BMC Immunology最新文献

Background: Chronic low-grade inflammation is often seen in individuals with insulin resistance, characterised by increased levels of pro-inflammatory cytokines, such as TNF-α (tumour necrosis factor-alpha) and IL-6 (interleukin-6). Insulin resistance (IR) and vitamin D deficiency are increasingly recognised as interconnected metabolic issues. Research indicated that low vitamin D levels may impair insulin sensitivity, while insulin resistance can worsen vitamin D deficiency, creating a vicious cycle. This study aims to explore the relationship between TNF-α and IL-6 expression levels and vitamin D levels in insulin-resistant patients with type 2 diabetes mellitus (DM), and compare them with non-diabetic controls to better understand the role of vitamin D in inflammation, disease development, and progression.

Methods: From a total of 150 participants, 30 were healthy individuals (the control group), and 120 were patients with type II diabetes. The current case-control study compared TNF-α, IL-6 expression levels, and serum vitamin D levels between insulin-resistant patients and non-diabetic controls.

Results: The demographic and clinical variables were statistically significant. The case-to-control ratio was 4:1. Higher levels of TNF-α and IL-6 were found in DM patients compared to non-diabetic controls. Insulin-resistant patients exhibited higher IL-6 levels (5.47 ± 0.30 pg/ml) than healthy participants (2.64 ± 0.83 pg/ml), with p-value < 0.001. Vitamin D levels were significantly lower in DM patients (22.33 ± 11.43 ng/ml) compared to healthy subjects (34.12 ± 2.08 ng/ml), with p-value < 0.001. TNF-α levels were also significantly higher in DM patients (7.99 ± 0.35 pg/ml) (p-value < 0.001) than in the healthy group (4.24 ± 0.27 pg/ml). Using qPCR and measuring disease severity, the relationship between cytokine gene expression and insulin resistance was assessed. The positive associations between TNF-α, IL-6, vitamin D deficiency, poor glycaemic control, and other disease conditions reflect a fundamental pathophysiological mechanism in insulin resistance in DM patients. This ultimately leads to increased inflammation and tissue damage, worsening the complications of diabetes.

Background: Malaria, a prevalent disease in Sudan, has a significant impact on socioeconomic conditions. Cytokines play a crucial role in regulating the immune response during infectious diseases. This study investigates the interplay between malaria and immune response modulation in the River Nile State, focusing on tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), transforming growth factor-beta1 (TGF-β1), and interleukin-10 (IL-10).

Method: Ninety participants with microscopy-confirmed malaria were enrolled. Parasite density and COVID-19 co-infection were assessed. Cytokine levels were measured using ELISA.

Results: TNF-α, IFN-γ, and TGF-β1 levels were significantly associated with parasite density (P < 0.05), but not IL-10. TGF-β1 was significantly higher in P. vivax infections, while IL-10 was elevated in P. falciparum cases. Uric acid levels were lower in participants co-infected with COVID-19 (P < 0.05).

Conclusion: The study's findings show how cytokines affect the immune response, impacting both parasite clearance. TNF-α, IFN-γ, and TGF-β1 are positively linked to parasite density (r = 0.42, 0.38, 0.51; P < 0.01). IL-10 levels were higher in P. falciparum compared to P. vivax (560.0 vs. 415.6 pg/mL, P = 0.019).

This study investigates the protective effects and underlying mechanisms of curcumin in sepsis-associated acute kidney injury (SA-AKI). Using a cecal ligation and puncture (CLP) model to simulate SA-AKI, our results demonstrate that curcumin significantly reduced serum creatinine and urea nitrogen levels, alleviated tubular damage and inflammation, improved cellular activity, and inhibited apoptosis. Further analysis revealed that curcumin inhibited the expression of p300 and decreased protein lactylation modification in renal tissue, thereby exerting anti-inflammatory and antioxidant effects. These findings suggest that curcumin may have potential therapeutic value for the prevention and treatment of SA-AKI.

Background: Autoimmune cytopenias (AICs) are among the most frequent non-infectious complications in inborn errors of immunity (IEIs) and may represent early or even initial manifestations. The genetic underpinnings of AICs in IEIs remain heterogeneous and incompletely defined.

Objective: This study aimed to determine the prevalence and distribution of AICs and to investigate their associations with underlying monogenic mutations and selected immunophenotypic parameters in adult patients with IEI.

Methods: A total of 121 adult IEI patients from a single tertiary immunology center were evaluated retrospectively. Clinical, immunophenotypic, and genetic data were obtained from electronic medical records. Comparisons were made between patients with and without autoimmune manifestations and AICs. Monogenic mutations were identified using targeted next-generation sequencing (NGS).

Results: Autoimmune manifestations were present in 48 of 121 patients (39.6%), and autoimmune cytopenias (AICs) were identified in 33 patients (27.5%). Autoimmune hemolytic anemia (AIHA) was the most frequently observed subtype, followed by combined cytopenias and immune thrombocytopenia (ITP). The most common genetic alteration detected was a mutation in TNFRSF13B (TACI), with additional variants identified in DOCK8, RAG1, LRBA, PRF1, PSTPIP1, CECR1, PRKDC, and MRTFA. Logistic regression revealed a strong independent association between TACI mutations and ITP (OR: 46.5, p = 0.002), while no significant relationship was found with autoimmune cytopenias overall. No statistically significant differences were found in class-switched memory B cells (CD27⁺IgD⁻) percentages, CD4⁺/CD8⁺ T-cell ratios, or baseline IgG concentrations between patients with and without autoimmune manifestations or AICs.

Conclusion: AICs represent a significant clinical burden in adult IEIs and may occur in association with a wide range of genetic variants. Class-switched memory B cells (CD27⁺IgD⁻) percentages, CD4⁺/CD8⁺ T-cell ratio, and baseline IgG were not significantly associated with autoimmunity in this cohort. These findings underscore the need for broader immunophenotypic and genetic screening to improve the early recognition and management of autoimmune complications in IEIs.

Introduction: An accurate assessment of prognostic risk is widely recognized to be important in improving the survival of patients with acute coronary syndrome (ACS). This study aimed to investigate the roles of neutrophil-to-lymphocyte * platelet (NLPR) and neutrophil-lymphocyte (NLR) ratios with high- and (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels in predicting the risk of major adverse cardiovascular events (MACEs) in patients with ACS undergoing percutaneous coronary intervention (PCI).

Results: Overall, 1,263 patients with ACS undergoing PCI between January 2016 and December 2018 were consecutively enrolled. The patients were divided into MACEs (n = 54) and non-MACEs (n = 1,209) groups. The study endpoints were MACEs, including cardiac-related mortality and re-hospitalization for severe heart failure (HF), myocardial infarction (MI), and in-stent restenosis (ISR). The Kaplan-Meier curve showed the low NLPR and NLR groups had higher cumulative survival than the high NLPR and NLR group. Patients with high NLPR/HDL-C, NLPR×LDL-C, NLR/HDL-C, and NLR×LDL-C also had significantly lower cumulative survival.

Conclusion: NLPR ≥ 2.843, NLPR/HDL-C ≥ 1.977, NLPR*LDL-C ≥ 4.608, NLR ≥ 0.025, NLR/HDL-C ≥ 0.030, and NLR*LDL-C ≥ 0.038 were all independent prognostic risk factors in patients with ACS undergoing PCI, which may be useful markers for long prognosis.

Background and aims: Common variable immunodeficiency (CVID) represents the most frequently diagnosed symptomatic primary immunodeficiency (PID), marked by a heterogeneous presentation involving infectious and non-infectious symptoms. This study investigated the association between serum copeptin levels and right ventricular functions (RVF) and pulmonary complications in patients diagnosed with CVID.

Methods: The study analyzed data from 60 individuals with a confirmed diagnosis of CVID and 30 age- and sex-matched healthy volunteers (HVs). Clinical and biochemical parameters were sourced from existing hospital records.CVID patients were categorized into two subgroups: those with and without pulmonary complications. Comparisons of serum copeptin levels were made between these groups and between the overall CVID cohort and healthy controls. RVF was evaluated using tricuspid annular plane systolic excursion (TAPSE) and supplementary echocardiographic indicators.

Results: The CVID group had a median age of 40 years (interquartile range [IQR]: 30-55), with 51.7% being male, while the HVs group had a median age of 37 years (IQR: 28-47.5), with 60% male. No significant differences in age (p = 0.226) or sex distribution (p = 0.45) were observed between the groups. CVID with pulmonary complications (CVID-P) exhibited significantly elevated copeptin levels compared to those without such complications (p < 0.001). According to ROC analysis, a copeptin cut-off value of 11 pmol/L significantly differentiated patients with CVID-P from those without pulmonary complications (p < 0.001). Moreover, overall copeptin levels were significantly higher in the CVID group than in HVs (p < 0.001). A copeptin cut-off value of 21 pmol/L effectively distinguished CVID patients with low TAPSE from those with normal TAPSE values (p < 0.001). Pulmonary complications and low TAPSE were independently associated with increased copeptin levels (p = 0.006 and p = 0.004, respectively).

Conclusion: The development of pulmonary complications and RV dysfunction were associated with elevated serum copeptin levels in CVID. Measuring serum copeptin concentration may be a useful biomarker in diagnosing and prognosis pulmonary diseases and RV dysfunction in CVID.