From the Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden; Department of Microbiology and Immunology, The Affiliated Hospital of GuiZhou Medical University, Guiyang, China; Department of Rheumatology, and Department of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
A. Mitander, MD, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, and Department of Rheumatology, Sahlgrenska University Hospital; Y. Fei, MSc, Professor, Department of Microbiology and Immunology, The Affiliated Hospital of GuiZhou Medical University; E. Trysberg, MD, PhD, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, and Department of Rheumatology, Sahlgrenska University Hospital; M. Mohammad, MSc, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg; Z. Hu, MSc, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, and Department of Microbiology and Immunology, The Affiliated Hospital of GuiZhou Medical University; E. Sakiniene, MD, PhD, Department of Rheumatology, Sahlgrenska University Hospital; R. Pullerits, MD, PhD, Associate Professor, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, and Department of Rheumatology, and Department of Clinical Immunology and Transfusion Medicine, Sahlgrenska University Hospital; T. Jin, MD, PhD, Associate Professor, Department of Rheumatology and Inflammation Research, Institution of Medicine, Sahlgrenska Academy at University of Gothenburg, and Department of Rheumatology, Sahlgrenska University Hospital.
J Rheumatol. 2018 Nov;45(11):1557-1564. doi: 10.3899/jrheum.171325. Epub 2018 Sep 1.
Infections remain a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). The high prevalence of infections in SLE is attributed to both the disease and its treatments. The complement system plays an important role in host immune responses against invading microorganisms. We sought to provide the experimental and clinical evidence supporting the hypothesis that low levels of complement factors cause defective complement-mediated opsonization in patients with SLE.
was opsonized with sera from healthy individuals (n = 16), SLE patients with normal (n = 5) or low complement (n = 8) levels. Phagocytosis of by healthy human neutrophils was analyzed by an imaging flow cytometry-based method. We retrospectively examined the infection incidence in relation to complement levels in a cohort of 165 patients with SLE during a 1.5-year period. The association was analyzed for infection incidence and disease-related variables.
Uptake of by neutrophils was decreased when was opsonized with sera from SLE patients with low complement levels compared to sera from healthy individuals and SLE patients with normal complement. In our SLE cohort, 44% of patients had at least 1 infection during the 1.5 years. No significant association was observed between complement levels and infection risk. Importantly, high-dose glucocorticoids (GC; prednisone ≥ 10 mg/day) were the most important predictive factor for infections in patients with SLE.
Low complement levels affect bacterial opsonization in SLE blood and lead to downregulated phagocytosis by neutrophils. High-dose GC increase the infection risk in patients with SLE.
感染仍然是红斑狼疮（SLE）患者发病率和死亡率的主要原因。SLE 感染率高归因于疾病及其治疗方法。补体系统在宿主对入侵微生物的免疫反应中起着重要作用。我们试图提供支持低水平补体因子导致 SLE 患者补体介导调理作用缺陷的假说的实验和临床证据。
用来自健康个体（n=16）、补体水平正常（n=5）或低（n=8）的 SLE 患者的血清对进行调理。通过基于成像流式细胞术的方法分析健康人中性粒细胞对的吞噬作用。我们回顾性地检查了 165 例 SLE 患者在 1.5 年期间与补体水平相关的感染发生率。分析了感染发生率与疾病相关变量之间的关联。
与用健康个体和补体水平正常的 SLE 患者的血清调理的相比，用补体水平低的 SLE 患者的血清调理时，中性粒细胞对的摄取减少。在我们的 SLE 队列中，44%的患者在 1.5 年内至少发生了 1 次感染。未观察到补体水平与感染风险之间存在显著相关性。重要的是，大剂量糖皮质激素（GC；泼尼松≥10mg/天）是 SLE 患者感染的最重要预测因素。
低补体水平会影响 SLE 血液中的细菌调理作用，并导致中性粒细胞吞噬作用下调。大剂量 GC 会增加 SLE 患者的感染风险。
