al-turath Medical Journal

Background: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder characterised by persistent synovial inflammation and progressive joint destruction. The immunomodulatory roles of IL-40, IL-37, and IL-38 in RA remain incompletely understood, particularly in Middle Eastern patient populations. Research question: Are serum levels of IL-40, IL-37, and IL-38 elevated in RA patients compared with healthy controls, and do they correlate with established pro-inflammatory markers? Methods: A cross-sectional comparative study was conducted at Tikrit Teaching Hospital, Salah al-Din, Iraq (January–September 2025), enrolling 60 RA patients and 30 age- and sex-matched healthy controls. Serum cytokines were quantified by ELISA. Normality was assessed by the Shapiro-Wilk test; Mann-Whitney U and Spearman rank correlation were applied. Results: IL-40 (8.91±1.08 vs 7.29±2.24 pg/mL; p=0.0002), IL-37 (398.44±72.95 vs 68.33±29.30 pg/mL; p<0.001), and IL-38 (635.48±197.43 vs 145.23±56.17 pg/mL; p<0.001) were all significantly elevated in RA. All pro-inflammatory markers were markedly elevated (p<0.001). Within the RA group, IL-37 correlated positively with CRP (r=0.352, r²=0.124, p=0.006) and ESR (r=0.311, r²=0.097, p=0.016). Conclusion: These findings suggest that IL-40, IL-37, and IL-38 may be actively involved in RA immunopathology. The moderate positive correlations between IL-37 and acute-phase reactants may reflect a counter-regulatory response proportional to systemic inflammatory burden. Confirmation in larger, longitudinal, multi-centre studies is required.

Background: Bacterial infections and type 2 diabetes mellitus (T2DM) independently dysregulate redox homeostasis and immune signalling; their co-occurrence may amplify these perturbations through shared transcriptional pathways. Aim: To quantify and compare oxidative stress and inflammatory biomarkers across healthy controls, patients with bacterial infection, patients with T2DM, and patients with concurrent bacterial infection and T2DM.

Methods: A cross-sectional comparative study enrolled 120 participants (30 per group) at a teaching hospital in Salah al-Din, Iraq (January–June 2024). Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), erythrocyte sedimentation rate (ESR), and a full metabolic panel were measured. One-way ANOVA with Duncan’s post hoc test and Pearson correlation were applied using SPSS v.26. Results: Group 4 (concurrent disease) showed the highest MDA (5.28 ± 0.74 nmol/mL; p=0.004 vs controls) and the lowest SOD (1.87 ± 0.39 U/mL; p<0.001). MDA correlated positively with IL-6 (r=+0.63, p=0.008) and negatively with SOD (r=−0.54, p=0.041). CRP and IL-6 were severalfold elevated in Group 4 relative to all other groups (p<0.001). Conclusion: Co-existing bacterial infection and T2DM synergistically intensify oxidative and inflammatory burden, underscoring the need for integrated antioxidant monitoring in dually affected patients.

This study showed the effect of chronic kidney disease (CKD) on serum protein balance and redox homeostasis through a comparative analysis of serum protein fractions and oxidation markers. The results showed a significant reduction in total protein, albumin, and ceruloplasmin ferroxidase activity coupled with marked elevation in globulin levels and total oxidant status(TOS), also a decline in catalase activity compared with the first (healthy) group. This alterations connected with a dual disturbance in nutritional and immune status: tubular damage, malnutrition, and protein loss which cause a decreased in proteins serum. While the increase in globulin levels indicates a chronic inflammatory response. The increase in (TOS) with reduced antioxidant defenses confirms the role of oxidative stress in (CKD) progression. Furthermore, the decrease in ceruloplasmin ferroxidase activity is caused by impaired iron and copper metabolism and the accumulation of labile iron, which promotes Fenton reactions and the generation of reactive oxygen species. Overall these results suggest that assessment of serum proteins and oxidative stress biomarkers provides important diagnostic and prognostic tools for evaluating disease severity and guiding therapeutic interventions, stressing in the importance to but a strategy that include nutritional support and oxidative stress mitigation to advance clinical outcomes in CKD patients.

Background: Parasitic infections remain a major constraint on global livestock productivity, contributing to substantial economic losses and compromised food security, particularly in developing regions. The biological complexity of host-parasite interactions — spanning protozoan, helminthic, and ectoparasitic infestations — governs infection outcomes, pathological severity, and therapeutic response through mechanisms that are only partially understood.

Objective: This narrative review critically analyzes the pathophysiology, immune polarization dynamics, oxidative stress mechanisms, and therapeutic landscape of major livestock parasites — including Theileria, Babesia, Trypanosoma, Fasciola, Haemonchus, Trichostrongylus, and Eimeria — with a focus on immune evasion strategies, anthelmintic resistance, and a systems biology perspective.

Key Findings: Protozoan parasites predominantly drive Th1 polarization (IFN-γ, TNF-α), while helminths classically elicit Th2 responses (IL-4, IL-5, IL-13, IgE). Regulatory T cell (Treg) expansion is common to most chronic parasitoses and undermines effector immunity. Oxidative stress — manifested by elevated MDA and depleted SOD, GPx, and GSH — is commonly associated with many major livestock parasitoses, though its magnitude varies considerably by parasite species, infection stage, and host immune status. Anthelmintic resistance represents a critical and escalating global challenge.

Conclusion: Effective management of livestock parasitosis requires integrated approaches combining targeted antiparasitic chemotherapy, resistance management, immunomodulatory nutritional support, host genetic resistance selection, and evidence-based vaccination. Future research must prioritize AI-assisted diagnostics, multi-omics characterization of resistance, and climate-adaptive epidemiological modeling.