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BACKGROUND: Venovenous extracorporeal membrane oxygenation (V-V ECMO) has become an important treatment for severe pneumonia, but there are various complications during the treatment. This article describes a case with severe pneumonia successfully treated by V-V ECMO, but during treatment, the retrovenous catheter, which was supposed to be in the right internal vein, entered the superior vena cava directly in the mediastinum. The ECMO was safely withdrawn after multidisciplinary consultation. Our experience with this case is expected to provide a reference for colleagues who will encounter similar situations. CASE SUMMARY: A 64-year-old man had severe pulmonary infection and respiratory failure. He was admitted to our hospital and was given ventilation support (fraction of inspired oxygen 100%). The respiratory failure was not improved and he was treated by V-V ECMO, during which the venous return catheter, which was supposed to be in the right internal vein, entered the superior vena cava directly in the mediastinum. There was a risk of massive mediastinal bleeding if the catheter was removed directly when the ECMO was withdrawn. Finally, the patient underwent vena cava angiography + balloon attachment + ECMO withdrawal in the operating room (prepared for conversion to thoracotomy for vascular exploration and repair at any time during surgery) after multidisciplinary consultation. ECMO was safely withdrawn, and the patient recovered and was discharged. CONCLUSION: Patients may have different vascular conditions. Multidisciplinary cooperation can ensure patient safety. Our experience will provide a reference for similar cases.
RESUMO
BACKGROUND: Mitofusin-2 (MFN2), a well-known mitochondrial fusion protein, has been shown to participate in innate immunity, but its role in mediating adaptive immunity remains poorly characterized. In this study, we explored the potential role of MFN2 in mediating the immune function of T lymphocytes. METHODS: We manipulated MFN2 gene expression in Jurkat cells via lentiviral transduction of MFN2 small interfering RNA (siRNA) or full-length MFN2. After transduction, the immune response and its underlying mechanism were determined in Jurkat cells. One-way analysis of variance and Student's t-test were performed to determine the statistical significance between the groups. RESULTS: Overexpression of MFN2 enhanced the immune response of T lymphocytes by upregulating Ca2+ (359.280 ± 10.130 vs. 266.940 ± 10.170, P = 0.000), calcineurin (0.513 ± 0.014 vs. 0.403 ± 0.020 nmol/L, P = 0.024), and nuclear factor of activated T cells (NFATs) activation (1.040 ± 0.086 vs. 0.700 ± 0.115, P = 0.005), whereas depletion of MFN2 impaired the immune function of T lymphocytes by downregulating Ca2+ (141.140 ± 14.670 vs. 267.060 ± 9.230, P = 0.000), calcineurin (0.054 ± 0.030 nmol/L vs. 0.404 ± 0.063 nmol/L, P = 0.000), and NFAT activation (0.500 ± 0.025 vs. 0.720 ± 0.061, P = 0.012). Furthermore, upregulated calcineurin partially reversed the negative effects of MFN2 siRNA on T cell-mediated immunity evidenced by elevations in T cell proliferation (1.120 ± 0.048 vs. 0.580 ± 0.078, P = 0.040), interleukin-2 (IL-2) production (473.300 ± 24.100 vs. 175.330 ± 12.900 pg/ml, P = 0.000), and the interferon-γ/IL-4 ratio (3.080 ± 0.156 vs. 0.953 ± 0.093, P = 0.000). Meanwhile, calcineurin activity inhibitor depleted the positive effects of overexpressed MFN2 on T cells function. CONCLUSIONS: Our findings suggest that MFN2 may regulate T cell immune functions primarily through the Ca2+-calcineurin-NFAT pathway. MFN2 may represent a potential therapeutic target for T cell immune dysfunction-related diseases.