splenocytes and DCs. Meanwhile, PHSML drainage enhanced the DC percentage in splenocytes and increased the TNF-α and IL-12 production by DCs and the expressions of CD80, CD86, and MHCII of DCs treated by LPS. Furthermore, PHSML treatment reduced the productions of TNF-α, IL-10, and IL-12 and the expressions of CD80 and CD86 in normal DCs after treatment with LPS. In summary, the current investigation demonstrated that PHSML inhibited the cytokine production and surface marker expressions of DCs stimulated by LPS, suggesting that PHSML plays an important role in hemorrhagic shock-induced immunosuppression through the impairment of DC function and maturation.

Clinical and pathological analysis of solitary fibrous tumors with portal vein widening: A case report.

RATIONALE: Solitary fibrous tumors (SFTs) are rare soft-tissue tumors characterized with spindle-cell, which occur more common in the chest and rarely seen in the abdomen. So far as we knew, SFTs accompanied with venopathy of portal vein has rarely been reported. PATIENT CONCERNS: A 36-year-old male presented with left-sided abdominal mass and portal vein expansion on ultrasound. DIAGNOSES: The post-operative histopathology confirmed the diagnosis of Solitary fibrous tumor. INTERVENTIONS: Laparotomy was performed and the mass was completely removed. OUTCOMES: Patients had no symptoms, recovered well without recurrence; the portal vein and splenic vein dilatation were alleviated and the symptoms of portal hypertension were relieved. LESSONS: SFTs presents with few symptoms in the early stage of the disease. A rich arteriovenous shunt is beneficial to the diagnosis of SFTs by B-ultrasound and computed tomography (CT) examinations. However, the diagnosis of SFTs must depend on histopathology.

Dynamic changes of IL-2/IL-10, sFas and expression of Fas in intestinal mucosa in rats with acute necrotizing pancreatitis.

AIM: To investigate dynamic changes of serum IL-2, IL-10, IL-2/IL-10 and sFas in rats with acute necrotizing pancreatitis. To explore the expression of Fas in intestinal mucosa of rats with acute necrotizing pancreatitis (ANP). METHODS: A total of 64 Sprague-Dawley (SD) rats were randomly divided into two groups: normal control group (C group), ANP group (P group). An ANP model was induced by injection of 50 g/L sodium taurocholate under the pancreatic membrane. Normal control group received isovolumetric injection of 9 g/L physiological saline solution using the same method. The blood samples of the rats in each group were obtained via superior mesenteric vein to measure levels of IL-2, IL-10, sFas and calculate the value of IL-2/IL-10. The levels of IL-2, IL-10 and sFas were determined by ELISA. The severity of intestinal mucosal injury was evaluated by pathologic score. The expression of Fas in intestinal mucosal tissue was determined by immunohistochemistry staining. RESULTS: Levels of serum IL-2 were significantly higher in P group than those of C group (2.79 +/- 0.51 vs 3.53 +/- 0.62, 2.93 +/- 0.89 vs 4.35 +/- 1.11, 4.81 +/- 1.23 vs 6.94 +/- 1.55 and 3.41 +/- 0.72 vs 4.80 +/- 1.10, respectively, P < 0.01, for all) and its reached peak at 6 h. Levels of serum IL-10 were significantly higher in P group than those of C group at 6 h and 12 h (54.61 +/- 15.81 vs 47.34 +/- 14.62, 141.15 +/- 40.21 vs 156.12 +/- 43.10, 89.18 +/- 32.52 vs 494.98 +/- 11.23 and 77.15 +/- 22.60 vs 93.28 +/- 25.81, respectively, P < 0.01, for all). The values of IL-2/IL-10 were higher significantly in P group than those of C group at 0.5 h and 2 h (0.05 +/- 0.01 vs 0.07 +/- 0.02 and 0.02 +/- 0.01 vs 0.03 +/- 0.01, respectively, P < 0.01, for all), and it were significantly lower than those of C group at 6 h (0.05 +/- 0.02 vs 0.01 +/- 0.01, P < 0.01) and returned to the control level at 12 h (0.04 +/- 0.01 vs 0.05 +/- 0.02, P > 0.05). In sFas assay, there was no significant difference between P group and C group (3.16 +/- 0.75 vs 3.31 +/- 0.80, 4.05 +/- 1.08 vs 4.32 +/- 1.11, 5.93 +/- 1.52 vs 5.41 +/- 1.47 and 4.62 +/- 1.23 vs 4.44 +/- 1.16, respectively, P > 0.05, for all). Comparison of P group and C group, the pathological changes were aggravated significantly in P group. Immunohistochemistry staining show the expression of Fas was absent in normal intestinal tissues, however, it gradually increased after induction of pancreatitis in intestinal tissue, then reached their peaks at 12 h. CONCLUSION: Fas were involved in the pathogenesis of pancreatitis associated intestinal injury. The mechanisms of Fas may be associated to Fas mediated T helper cell apoptosis.

Hemogram and bone marrow morphology in children with chronic aplastic anemia and myelodysplastic syndrome.

BACKGROUND: Aplastic anemia (AA) and myelodysplastic syndrome (MDS) are both acquired disorders in which bone marrow fails to produce or release sufficient blood cells. Anemia, infections and thrombocytopenia are common signs of such diseases. Clinically, it is difficult to distinguish chronic aplastic anemia (CAA) from MDS, especially from MDS without splenomegaly. As prognosis and treatment of AA and MDS are different, it is extremely important to make a differential diagnosis for the two diseases. METHODS: The medical records of 31 patients with CAA and 17 patients with MDS were retrospectively reviewed. Hemogram, bone marrow smear and biopsy for those patients were analyzed. RESULTS: The mean counts of monocytes and platelets in the peripheral blood of the CAA patients were significantly lower than those of the MDS patients. Bone marrow smear showed a reduction of cellularity in CAA patients. The mean counts of myeloblasts+promyelocytes, myeloblasts+proerythroblasts, and megakaryocytes in the bone marrow of CAA patients were markedly lower than those in MDS patients. But the mean lymphocyte count was reversed. Bone marrow cells showed morphological abnormalities in MDS. Hematopoietic tissue in the bone marrow biopsy decreased obviously in more than 96% of the patients with CAA. Adipose tissue in the bone marrow of CAA patients increased obviously. A reduction or deficiency (<2 cell/piece) of megakaryocytes was noted in 28 patients with CAA. Fibrous tissue in the bone marrow was detected in 5 patients with CAA. Bone marrow biopsy results showed hypercellular changes in 12 MDS patients. Ten patients showed aggregated erythroblasts which were in the same stage of development, and 15 patients had abnormal localization of immature precursors (ALIP). CONCLUSIONS: Blood cell counts can be decreased in addition to the reduction of cellularity in the bone marrow without dyshematopoiesis in CAA patients. Peripheral blood monocytes, fibrous tissue and cellularity in bone marrow are increased in MDS. Dyshematopoiesis and ALIP may appear characteristically in the children with MDS. Histology of bone marrow is important in the differential diagnosis of MDS and CAA.