COVID-19 pneumonia is distinct from pneumonia of other origins due to the sudden deterioration 7-9 days after the commencement of symptoms, the severity of hypoxemia that contrasts with the relatively well-preserved lung mechanics, and the prolonged nature of acute respiratory distress syndrome [1]. ARDS. Several studies have shown that COVID-19 have elevated levels of circulating proinflammatory cytokines [2, 3]. During the rapid progression of COVID-19, a cytokine storm can occur, modifying the immune system by lowering lymphocyte and T-cell counts [4]. Immune dysregulation is a characteristic of the more severe stages of SARS-CoV-2 infection; therefore, understanding the processes by which the immune system contributes to the severity of COVID-19 may lead to the development of new treatment options. Cytokine release syndrome (CRS), also called a cytokine storm, is a life-threatening systemic inflammatory syndrome. It is marked by high amounts of cytokines in the blood, especially IL-1, IL-1, IL-6, TNF-, IL-17, and Chemokines like CXCL 8 and CXCL 10, as well as overactive immune cells. Different pathogens, autoimmune diseases, cancers and T-cell-based treatments can cause it [5], in COVID-19 the inflammatory mediators are not as highly expressed as in some of these other diseases. The most important indicator of severe disease and poor outcome in COVID-19 is an immune response that is disordered and not markedly enhanced [6]. Inflammatory cells are attracted to the site of inflammation by chemoattractant cytokines called chemokines, which travel from the intravascular space via the endothelium and epithelium [7]. Covid-19’s role in the dysregulation of chemokines is not well established. Some proinflammatory chemokines, including CXCL10, CXCL8, and CCL2, have been found in the plasma of Covid-19 patients at significantly greater concentrations than in the plasma of healthy controls. individuals requiring critical care unit admission had substantially greater circulation concentrations of CXCL10 and CCL2 compared to individuals with a milder clinical history [8, 9]. Transcriptome sequencing of bronchoalveolar lavage fluid (BALF) revealed that neutrophils, monocytes, and T lymphocytes were recruited to the lungs due to an abundance of these two chemokines [10]. Pulmonary inflammation and involvement in SARS patients were associated with elevated circulating levels of CXCL10 and CCL2 [9, 11]. When compared to type 1 response, type II immunity is anti-inflammatory and repairs tissue, which is a stark difference. In the case of an illness, both type 1 and type 17 reactions work to stop the infection. However, they often have dangerous side effects because antibiotic agents like reactive oxygen and nitrogen species damage tissue [12]. Interleukin 10 is an important antipyretic and immunosuppressant. It acts as a neutrophil inhibitor and a macrophage deactivation agent. In fact, several pathogens decrease host immune responses by inducing IL-10 production or encoding their own IL-10 homologs [13].
The thesis project has been approved according to the decision of the Research Committee in the Thi-Qar Health Directorate (issue No. 208/2022 on 15/8/2022) and facilitation task issued by the Thi-Qar Health Directorate, Department of Training and Development (issue No. 617 on 17/8/2022), which are attached to the document of University of Thi-Qar /College of Science (issue No. 3/11/982 on 17/7/2022), where the patient’s consent is taken verbally when reviewing hospitals designated for Covid-19.
A total of 180 blood samples were collected for this investigation, arterial blood samples were taken from COVID-19 patients while control group venous samples were drawn as follows. About five ml were collected from each sample and placed in a gel tube and left at room temperature for about 30 minutes. The gel tubes containing samples were centrifuge at 4000 RPM for 5 minutes and the serum sample was divided into three replicates in Eppendorf tubes, each part contains approximately 500 μl and stored in a deep freeze at -20 C°. The serum samples were used for evaluation CXCL 10 and IL-10 by Enzyme-Linked-Immuno-Sorbent-Assay Technique (ELISA).
The current study included patients with Covid-19 hospitalized in Thi-Qar Health Directorate of both sexes up to the age of 70 years, with the exception of patients with chronic diseases and pregnant women, as well as those over 70 years old.
The data of this study were statistically analysis by using the statistical package for social sciences version 26 SPSS, based on the use of an independent sample t-test to compare rates between patients and the control group, and ANOVA was used for mean comparison according to disease severity and body mass index. Also, person correlation was used to determine the relationship between CXCL 10 and CRP, as well as the ROC test to provide predictive values for the level of proinflammatory mediators according to body mass and disease severity.
The Table 1 showed the COVID-19 patients had a high level of CXCL 10 than control group, while the IL-10 decreased significantly in patients than control group at
Levels of CXCL 10 and IL-10 in COVID-19 patients and control group
Patients No. 120 | Control No. 60 | ||
---|---|---|---|
Mean ± SD | |||
CXCL10 ng/l | 888.4 ± 286.8 | 366.9 ± 108.3 | <0.01** |
IL-10 ng/l | 3.38 ± 1.36 | 5.46 ± 1.49 | <0.01** |
significant.
The Table 2 showed the critical COVID-19 patients had a high level of CXCL 10 than other severity of disease categories, the study also noted the IL-10 was increased sever COVID-19 patients at
Levels of CXCL 10 and CRP in COVID-19 according to severity of disease
Moderate No. 62 | Severe No. 24 | Critical No. 34 | ||
---|---|---|---|---|
Mean ± SD | ||||
CXCL10 | 873.0 ± 263.0b | 770.5 ± 236.7b | 999.7 ± 326.1a | 0.1281,2, 0.0341,3, <0.012,3 |
IL-10 | 2.80 ± 0.85c | 4.27 ± 1.22a | 3.80 ± 1.16b | <0.011-2, <0.011-3, 0.0122-3 |
significant at <0.001.
significant at <0.01.
significant at <0.05.
groups (moderate, severe, critical).
The Table 3 showed the obese COVID-19 patients had a lowest level of CXCL 10, while both normal weight and overweight patients scored high level of CXCL 10 with non-significant difference between them. In contrast the IL-10 was increased normal weight of patients at
Levels of CXCL 10 and IL-10 in COVID-19 according to BMI
Normal No. 50 | Overweight No. 31 | Obesity No. 39 | ||
---|---|---|---|---|
Mean ± SD | ||||
CXCL10 | 992.7 ± 295.1a | 964.9 ± 265.1a | 693.8 ± 178.6b | 0.1281,2, < 0.011,3 < 0.012,3 |
IL-10 | 4.12 ± 1.60a | 2.37 ± 0.59c | 3.23 ± 0.80b | < 0.01 for all |
significant at <0.001.
significant at <0.01.
significant at <0.05.
groups (normal, over weight, obesity).
The level of CXCL-10 increases significantly in patients than control group, while the IL-10 decreased significantly in patients, within disease severity CXCL 10 increased with progress of disease, according to BMI the CXCL 10 decrease in obese patients than over and normal weight, while IL-10 increase in sever and critical than moderate patients, and scored high level in normal weight patients than other BMI categories. CXC chemokine ligand 10 CXCL10, is a type of protein that can be induced by interferon to chemoattract lymphocytes. It has been confirmed that CXCL10 has many biological functions, such as chemotaxis monocytes, activated T cells and NK cells for expansion [14]. The study of Zhang
The present study agreed with study of Zhao
The study of Ahmed and Salih, [30], showed the IL-10 increased significantly after vaccination in female more than male. This may be the women exhibition a greater immune response to vaccine and facilities their activity, they also experience more frequency and severity than men. The study of Chang
This study investigated the CXCL 10 was highly elevated in COVID-19 patients than control group, also noted the CXCL 10 increased with disease progress, therefor consider a good marker for poor outcome, furthermore the obese patients are more likely to have severe outcomes than others, so BMI is considered a risk factor for patients.