Unilateral pulmonary oedema: a case report and literature review.

Acute myocarditis is often secondary to an acute virus infection, which can be the first manifestation of upper respiratory tract symptoms, followed by chest tightness, shortness of breath, palpitations, chest pain and other non-specific symptoms. In severe cases, it can quickly progress to serious complications such as heart failure, shock and respiratory failure. Laboratory examinations can show an increase of myocardial injury markers, infection and inflammatory indicators. Cardiac ultrasound can detect the weakening of the myocardial contraction and valve regurgitation. On imaging, bilateral pulmonary oedema demonstrates symmetrical infiltration along the hilum of lung, called the "butterfly shadow". This current case report describes a patient with unilateral pulmonary oedema caused by myocarditis that was initially misdiagnosed and treated as pneumonia. The patient was subsequently treated with the application of extracorporeal membrane oxygenation and he made a full recovery. A review of this case highlights that when a patient's symptoms are not typical, a comprehensive examination and evaluation are required to avoid incorrect treatment.

18ß-glycyrrhetinic acid inhibits hepatocellular carcinoma development by reversing hepatic stellate cell-mediated immunosuppression in mice.

Hepatic stellate cells (HSCs) have immunosuppressive capabilities and contribute to the occurrence and development of hepatocellular carcinoma (HCC). Thus, activated HSCs may be a suitable target for HCC therapy. Our study used mixed leukocyte reactions (MLR) in vitro to demonstrate that 18ß-glycyrrhetinic acid (GA) could reverse HSC-mediated immunosuppression by reducing T-cell apoptosis and regulatory T (Treg) cells expression, thereby enhancing the ability of T cells to attack tumor cells and attenuating HCC cell invasiveness. Moreover, we established a HCC orthotopic implantation model in immunocompetent C57BL/6 mice, which suggested that GA played a protective role in HCC development by reducing immunosuppression mediated by HSCs in the tumor microenvironment.

Bear bile inhibits the immunosuppression activity of hepatic stellate cells in vivo.

BACKGROUND/AIMS: In the injured liver, hepatic stellate cells (HSCs) induce immunosuppression activity and thus participate in the pathogenesis of liver disease, including HCC. Therefore, finding new drugs to inhibit their immunosuppression activity is necessary. This study tests whether bear bile can affect the immunosuppression activities of HSCs. METHODOLOGY: The mice were gavaged with bear bile for 4 weeks. The expression of HSCs was detected through desmin and ±-smooth muscle antibody immunohistochemistry. HSCs were isolated from these mice liver and then cultured with T cells in a mixed leukocyte reaction for 3 days. Stellate cell surface makers, T-cell apoptosis, regulatory T cells and the ability of T cells to kill hepatocellular carcinoma were determined via flow cytometry. Cytokines were determined by a mouse cytokine array panel and T-cell proliferation was determined through a BrdU kit. RESULTS: Bear bile decreased HSCs and their surface molecules, and affected cytokine secretion. Interestingly, HSCs from the mice gavaged with bear bile promoted T-cell proliferation, inhibited T-cell apoptosis, decreased CD4+CD25+Foxp3+ regulatory T cells and enhanced the activation of T cells killing hepatocellular carcinoma. CONCLUSIONS: Bear bile can inhibit the immunosuppression activity of HSCs and enhance immune response especial anti-tumor immune response.

The role of hepatic stellate cells in the regulation of T-cell function and the promotion of hepatocellular carcinoma.

Hepatic stellate cells (HSCs) have immunosuppressive abilities and may be responsible for the occurrence and development of hepatocellular carcinoma (HCC). However, the mechanisms through which HSCs affect T-cell-mediated immune responses remain unclear. The aim of this study was to elucidate these mechanisms. We examined the effect of HSCs on T-cell proliferation and apoptosis, regulatory T cells (Treg cells) and T-cell-mediated cytotoxicity using mixed leukocyte reactions (MLRs). Furthermore, we examined the cytokines present in the supernatant and the effect of this supernatant on the proliferation and migration of cancer cells. Finally, we examined the effect of HSCs on HCC cells in vivo. We found that activated HSCs induced T-cell hyporesponsiveness, accelerated activated T-cell apoptosis, increased the number of Treg cells and inhibited T-cell-mediated cytotoxicity. HSCs also enhanced the expression of some cytokines and promoted the proliferation and migration of cancer cells. Furthermore, activated HSCs were able to induce HCC proliferation and Treg cells expansion in vivo. Activated HSCs may induce T cell anergy, thereby facilitating the immunologic escape of HCC cells.

Activated hepatic stellate cells promote hepatocellular carcinoma development in immunocompetent mice.

Activated hepatic stellate cells (HSCs) play a central role in the hepatic fibrosis and cirrhosis. Recently, HSCs were reported to have strong immune modulatory activities. However, the role of HSCs in hepatocellular carcinoma (HCC) remains unclear. In this study, we showed that HSCs could promote HCC growth both in vitro and in vivo. We examined the HSC-mediated inhibition of T-cell proliferation and the ability of conditioned medium from activated HSCs to promote the growth of murine HCC cell lines in vitro. We also assessed the immune suppression by HSCs during the development of HCC in immunocompetent mice. Cotransplantation of HSCs promoted HCC growth and progression by enhancing tumor angiogenesis and tumor cell proliferation and by creating an immunosuppressed microenvironment. Cotransplanted HSCs inhibited the lymphocyte infiltration in tumors and the spleens of mice bearing tumors, induced apoptosis of infiltrating mononuclear cells, and enhanced the expression of B7H1 and CD4(+) CD25(+) Treg cells. The immune modulation by HSCs seemed to be systemic. In conclusion, our data provide new information to support an integral role for HSCs in promoting HCC progression in part via their immune regulatory activities, and suggest that HSCs may serve as a therapeutic target in HCC.