Progressive enlargement of a mass lesion in late cerebral radionecrosis

The progressive enlargement of a mass lesion in late cerebral radionecrosis (LCR) was studied using a surgical specimen from a woman’s irradiated brain. Using immunohistochemical (IHC) staining on paraffin-embedded sections, expression of tumor necrosis factor-alpha (TNF??), interleukin (IL)6, Flk-1, and vascular endothelial growth factor (VEGF) was semi-quantitatively evaluated in the necrotic area and areas distant and adjacent to the necrotic area. High immunoreactivity for TNF??, IL6, and VEGF in regions distant to the necrotic core were strongly associated with inflammatory cell density, hyalinized vessels, and vascularization. Ghost cells stained with glial fibrillary acidic protein (GFAP), Ki-M1P, KP-1, ubiquitin-C-terminal hydrolase 1, and fibrinoid necrosis were observed in the necrotic area and adjacent regions. These results suggest that necrotic factors, inflammatory reaction, and angiogenetic factors act temporally and spatially through radiation-induced vascular endothelial cell damage to contribute to the progressive enlargement of an enhancing mass lesion in LCR.     

内毒素增敏系统与严重烧伤脓毒症的关系及其临床意义

目的 探讨严重烧伤患者内毒素增敏系统--脂多糖结合蛋白/脂多糖受体CD14(LBP/CD14)的变化与严重脓毒症的关系及其临床意义.方法 选择35例烧伤体表总面积大于30%患者,根据烧伤脓毒症的定义和诊断标准分为脓毒症组(19例)和非脓毒症组(16例),应用酶联免疫吸附试验检测患者烧伤后1、3、5、7、14、21、28...     

高血压大鼠局灶性脑缺血再灌注后IL-6mRNA在神经元和星形胶质细胞的表达

目的观察白细胞介素-6(IL-6)mRNA在高血压大鼠局灶性脑缺血一再灌注(isehemia reperfusion，IR)后不同部位及细胞来源的表达。方法采用双肾双夹法制成高血压模型和线栓法制成大脑中动脉栓塞模型。采用原位杂交免疫组化和免疫组化双重染色方法检测IL-6mRNA，并做脑组织HE染色。结果缺血2h再灌注不同时间IL-6mRNA在缺血周边区有明显表达，以再灌注24h后表达最高，且IL-6mRNA表达主要在神经元。结论脑IR后以神经元表达IL-6mRNA为主，且缺血周围区表达最明显，并在IR后期仍维持较高水平。     

Placental p,p''-dichlorodiphenyldichloroethylene and cord blood immune markers

Placental p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) concentration and cord blood atopic markers were determined in 19 neonates. Increased placental p,p'-DDE was associated with a statistically significant increase in cord plasma interleukin (IL)-13. Furthermore, both cord plasma IL-4/interferon (IFN)-gamma and IL-13/IFN-gamma ratios were significantly positively associated with placental p,p'-DDE concentration.     

Immunomodulatory constituents of human milk change in response to infant bronchiolitis

Although epidemiological evidence is generally supportive of a causal association between respiratory syncytial virus (RSV) bronchiolitis during infancy and the development of persistent wheeze/asthma, if not allergy, the mechanism by which this occurs and an explanation for why all children do not succumb remains to be elucidated. Breast feeding has been found to confer a protective effect against respiratory infections such as RSV bronchiolitis and allergy; however, again there is little direct evidence and no clear mechanism. In this study, we examined whether human milk immunomodulatory factors (cells, cytokines) change in response to clinically diagnosed, severe bronchiolitis in the recipient breast-fed infant. We examined milk from 36 breast feeding mothers of infants hospitalized with bronchiolitis and compared them with milk from 63 mothers of postpartum age-matched healthy controls. Milks from mothers of infants hospitalized with bronchiolitis had significantly greater numbers of viable cells when compared with the milks obtained from mothers of healthy infants (1.3 +/- 0.4 vs. 0.3 +/- 0.03 x 10(6) cells/ml, mean +/- s.e.m.; p < or = 0.001). Further, the cells obtained from the mothers of infants hospitalized with bronchiolitis were found to produce a skewed cytokine profile ex vivo in response to stimulation by live RSV but not when cultured with a non-specific mitogen (concanavalin A). This study provides preliminary evidence for an immunological link between mothers and their breast-fed infants during severe respiratory infections as well as a possible contributing factor to the development of persistent wheeze in these infants.     

Allergen-induced cytokine phenotypes in mice: role of CD4+ and CD8+ T cell populations

BACKGROUND: CD4+ T cells expressing type 2 cytokines have been implicated in the pathogenesis of asthma to high-molecular-weight allergens. Topical exposure of BALB/c strain mice to low-molecular-weight chemical contact and respiratory allergens stimulates type 1 and type 2 cytokine secretion phenotypes, respectively. OBJECTIVE: To examine the relative frequencies of cytokine-positive CD4+ and CD8+ T cells and their contributions to these cytokine secretion profiles. Methods Draining auricular lymph nodes were isolated 13 days after initiation of topical exposure of female BALB/c strain mice to chemical allergen, or to vehicle alone. The frequency of intracellular cytokine (IL-4 and IFN-gamma)-positive CD4+ and CD8+ lymphocytes was enumerated by flow cytometry. The relative contribution of CD4+ and CD8+ cells to cytokine secretion profiles was assessed by negative selection. RESULTS: Exposure to allergen resulted in an increased frequency of both IFN-gamma+ CD4+ and CD8+ lymphocytes, although there were no marked differences between trimellitic anhydride (TMA)- and 2,4-dinitrochlorobenzene (DNCB)-activated lymph node cells. Treatment with TMA induced approximately five times as many IL-4+ CD4+ cells as did exposure to DNCB. This pattern of cytokine staining was also observed for a further pair of contact and respiratory allergens; respectively, formalin and fluorescein isothiocyanate. CONCLUSION: These data demonstrate that the divergent immune responses induced in mice by different classes of chemical allergen are independent of changes in the frequency of IFN-gamma+ cells, but are associated with differential frequencies of IL-4-expressing CD4+ T cells.     

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by α-adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.     

Modulation of Langerhans cell surface antigen expression by recombinant cytokines

This study examined the influence of cytokines on surface antigen expression by gingival Langerhans cells (LC) in organ culture, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) upregulated the expression of CD1a, HLA-DR and HLA-DP antigens on LC. TNF-alpha, interleukin-4 (IL-4), and transforming growth factor beta (TGF-beta) suppressed CD29 expression, while other cytokines, including interleukin-3 and granulocyte-macrophage colony stimulating factor, were without effect. No cytokines induced CD3, CD4, CD23, CD25 or CD45 RA antigen expression in organ culture. Since TNF-alpha and IL-6 can be secreted by keratinocytes, these molecules, together with interleukin-1, are likely to play a role in the local control of LC number and function within the epithelial milleu. Thus, alterations in cytokine secretion by keratinocytes may at least in part be responsible for variations in LC number and antigen expression which occur in oral mucosal disorders.