Clinical importance of cytokine (IL-6, IL-8, and IL-10) and vitamin D levels among patients with Type-1 diabetes | Scientific Reports

Oct 16, 2024

Scientific Reports volume 14, Article number: 24225 (2024) Cite this article

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Type-1 diabetes (T1D) is an autoimmune disorder characterized by impaired insulin release by islet β cells. It has been shown that proinflammatory cytokines released during the disease can exacerbate the condition, while anti-inflammatory cytokines offer protection. This study analyzed the clinical role of interleukin (IL)-6, -8, -10, and vitamin D levels in T1D patients compared to healthy controls. The levels of IL-6, IL-8, IL-10, and vitamin D in the participants’ serum samples were analyzed using ELISA. The findings showed that T1D patients had significantly increased levels (p < 0.0001) of fasting blood glucose, HbA1c, systolic blood pressure, low-density lipoprotein, triglycerides, cholesterol, and very low-density lipoprotein and decreased levels of high-density lipoprotein and vitamin D (p < 0.0001) compared to healthy controls. Moreover, the levels of IL-6, IL-8, and IL-10 were also significantly greater (p < 0.0001) in T1D patients. The study also determined the significance of these cytokines among T1D patients and healthy controls using ROC curves. Furthermore, we found that smokers had significantly higher levels of IL-6 (p = 0.01) and IL-8 (p = 0.003) than non-smokers. These results showed that elevated levels of IL-6, IL-8, and IL-10, decreased vitamin D levels, and smoking among T1D participants could contribute to the worsening of T1D disease and could serve as predictive indicators.

Type-1 diabetes (T1D) is a non-communicable autoimmune disorder that arises due to impaired release of insulin by islet β cells. Autoreactive immune cells, especially T cells, improperly target islet β cells, resulting in progressive damage to insulin secretion and destruction of approximately 70–80% of the β cell mass1. According to the International Diabetes Federation (IDF), approximately 8.75 million people worldwide were diagnosed with T1D in 2022. Among these individuals, 17% were under 20 years old, 64% were between 20 and 59 years old, and 19.9% were 60 years or older2. T1D is particularly prevalent in Saudi Arabia and other Middle Eastern nations3. In fact, the IDF reports that Saudi Arabia has the second highest incidence of diabetes in the Arabian region and the seventh highest incidence in the world2,4,5. The activation of the immune system and islet infiltration of immune cells contribute to the destruction of pancreatic beta cells, leading to high blood glucose levels6. The infiltration of autoreactive immune cells results in the inflammation of islet cells and further exacerbates the disease. Additionally, beta cells are exposed to outside stimuli, such as cytokines, that cause inflammation7. This condition is worsened by high levels of proinflammatory cytokines, such as interleukins, interferons, transforming growth factor-β, tumor necrosis factors, and nitric oxide cascades8. In contrast, anti-inflammatory cytokines are associated with protective effects against β-cell survival9.

Interleukin-6 (IL-6) plays an important role in the progression of various autoimmune diseases by targeting the IL-6/IL-6 receptor10. IL-8, a member of the C-X-C motif subfamily of chemokines, acts as a chemoattractant and polymorph activator via interaction with two receptors (CXCR1 and CXCR2). Several studies have demonstrated the role of IL-8 in the pathogenesis of T1D11,12,13. IL-10 has diverse anti-inflammatory effects on antigen-presenting cells, promoting tissue repair mechanisms14. IL-10 is produced by different immune cells, including regulatory T cells, immature dendritic cells15, and regulatory B cells in T1DM16. Low serum vitamin D concentrations lead to impaired insulin secretion, poor glucose homeostasis, and increased risk of metabolic syndrome17. It also increases the risk of both T1D and T2D development18. In particular, vitamin D affects T cells by encouraging CD4 + T cells to differentiate into Th2 and Treg cells while reducing the generation of Th1 and Th17 cells and the proportion of Th1/Th2 cells. IL-4, IL-10, and TGF-β synthesis in immune cells is stimulated by vitamin D, but the production of proinflammatory cytokines, including IL-2, IL-6, IL-12, IL-17, and IL-22, is decreased19. Therefore, the present study aimed to explore the involvement of IL-6, IL-8, IL-10, and vitamin D in T1D.

Two hundred individuals were enrolled in the present research; 100 were T1D patients, and 100 were healthy controls. Individuals who presented symptoms, including polyuria, polydipsia, polyphagia, weight loss linked to hyperglycemia, ketonuria, and glycosuria, as well as the existence or absence of acidosis, were considered. Only GAD antibody-positive participants were included in the present study. Fasting glucose (100–125 mg/dL) and 2-hour postprandial blood glucose (140–199 mg/dL) were measured to confirm hyperglycemic conditions.

Individuals who had conditions such as acute or chronic infectious diseases, cancer, endocrine disorders, cardiovascular diseases, inflammatory or other autoimmune disorders, or chronic hepatitis or renal disease were excluded from the study. All the healthy controls were free of any illness or complications.

Peripheral blood samples (4 ml) were collected from the participants for various analyses. Briefly, 2 ml of blood was transferred to plain vials for analysis of lipid parameters, GAD antibodies, interleukins, and vitamin D. One milliliter of blood was collected in a fluoride vial for fasting blood glucose analysis, and another 1 ml was taken in an EDTA vial for analysis of HbA1c. Additionally, 1 ml of blood was collected in a fluoride vial after a meal to analyze 2-hour blood glucose levels. From healthy controls, a total of 3 ml of peripheral blood was collected, with 1 ml stored in EDTA vials, another 1 ml collected in a fluoride vial before eating, and the remaining 1 ml placed in plain vials to measure interleukins, vitamin D levels, and lipid parameters. Blood samples collected in plain vials were centrifuged, and the serum was separated and stored at -80 °C.

The stored serum samples from the participants at -80 °C were thawed, centrifuged to remove RBC residue, and used for lipid profile analysis via a kit from Randox Laboratories Limited (Antrim, United Kingdom). IL-6 (catalog # KHC0061), IL-8 (catalog #KHC0081), and IL-10 (catalog #KHC0101) ELISA kits were purchased from Thermo Scientific and were analyzed following the manufacturer’s protocol.

Using an electrochemiluminescence immunoassay (Cobas e411, Roche, Basel, Switzerland), vitamin D levels in the serum of T1D patients and healthy controls frozen at -80 °C were determined. Vitamin D deficiency was defined as a serum 25-hydroxyvitamin D [25(OH)D] concentration of less than 20 ng/mL. In comparison, serum 25[OH]D concentrations ranging from 21 to 29 ng/mL were classified as insufficient, and concentrations of 30 ng/mL or higher were considered sufficient, representing levels generally deemed adequate to support bone health, immune function, and other physiological processes dependent on vitamin D20,21.

All the qualitative and quantitative data were recorded in Microsoft Excel and analyzed via SPSS version 21 and GraphPad Prism software. The Mann‒Whitney U test was used to compare quantitative data, and Spearman correlation analysis was used to determine any correlation between the quantitative results. A p value less than 0.05 was considered to indicate statistical significance.

For this study, 200 participants were included: 100 individuals with T1D and 100 healthy controls. The demographic characteristics of the study participants are presented in Table 1. Among the T1D participants, 86% were male, whereas 88% of the healthy controls were male. On the other hand, 14% of the T1D participants were female, whereas 12% of the healthy controls were female. The median age of the T1D patients was 19.31 years (95% confidence interval (CI) 18.40–20.22), whereas the median age of the healthy controls was 19.61 years (95% CI 18.22–20.09). According to our health questionnaire, 28% of those with T1D were smokers, and 72% were nonsmokers. However, 27% of the healthy controls were smokers, and 73% were nonsmokers. With respect to physical activity, only 27% of the T1D participants engaged in physical activity, whereas 73% did not. In contrast, 57% of the healthy controls performed some form of physical activity, whereas 43% did not. With respect to body mass index (BMI), 67% of the T1D participants had a normal BMI, compared to 63% of the healthy controls. Additionally, 21% of the T1D participants were overweight, compared with 27% of the healthy controls, and 12% of the T1D participants were obese, compared with 10% of the healthy controls.

The biochemical indicators were compared between individuals with T1D and healthy controls and are shown in Table 2. Fasting blood glucose (FBG) levels were significantly elevated in T1D patients, with a mean value of 205.8 ± 38.54 mg/dL, compared with 80.42 ± 6.61 mg/dL in healthy controls, and this difference was statistically significant (p < 0.0001). Similarly, glycated hemoglobin (HbA1c) levels were markedly higher in T1D patients (7.74 ± 0.52%) than in controls (5.03 ± 0.57%), with a p value of < 0.0001, underscoring poor glycemic control in the diabetic group. Blood pressure measurements revealed that systolic blood pressure was significantly greater in T1D patients (140 ± 17.25 mmHg) than in healthy controls (122 ± 6.20 mmHg; p < 0.0001). There were also differences in diastolic blood pressure between the two groups (80.88 ± 10.65 mmHg vs. 77.62 ± 5.44 mmHg), but these differences were not statistically significant (p = 0.08).

Lipid profile analysis revealed that T1D patients had significantly lower levels of high-density lipoprotein (HDL) than healthy controls did (33.50 ± 9.20 mg/dL in T1D patients vs. 39.65 ± 7.55 mg/dL in healthy controls; p < 0.0001). Conversely, low-density lipoprotein (LDL) levels were substantially higher in T1D patients than in controls (195.3 ± 28.20 mg/dL in T1D patients vs. 102.6 ± 19.41 mg/dL in controls; p < 0.0001). Additionally, triglyceride (TG, 212.1 ± 37.89 mg/dL vs. 140.2 ± 21.55 mg/dL) and total cholesterol levels (233.0 ± 25.38 mg/dL vs. 168.5 ± 25.0 mg/dL) were significantly elevated in T1D patients compared with healthy controls. Very low-density lipoprotein (VLDL) levels were also significantly higher in T1D patients than in controls. Furthermore, we found that T1D patients had considerably lower levels of vitamin D (16.93 ± 6.55 ng/dL) than healthy controls did (25.6 ± 8.12 ng/dl; p = 0.0001).

A correlation analysis was also performed between vitamin D levels and biochemical indicators among the T1D patients and healthy controls (Table 3). The analysis revealed a significant inverse correlation between vitamin D levels and both FBG and HbA1c, with correlation coefficients of -0.52 and − 0.53, respectively (p < 0.0001 for both), suggesting that lower vitamin D levels are associated with poorer glycemic control in the study population. Systolic blood pressure was also significantly negatively correlated with vitamin D levels (r = -0.31, p < 0.0001). However, the correlation between diastolic blood pressure and vitamin D was weaker and not statistically significant (r = -0.10, p = 0.14).

With respect to the lipid profile, HDL levels were positively correlated with vitamin D status (r = 0.30, p < 0.0001), suggesting that higher vitamin D levels may be associated with better HDL cholesterol levels. Conversely, LDL, TG, total cholesterol, and VLDL were significantly negatively correlated with vitamin D, with correlation coefficients of -0.50, -0.53, -0.50, and − 0.52, respectively (all p < 0.0001). Overall, these results underscore the potential role of vitamin D in modulating glycemic control and lipid metabolism, particularly in individuals with T1D. The observed significant correlations suggest that vitamin D deficiency may contribute to poor metabolic control and unfavorable lipid profiles in this population.

In the present study, the levels of IL-6, IL-8, and IL-10 were compared between T1D patients and healthy controls (Fig. 1). Compared with healthy controls (1.40 ± 0.76 pg/ml), the T1D group presented significantly elevated serum IL-6 levels (2.46 ± 0.83 pg/ml) (p < 0.0001) (Fig. 1a). Similarly, serum IL-8 levels were markedly higher in T1D patients (11.02 ± 6.51 pg/ml) than in healthy controls (1.87 ± 0.93 pg/ml) (p < 0.0001) (Fig. 1b). The serum IL-10 level was also significantly greater in the T1D group (6.84 ± 1.43 pg/ml) than in the healthy control group (2.51 ± 0.80 pg/ml) (p < 0.0001) (Fig. 1c). The data suggest a notable difference in inflammatory cytokine levels between individuals with T1D and healthy controls, highlighting the immune dysregulation associated with T1D.

Serum levels of inflammatory cytokines, IL-6 (a), IL-8 (b), and IL-10 (c) in individuals with T1D (n = 100) compared to healthy controls (n = 100). The error bars represent the standard deviations. A p value of ˂ 0.01 was considered significant.

The relationships between vitamin D and the concentrations of three distinct interleukins—IL-6, IL-8, and IL-10—were also examined in our investigation (Fig. 2). We observed a nonsignificant negative correlation between vitamin D levels and IL-6 (r=-14, p = 0.22, Fig. 2a) and IL-10 (r=-12, p = 0.73, Fig. 2c), suggesting a potential decrease in these interleukins with higher vitamin D levels. We also found a nonsignificant positive correlation between vitamin D and IL-8 (r = 0.15, p = 0.19) (Fig. 2b), indicating higher vitamin D levels may result in a possible increase in IL-8 levels among T1D patients. These findings suggest that while there are trends in the associations between vitamin D levels and IL-6, IL-8, and IL-10 concentrations in T1D patients, the correlations observed were not statistically significant in this study.

Correlations between serum vitamin D levels and the levels of the inflammatory cytokines IL-6 (a), IL-8 (b), and IL-10 (c) in individuals with T1D. Each point represents an individual with T1D.

The importance of the cytokines IL-6, IL-8, and IL-10 in T1D patients and healthy controls was assessed via receiver operating characteristic (ROC) curves (Table 4; Fig. 3). These cytokine levels were compared between T1D patients and healthy individuals. The level of interleukins among the healthy controls served as a reference group. After the analysis, the AUC for IL-6 was 0.82, with a sensitivity of 79% and specificity of 70% at the cutoff value of 1.72 pg/ml (p < 0.0001). For IL-8, the AUC was 1.00, with a sensitivity of 93% and specificity of 100% at the cutoff value of 5.50 pg/ml (p < 0.0001). Finally, for IL-10, the AUC was 0.99, with a sensitivity of 96% and specificity of 89% at the cutoff value of 3.55 pg/ml (p < 0.0001). These data demonstrate the strong prognostic potential of IL-6, IL-8, and IL-10 in distinguishing T1D patients from healthy controls.

Receiver operating characteristic (ROC) curves illustrating the prognostic significance of (a) IL-6, (b) IL-8, and (c) IL-10 cytokine levels in T1D patients compared to healthy controls.

We compared the levels of the cytokines IL-6, IL-8, and IL-10 among the T1D patients with respect to smoking status (Fig. 4). Our study revealed that smokers had significantly higher levels of IL-6 (2.88 pg/ml vs. 2.31 pg/ml; p = 0.01) and IL-8 (12.24 pg/ml vs. 9.91 pg/ml; p = 0.003) than nonsmokers did, indicating a statistically significant increase in these proinflammatory cytokines among smokers. In contrast, the IL-10 level was slightly lower in smokers (6.56 ± 1.70 pg/mL) than in nonsmokers (6.94 ± 1.32 pg/mL), but this difference was not statistically significant (p = 0.35). These findings suggest that in T1D patients, smoking is associated with increased levels of proinflammatory cytokines (IL-6 and IL-8) but does not significantly affect the levels of the anti-inflammatory cytokine IL-10.

Comparison of interleukin (IL) (a) IL-6, (b) IL-8, and (c) IL-10 levels between nonsmokers (n = 72) and smokers (n = 28). Data are presented as box plots showing the median, interquartile range, and minimum/maximum values. The mean ± standard deviation values are displayed above each box. The p values indicate the statistical significance of differences between nonsmokers and smokers for each interleukin.

Additionally, we examined how the hypertensive condition of T1D patients affects variations in IL-6, IL-8, and IL-10 levels. The nonhypertensive and hypertensive T1D subjects presented slight differences in IL-6, IL-8, and IL-10 levels, but these differences were not statistically significant (Fig. 5).

Comparison of interleukin (IL) (a) IL-6, (b) IL-8, and (c) IL-10 levels between nonhypertensive and hypertensive T1D patients. Data are presented as box plots showing the median, interquartile range, and minimum/maximum values. The mean ± standard deviation values are displayed above each box.

The present study compared various clinical and biochemical parameters between T1D patients and healthy controls. Significant differences in FBG, HbA1c, HDL, LDL, triglyceride, and very low-density lipoprotein levels were detected between the two groups. In line with our findings, previous studies have shown that patients with poorly controlled diabetes, indicated by poor glycemic control, tend to have unfavorable lipid profiles22. Specifically, alterations in lipid levels, such as reduced HDL cholesterol23 and triglyceride levels24, have been associated with an increased risk of cardiovascular disease (CVD) in T1D patients. Our study similarly revealed low HDL and high triglyceride levels among T1D patients. A study on children and young people with T1DM found a direct correlation between total dyslipidemia and glycemic control25 and LDL cholesterol26. Diabetic dyslipidemia, characterized by low HDL cholesterol, high triglycerides, elevated LDL, and primarily small dense LDL-C particles, is a major contributor to diabetes and atherosclerosis27. For example, Kantoosh et al. (2002) reported that hypertriglyceridemia is the most prevalent form of dyslipidemia in Egyptian children with newly diagnosed T1D, who also had significantly higher blood triglyceride and HbA1c levels28. Studies by Patiakas et al. (2007) and Alrabaty et al. (2009) similarly reported that diabetic patients have the highest prevalence of hypercholesterolemia29 and that hypertriglyceridemia is common in children and adolescents with T1D30. Compared with healthy controls, a significantly greater proportion of young people with T1D showed dyslipidemia compared to healthy controls31. Metabolic problems in T1D are often associated with excess weight, hypertension, dyslipidemia32, and chronic inflammation of the pancreatic islets33, leading to the destruction of insulin-secreting beta cells34 by autoreactive CD8 + and CD4 + T cells35. These immune cells frequently release cytokines throughout T1D development36. In this study, we found increased levels of IL-6, IL-8, and IL-10 in T1D patients, with IL-6 levels being 1.75 times higher, IL-8 levels being 5.89 times higher, and IL-10 levels being 2.72 times higher than those in healthy controls, suggesting their potential involvement in T1D pathology.

T1D patients have consistently reported higher IL-6 levels than nondiabetic individuals do37. Cytokines, particularly in autoimmune diseases such as T1D, are crucial for the formation and activation of immune cells38. IL-6, produced by T cells and macrophages, plays a role in the inflammatory response linked to insulin resistance39. Studies in mouse models have shown that the overexpression of IL-6 causes increased infiltration of islets by B cells and other immune cells40, with similar increases in IL-6 signaling observed in T1D patients41. Elevated IL-6 secretion has been reported in T1D patients42, and IL-6 concentrations are significantly increased in patients with autoimmune diseases, suggesting that this proinflammatory cytokine is involved in the etiology of diabetes43. IL-8 has also been identified as a potential marker for determining diabetic risk and managing complications44. T1D children have significantly higher salivary IL-8 levels than healthy controls do45. Erbagci et al. reported that even after adjusting for age, body mass index, lipids, apolipoproteins, and glycemic management, serum IL-8 concentrations remained significantly higher in children with T1D than in those without46.

Elevated serum IL-8 levels have been observed in both adults and adolescents with T1D47. Hyperglycemia and ketosis can regulate IL-8 synthesis in cultured monocytes, and hyperglycemia can activate IL-8 gene transcription in human endothelial cells48. The degree of metabolic control may directly influence the regulation of IL-8 more than the overall proinflammatory state associated with T1D49. Increased IL-8 levels may also contribute to the pathogenesis of atherosclerosis and diabetic macroangiopathy, suggesting its potential role in the detection, prevention, and management of diabetes complications50. Devaraj S et al. (2006) revealed that compared with nondiabetic individuals, T1D patients have higher serum concentrations of IL-6 and IL-851. IL-10, on the other hand, plays a critical role in maintaining the balance of the immune response, protecting tissues from infection and defending the body52. IL-10 gene expression is higher in diabetic patients than in nondiabetic individuals, indicating increased inflammatory activity53. A change in cytokine profiles, with reduced IL-10 expression as HbA1c levels decrease, suggests a compensatory defense cytokine response54. Severe diabetes may lead to increased IL-10 expression in response to metabolic stress caused by ketoacidosis or hyperglycemia55.

We evaluated the prognostic efficacy of these cytokines and found that the AUC for IL-8 was 1.00, with a sensitivity of 93% and specificity of 100% at a cutoff value of 5.50 pg/ml. For IL-10, the AUC was 0.99, with a sensitivity of 96% and specificity of 89% at a cutoff value of 3.55 pg/ml, indicating that IL-8 and IL-10 could be reliable prognostic indicators for T1D. Smoking has been shown to alter the levels of anti- and proinflammatory cytokines56. IL-6 levels are significantly higher in smokers with pancreatitis than in nonsmokers57. Tobacco smoke exposure causes oxidative stress and increases the release of inflammatory cytokines, including IL-6 and IL-858. Smoking exacerbates the production of these cytokines, contributing to inflammation59. Our study also observed that T1D patients who smoke have higher levels of IL-6 and IL-8 than nonsmokers do, suggesting that smoking could worsen disease severity and lead to adverse health outcomes.

This study has several limitations that should be considered. A primary limitation is the sex imbalance among the participants, with only 12–14% of the study population being female. This significant underrepresentation of women limits the generalizability of our findings across both sexes and prevents direct comparisons between male and female T1D patients. Given the known sex dimorphism in the prevalence and pathophysiology of T1D, the results of this study may not fully capture the variations in disease manifestation and progression between men and women. While the study provides valuable insights, particularly for the male T1D population, the findings should be interpreted with caution regarding their applicability to female patients. Future studies with a more balanced sex distribution are needed to explore potential sex-specific differences and to validate the broader applicability of these results.

Additionally, the study did not include any treated T1D participants and had a small sample size, which could have affected the accuracy of the results. The smoking history was recorded on the basis of a health questionnaire, which may have introduced inaccuracies. The participants were simply categorized as smokers or nonsmokers without further details or verification, which could have led to some misreporting of smoking habits. Moreover, no staging was performed for T1D patients, as only GAD antibody-positive participants were included, which could affect the generalizability of the results since the study did not account for the full spectrum of T1D participants. Despite these limitations, the study’s findings remain valuable, and further research could address these issues to increase the robustness of future studies.

The present study revealed decreased vitamin D levels in T1D patients compared with healthy controls. Vitamin D was negatively correlated with IL-6 and IL-10 and positively correlated with IL-8, but these correlations were not significant. The higher IL-6, IL-8, and IL-10 expression in patients with T1D suggested that ROC analysis was a significant prognostic indicator. Furthermore, T1D participants who smoked had higher IL-6 and IL-10 levels than did T1D participants who did not smoke. In summary, the present study provides important insights into the potential role of interleukins and vitamin D in the development and progression of T1D.

The experimental data generated and analyzed during the current study is provided within the manuscript.

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The authors acknowledge all the study participants. This research has been funded by the Scientific Research Deanship at the University of Ha’il - Saudi Arabia through Project number MDR-22 024.

This research has been funded by the Scientific Research Deanship at the University of Ha’il - Saudi Arabia through Project number MDR-22 024.

Department of Pathology, College of Medicine, University of Hail, Hail, 55476, Saudi Arabia

Azharuddin Sajid Syed Khaja & Mohd Saleem

Medical and Diagnostic Research Centre, University of Hail, Hail, 55476, Saudi Arabia

Azharuddin Sajid Syed Khaja, Naif K. Binsaleh, Husam Qanash & Mohd Saleem

Department of Medical Laboratory Science, College of Applied Medical Sciences, University of Hail, Hail, 55476, Saudi Arabia

Naif K. Binsaleh & Husam Qanash

Faculty of Medicine, Alatoo International University, Bishkek, 720048, Kyrgyzstan

Mirza Masroor Ali Beg

Centre for Promotion of Medical Research, Alatoo International University, Bishkek, 720048, Kyrgyzstan

Mirza Masroor Ali Beg

Department of Clinical Nutrition, College of Nursing and Health Sciences, Jazan University, Jazan, 82817, Saudi Arabia

Fauzia Ashfaq

Department of Basic Health Sciences, College of Applied Medical Sciences, Qassim University, Buraydah, 51452, Saudi Arabia

Mohammad Idreesh Khan

Department of Clinical Nutrition, College of Applied Medical Sciences, University of Hafr Albatin, Hafr Albatin, Saudi Arabia

Malak Ghazi Almutairi

General Directorate of Public Health Hail, Ministry of Health, Hail, 2440, Saudi Arabia

Ibrahim Abdelmageed Mohamed Ginawi

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Conceptualization, A.S.S.K, and M.M.A.B.; methodology, A.S.S.K, N.B, M.M.A.B., F.A., M.I.K., and M.S.; Figure preparation, A.S.S.K, M.M.A.B., F.A., M.I.K., M.G.A., H.A.Q., and M.S.; validation, F.A., M.I.K., and M.S.; formal analysis, A.S.S.K, N.B, M.M.A.B., F.A., M.I.K., I.A.M.G., and M.S.; investigation, A.S.S.K., M.M.A.B., F.A., M.I.K., and M.S.; data curation, A.S.S.K, N.B, M.M.A.B., F.A., M.I.K., and H.A.Q.; writing—original draft preparation, A.S.S.K, and M.M.A.B.; writing—review and editing, A.S.S.K, N.B, M.M.A.B., F.A., M.I.K., M.G.A., H.A.Q., I.A.M.G., and M.S.; supervision, A.S.S.K, M.M.A.B., and M.S.; project administration, A.S.S.K, M.M.A.B., and M.S.; funding acquisition, A.S.S.K. All authors have read and agreed to the published version of the manuscript.

Correspondence to Azharuddin Sajid Syed Khaja or Mirza Masroor Ali Beg.

The authors declare no competing interests.

The study was approved by the Institutional Ethics Review Board (H-08-L-074) at the University of Hail, Hail, Saudi Arabia. Before the study commenced, the participants provided written informed consent. The study was carried out in accordance with the Declaration of Helsinki, and all ethical principles concerning human experimentation were followed.

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Syed Khaja, A., Binsaleh, N.K., Beg, M.M.A. et al. Clinical importance of cytokine (IL-6, IL-8, and IL-10) and vitamin D levels among patients with Type-1 diabetes. Sci Rep 14, 24225 (2024). https://doi.org/10.1038/s41598-024-73737-6

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Received: 15 May 2024

Accepted: 20 September 2024

Published: 16 October 2024

DOI: https://doi.org/10.1038/s41598-024-73737-6

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