Modulation of cytokine production from an EpiOcular corneal cell culture model in response to Staphylococcus aureus superantigen

The present study investigated the hypothesis that Staphylococcus aureus enterotoxin B (SEE) produces epithelial cell death and releases inflammatory cytokines that produce stromal infiltration during contact lens induced peripheral ulceration. Epithelial cells were incubated with different doses of SEB for various time periods. Culture supernatants were assayed for cytokines IL- lo, IL-6 and chemotactic agents IL-8 and LTB,. SEE induced the production of IL- I p and IL-8. Epithelial cells exposed for longer periods (48 h) with low concentrations of SEB produced significantly higher levels (N0.02) of IL-Ip and IL-8 (P<0.05) compared t o a 24 h exposure. SEB did not induce the production o f IL-6 and     

Localization of mRNA for inflammatory cytokines in radicular cyst tissue by in situ hybridization, and induction of inflammatory cytokines by human gingival fibroblasts in response to radicular cyst contents

The expression of mRNA encoding the inflammatory cytokines interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor α (TNF-α) have been examined in radicular cysts by in situ hybridization. Furthermore, the biological activity of the contents of radicular cysts (RCC) has been assayed by adding extracts of RCC to cultured human gingival fibroblasts (HGFs) and analyzing the culture medium for the release of inflammatory cytokines. In the epithelial layer, keratinocytes expressed all cytokine mRNAs examined at various levels. Basal layer cells expressed mRNA for each cytokine. In the subepithelial granulation tissue of the cysts, fibroblasts and macrophages expressed mRNA for IL-6, IL-8, IL-1β and TNF-α mRNA at varying levels; especially clear expression of TNF-α and IL-1β mRNA was detected on macrophages. The infiltrating lymphoid cells, largely composed of T cells and plasma cells, expressed these cytokine mRNAs, especially those encoding IL-6 and IL-8, at various levels. In vitro analysis indicated dose-dependent release of both IL-6 and IL-8 by HGFs in response to RCC. After heating to 100°C for 10 min, RCC almost completely failed to stimulate IL-6 release from HGFs. Furthermore, anti-IL-1β antibody (neutralization test) did not prevent the stimulation of IL-6 release by RCC. Significant amounts of IL-6 and IL-8 were detected in RCC in two cases, and a trace amount of IL-1β was detected in one case. This study demonstrated the wide expression of mRNA encoding inflammatory cytokines in radicular cyst tissues, and RCC itself was capable of stimulating 1L-6 and 1L-8 production from HGFs.     

Detection of cytoplasmic IL-1 beta in peripheral blood mononuclear cells from intensive care unit (ICU) patients.

Cytokines including IL-1 beta have been implicated in the pathophysiology of sepsis and the systemic inflammatory response. It is believed that certain critically ill patients may be 'primed' with respect to cytokine production, and that subsequent 'triggers' may cause exaggerated cytokine production in these patients with exacerbation of their clinical condition; however, no means of identifying 'primed' patients has been described. The presence of cytoplasmic IL-1 beta within peripheral blood mononuclear cells (PBMC) from patients in the ICU was investigated as a means of identifying 'primed' patients, using fluorescent antibody labelling and flow cytometry. The study revealed that PBMC from ICU patients had a different staining pattern for IL-1 beta than those from healthy subjects, and that PBMC from certain ICU patients did indeed stain strongly for IL-1 beta; however, the presence of these strongly staining cells was not associated with clinical condition or outcome. It is concluded that whilst it might be possible to identify 'primed' patients in the ICU using this technique, this is of no clinical value as a predictor of clinical course.     

Contraception and sexually transmitted diseases: Interactions and opportunities

Today "safe sex" means protection from both unintended pregnancy and sexually transmitted disease and human immunodeficiency virus. These parallel complications of sexual activity have serious biologic and clinical sequelae that should be considered at the time of contraceptive selection. In addition, there is ongoing debate regarding potential interactions between antibiotic intervention and contraceptive steroids. This article assesses the impact of hormonal contraception, spermicides, barrier methods, intrauterine devices, and douching on the pathogenesis of sexually transmitted disease and the human immunodeficiency virus infection. It discusses the direct and indirect effects of contraception methods on clinical physiology and host immune responses while also considering the possible consequences on maternal and infant health if pregnancy results from the use of ineffective contraception. Counseling and care for both family planning and infectious disease protection must be provided to all sexually active individuals. (Ann J OBSTET GVNECOL 1993;168:2033-41.)     

Overexpression of suppressor of cytokine signalling-5 augments eosinophilic airway inflammation in mice

BACKGROUND: Enhanced expression of the suppressor of cytokine signalling (SOCS)-5 might be of therapeutic benefit for T-helper type 2 (Th2) dominant diseases, as its expression is reported to result in a reduction of Th2 differentiation in vitro due to the inhibition of IL-4 signalling. OBJECTIVE: To investigate the regulatory role of SOCS-5 in vivo, we explored the phenotype of an experimental asthma model developed in SOCS-5 transgenic (Tg) mice. METHODS: The SOCS-5 Tg mice or wild-type (WT) mice were sensitized and repeatedly challenged with ovalbumin (OVA). We examined bronchoalveolar lavage fluid (BALF), lung specimens, and airway hyperresponsiveness (AHR) to methacholine. RESULTS: The production of IFN-gamma by CD4(+) T cells from unprimed SOCS-5 Tg mice was significantly increased in comparison with unprimed wild-type mice, indicating that SOCS-5 Tg mice have a Th1-polarizing condition under natural conditions. However, in an asthma model, significantly more eosinophils in the airways and higher levels of IL-5 and IL-13 in BALF were observed in the SOCS-5 Tg than the wild-type mice. AHR in the asthma model of SOCS-5 Tg was also more enhanced than that of wild-type mice. OVA-stimulated CD4(+) T cells from the primed SOCS-5 Tg mice produced significantly more IL-5 and IL-13 than CD4(+) T cells from wild-type mice. CONCLUSION: Our results demonstrate that the overexpression of SOCS-5 does not inhibit Th2 response, but rather augments the phenotype of the asthma model in vivo. This finding throws into question the therapeutic utility of using enhancement of SOCS-5 expression for Th2-dominant disease.     

Fallopian tube carcinoma presenting as tubo-ovarian abscess: a report of two cases with literature review

Preoperative diagnosis of fallopian tube carcinoma is difficult, with fewer than 5% being diagnosed preoperatively. We describe tubal carcinoma, presenting as a tubo-ovarian abscess in two 47-year-old women. Both patients presented with abdominal pain, pelvic mass, and fever. Both patients were treated as having a tubo-ovarian abscess but failed to respond to therapy. During surgery a metastatic right tubal carcinoma was found. A definite operation was performed in both patients. Three additional cases of fallopian tube carcinoma, presenting as acute pelvic inflammatory disease, were found while reviewing the English literature. Actually all these three cases presented as tubo-ovarian abscess because of the existence of tender pelvic mass. Carcinoma of the fallopian tube should be considered in the differential diagnosis of tubo-ovarian abscess in those who failed to respond to a previously unreported clinical presentation.     

急性冠脉综合征患者循环内皮祖细胞与炎性相关因子的研究

目的:探讨急性心肌梗死(AMI)、不稳定性心绞痛(UA)患者外周血中循环内皮祖细胞(EPCs)与炎性相关因子C反应蛋白质(CRP)、白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)的相关性。方法:取AMI(25例)UA患者(28例)及健康体检者(对照组32例)静脉血,采用密度梯度离心法从外周血获得单个核细胞;激光共聚焦显微镜鉴定FITC-UEA-I和Dil-acLDL双染色阳性细胞为正在分化的EPCs,并在倒置荧光显微镜下计数;酶联免疫法检测各种炎性相关因子。结果:AMI组及UA组的EPCs数量和血清CRPI、L-6、TNF-α水平显著高于正常对照组。结论:AMI及UA患者EPCs数量增加与炎性相关因子增加有关。     

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.