ABSTRACT
Objective: To describe the prevalence of antiphospholipid antibodies in coronavirus disease-19 (COVID-19) and to find potential associations between antiphospholipid antibody positivity and clinical outcomes. Methods: From September to November 2020, clinical and laboratory data were collected from 50 COVID-19 patients hospitalized at Saiful Anwar General Hospital in Malang, Indonesia. Antiphospholipid antibodies were measured by finding IgM anti-β2 glycoprotein, lupus anticoagulant, and IgM/IgG anticardiolipin. Clinical characteristics, thrombotic events, ICU admission, and mortality during hospitalization were recorded. Disease severity was defined by the Guidelines for the Prevention and Control of COVID-19, Indonesia. Results: Among 50 patients, 5 patients (10.0%) were positive for antiphospholipid antibodies: 4 patients (80.0%) had IgM anti-β2 glycoprotein and 1 patient had IgG anti-cardiolipin (20.0%) and IgM anti-cardiolipin (20.0%), none of lupus anticoagulant was detected. Antiphospholipid antibodies were associated with anosmia (OR 8.1; 95% CI 1.1-57.9; P=0.018), nausea and vomiting (OR 12.4; 95% CI 1.2-122.6; P=0.010), diarrhea (OR 9.8; 95% CI 1.3-70.9; P=0.010), cardiovascular disease (OR 1.4; 95% CI 1.0-1.9; P=0.001), chronic kidney disease (OR 12.0; 95% CI 1.6-90.1; P=0.05), acute coronary syndrome (OR 29.3; 95% CI 2.0-423.7; P=0.001), moderate (OR 0.11; 95% CI 0.01-1.10; P=0.031) and severe (OR 18.5; 95% CI 1.8-188.4; P=0.002) disease severity, and in-hospital mortality (OR 8.1; 95% CI 1.1-57.9; P=0.018). However, there is no correlation between the presence of antiphospholipid antibody and ICU admission. Conclusions: In summary, the prevalence of antiphospholipid antibodies in COVID-19 patients is low, mainly against IgM anticardiolipin, and is associated with an acute coronary syndrome, gastrointestinal manifestations, moderate and severe disease severity, and increased risk of mortality.
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Introduction: Regulatory T cells’ (Tregs’) role remains unclear in the pathogenesis ofsystemic lupus erythematosus (SLE). This study was aimed at monitoring the percentage of Tregswithin 32 weeks and monitoring its relationship with the percentage of other T helper (Th) cellsubsets and the levels of autoantibodies and pro-inflammatory cytokines in a murine SLE modelinduced by pristane.Methods: Forty-eight female BALB/c mice were divided into a healthy control (HC) and apristine-induced (PI) group. SLE was induced by a single 0.5 cc pristane intraperitoneal injection.Six from each group were sacrificed every eight weeks until 32 weeks post-pristane injection. Treg,Th1, Th2 and Th17 percentages from the spleen were measured using flowcytometry. ANA, IL-6 andIFN-α levels were measured from serum using ELISA.Results: The Treg percentage from the PI group increased significantly at 16 weekscompared to the HC group, while Th1, Th2 and Th17 percentages decreased. Tregs in the PIgroup began to reduce from the 24th to 32nd weeks, followed by an elevation of the Th1, Th2and Th17 percentages. Tregs were negatively correlated with Th1 and Th2. Tregs in the PI grouphad a negative correlation with ANA and IFN-α levels from serum, whereas Tregs had a positivecorrelation with IL-6 levels.Conclusion: The compensation of Tregs observed at 16 weeks after pristane injectionfailed, marked by a decreasing number of Tregs, followed by an increase of Th subsets, proinflammatorycytokines and autoantibodies. This compensatory failure of Tregs could be affectedby pro-inflammatory cytokines, such as IFN-α and IL-6.
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Background: The innate immune response to tuberculosis infection may involve the increased production of nitric oxide and cathelicidin due to the up-regulated expression of the vitamin D receptor (VDR), though this proposed mechanism remains controversial. The aim of this study was to determine how the exposure of human monocytes to Mycobacterium tuberculosis (M. tuberculosis) DNA affects the production of nitric oxide and cathelicidin, as well as the expression of VDR. Methods: This study was performed using monocytes obtained from healthy donors. After 24 h incubation, monocytes were stimulated with M. tuberculosis DNA for 18 h to determine the expression of VDR mRNA and the production of nitric oxide and cathelicidin versus non-stimulated cells (the control group). Results: The expression of VDR mRNA was higher in the monocytes exposed to M. tuberculosis DNA compared to the control group (P = 0.020). Monocytes exposed to M. tuberculosis DNA also showed significantly increased production of nitric oxide and cathelicidin compared to the control group (P = 0.0001; P = 0.028). Conclusion: The stimulation of human monocytes with M. tuberculosis DNA increases the expression of the VDR mRNA and the production of nitric oxide and cathelicidin.
ABSTRACT
The sequestration of infected erythrocytes in the placenta can activate the syncytiotrophoblast to release cytokines that affect the micro-environment and influence the delivery of nutrients and oxygen to fetus. The high level of IL-10 has been reported in the intervillous space and could prevent the pathological effects. There is still no data of Th17 involvement in the pathogenesis of placental malaria. This study was conducted to reveal the influence of placental IL-17 and IL-10 levels on fetal weights in malaria placenta. Seventeen pregnant BALB/C mice were divided into control (8 pregnant mice) and treatment group (9 pregnant mice infected by Plasmodium berghei). Placental specimens stained with hematoxylin and eosin were examined to determine the level of cytoadherence by counting the infected erythrocytes in the intervillous space of placenta. Levels of IL-17 and IL-10 in the placenta were measured using ELISA. All fetuses were weighed by analytical balance. Statistical analysis using Structural Equation Modeling showed that cytoadherence caused an increased level of placental IL-17 and a decreased level of placental IL-10. Cytoadherence also caused low fetal weight. The increased level of placental IL-17 caused low fetal weight, and interestingly low fetal weight was caused by a decrease of placental IL-10. It can be concluded that low fetal weight in placental malaria is directly caused by sequestration of the parasites and indirectly by the local imbalance of IL-17 and IL-10 levels.