Published online Sep 19, 2026. doi: 10.5498/wjp.117289
Revised: February 27, 2026
Accepted: July 29, 2026
Published online: September 19, 2026
Processing time: 215 Days and 21.2 Hours
The increasing prevalence of depression among adolescents is a global public health concern. Although inflammation has been implicated in adult depression, the relationship between plasma cytokine levels and the severity of depression in adolescents remains unclear.
To investigate plasma cytokine dynamics in first-episode adolescent depression and their correlation with depression severity to identify potential diagnostic bio
In this observational, cross-sectional study, 100 adolescents with first-episode depression and 50 healthy controls were enrolled. Fasting plasma levels of inter
The effective response rates were 91.74% (patient group) and 94.34% (control groups). Baseline levels of IL-10, IL-6, and TNF-α were significantly higher in the severe depression group than in the mild-to-moderate group (all P < 0.05). After 8 weeks of treatment, no significant differences in the levels of these cytokines persisted between the severity groups (P > 0.05). Binary logistic regression identified log-transformed IL-6 as an independent risk factor (odds ratio = 6.290, 95%CI: 2.708-14.608).
IL-10, IL-6, and TNF-α are dysregulated in first-episode adolescent depression and significantly associated with baseline severity. These cytokines are potential biomarkers for diagnosing adolescent depression, assessing seve
Core Tip: In this study, we investigated the relationship between plasma cytokine levels and severity of first-episode adolescent depression. A cross-sectional analysis of 100 patients and 50 controls revealed that levels of interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha were significantly higher in severe cases than in mild-to-moderate cases before treatment. These differences normalized after 8 weeks of treatment. Logistic regression analysis identified IL-6 level as an independent risk factor. These findings suggest that these cytokines are dysregulated and are correlated with depression severity, indicating their potential use as biomarkers for diagnosis and clinical assessment.
- Citation: Dai H, Chen J, Yin ZP. Correlational study on plasma cytokine levels and severity of depression in first-episode adolescent depression patients. World J Psychiatry 2026; 16(9): 117289
- URL: https://www.wjgnet.com/2220-3206/full/v16/i9/117289.htm
- DOI: https://dx.doi.org/10.5498/wjp.117289
Adolescent depression is on the rise and is affecting an estimated 300 million people worldwide according to the World Health Organization[1]. Depression amongst adolescents is common in China[2]. Environmental, genetic, social, cultural, and psychological factors are involved in its emergence[3]. Recently, immune and inflammatory responses have been shown to play crucial roles in the development of depression[4,5]. Dementia increases cytokine levels, leading to inflammation. Among these inflammatory cytokines are tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6. The pathophysiology of depression is strongly affected by these cytokines. Neuroendocrine dysregulation stimulates the hypothalamic-pituitary-adrenal axis, which may cause an increase in TNF-α and IL-6 concentrations in individuals with depression[6]. Moreover, these pro-inflammatory cytokines can also affect neuronal plasticity and, consequently, brain-derived neurotrophic factor production, and by proxy, neural development, and synapse formation[7]. Furthermore, these inflammatory mediators may activate the immune cells in the central nervous system and affect the permeability of the blood-brain barrier, both of which can worsen the symptoms of depression[8].
The particular characteristics of the immune inflammatory response become evident throughout puberty because of the substantial changes in the maturation of the immunological system[9]. Recent research has revealed that teenagers with depression have increased blood levels of certain pro-inflammatory cytokines; therefore, inflammation may plausibly be instrumental in the development and progression of depression in this age group[10-12]. Owing to developmental changes, the immune-inflammatory responses of teenagers are different from those of younger people. Levels of IL-6 and TNF-α are much higher in teenage girls with a mood disorder than in healthy controls[13,14]. There is considerable evidence that compromised immune systems in adolescents with depression are linked to an increase in pro-inflammatory cytokines, which may result in an altered Th1/Th2 cytokine ratio towards Th1 predominance[15].
Currently, the diagnosis of depression in clinical practice primarily relies on subjective clinical interviews and scale assessments, such as the 24-item Hamilton Depression Rating Scale (HAMD-24), which lacks objective biological markers[16]. In adults, the correlation between plasma cytokine levels and disease severity has been extensively investigated, with many studies reporting elevated levels of pro-inflammatory cytokines like IL-6 and TNF-α in adults with depression, which are often associated with symptom severity[17]. However, findings remain inconsistent[18], and research specifically focusing on first-episode drug-naïve adolescents is scarce[19,20]. The dynamic changes in the levels of these cytokines during treatment and their precise relationship with depression severity in this vulnerable population are yet to be fully elucidated[12].
This study compared plasma cytokine levels in patients and healthy controls to study the role of inflammation in teenage depression. We sought to determine the correlation between these variables and the degree of depression to enable early diagnosis and individual treatment.
In this observational cross-sectional study, 100 adolescents, who were treated in Wenzhou Seventh People’s Hospital for a first episode of depression between June 2023 to June 2024, were enrolled. In addition, we recruited 50 healthy volunteers as controls concurrently and matched them on a sex and age basis. All 100 participants underwent a comprehensive assessment, which included the HAMD-24, administered by two trained physicians to ensure reliability. Subsequently, the patients were classified into groups according to the severity of their depressive conditions using their HAMD-24 scores: (1) A mild-to-moderate depression group (HAMD-24 score: 20-34, n = 54); and (2) A severe depression group (HAMD-24 score: ≥ 35, n = 46). The standardized treatment regimen for the teenage patients was 8 weeks and involved psychotherapy and the selective serotonin reuptake inhibitor (SSRI) fluoxetine; benzodiazepines were administered only when necessary. Informed consent was obtained from the guardians before the initiation of therapy. Patients were instructed to follow a specific eating plan for the duration of therapy.
Sample size was estimated based on pro-inflammatory cytokine level differences reported in prior studies and the expected effect size of this study[21], using the following statistical formula: n = (Z1-α/2 +Z1-β)2/(δ/σ) 2.
To gain statistical power, we introduced a 20% buffer and planned to have a minimum of 50 patients and 50 healthy controls in each group to ensure reliability.
Parameters: (1) The n is the size of the sample for each category; (2) The critical value for a two-tailed test for a = 0.05 is 1.96, which is given by Z1 minus a/2; (3) The critical value for 80% power (between 0.20 and 0.84) is Z1 minus β; (4) The d: The anticipated means of the two groups are 2.5; and (5) The s: SD of the pooled data (3.0).
Study group (patients): The following are some of the inclusion criteria for this study: (1) Age between 12 years and 18 years; (2) Diagnosed with depression according to the International Classification of Diseases-10; (3) HAMD-24 score of 20 or higher at the beginning of the study; (4) First episode of depression; (5) Not taking any medication for at least 2 weeks before enrollment in the study; (6) Regular eating habits; and (7) The ability to complete some assessments by themselves with the help of parents or guardians. The exclusion criteria were as follows: (1) Other mental conditions (such as bipolar illness, drug abuse, or mental retardation) and co-occurring infectious or neurological illnesses or diseases that are correlated with inflammation (such as autoimmune disease); (2) Individuals with cognitive or communicative problems that prevent their evaluation; (3) Guardians who were unable to cooperate in the research protocol; and (4) People who had recently used immunomodulators, corticosteroids, or nonsteroidal anti-inflammatory medications in the last 4 weeks.
Control group: Healthy volunteers.
Group C: Healthier volunteers.
Children between the ages of 12 and 18 who were able to understand and comply with research protocols were allowed to participate.
Inclusion requirements + history of mental illness, either in the patient's immediate family or in distant generations NOT (International Classification of Diseases-10 criteria): The inflammatory state is altered by infectious illnesses and systemic disorders, and immunomodulators, corticosteroids, or nonsteroidal anti-inflammatory medications are utilized during the last 4 weeks.
Each participant (or legal guardian) provided written informed consent before the study started. The Ethics Committee of Wenzhou Seventh People’s Hospital approved the research.
The participants’ age, sex, first-episode status, age at onset, body mass index (BMI), current medications, and illness duration were collected using a self-designed questionnaire. Diagnostic interviews and evaluations were conducted by two doctors or other highly trained medical professionals. To collect demographic and clinical data from eligible patients, trained research assistants accompanied the participants and obtained their and their guardians’ permission.
All study participants had to control their emotions, not exercise too hard, or fast the previous night. Using known techniques, experienced clinicians collected 10 mL of fasting venous blood from the cubital vein the following morning into anticoagulant tubes. In particular, anticoagulant tubes without RNase were used to collect 5 mL of venous blood. After centrifugation of the plasma samples at 3000 rpm for 10 minutes at ambient temperature and climatic conditions, the samples were stored at -80 °C until analysis. Plasma cytokines were quantified using ultra-sensitive multiplex electrochemiluminescence immunoassays. Measurements was performed under strict control of storage, testing, and sampling conditions to ensure consistent and valid results.
The variables of interest were the concentrations of plasma cytokines, including pro-inflammatory cytokines IL-6, IL-10 and TNF-α. The HAMD-24 was used to grade depression. Two trained physicians separately assessed each patient to ensure interrater reliability. Each item on the HAMD-24 was scored on a 5-point Likert scale. An HAMD-24 score of 20-34 indicated mild to moderate depression and a score of 35 or more indicated severe depression. Using correlational analysis, we examined the correlation between the levels of cytokines (IL-6, IL-10, and TNF-α) in the plasma and depression severity.
This study used the Supreme Statistical Program software version 26.0 for statistical analyses. The mean ± SD was used to describe continuous variables with a normal distribution, and group comparisons were performed using independent t-tests. Comparisons between groups were performed using Kruskal-Wallis tests, and median and interquartile range were provided for data that were not normally distributed. The n (%) were used to describe categorical variables, and dif
The sample size was 109 survey questionnaires, which provided 100 valid responses (91.74) to the patient group. Of the 53 surveys mailed to the control group, 50 (94.34) were valid.
Of the 100 patients that were included, 48 were males and 52 females. The mean age was 15.58 ± 1.98 years and mean BMI was 22.34 ± 3.18 kg/m2. The control group consisted of 50 participants, including 27 females and 23 males, with a mean age of 15.20 years (SD = 2.00) and a BMI of 22.07 (SD = 2.94). No significant differences were observed between the research and control groups in terms of age, sex, BMI, or being an only child (P > 0.05), as shown in Table 1.
| Variables | Study group (n = 100) | Control group (n = 50) | P value |
| Age (years) | 15.58 ± 1.98 | 15.20 ± 2.00 | 0.271 |
| Gender (female/male) | 52/48 | 27/23 | 0.624 |
| BMI (kg/m2) | 22.34 ± 3.18 | 22.07 ± 2.94 | 0.616 |
| Only child | 0.651 | ||
| Yes | 89 (89.00) | 46 (92.00) | |
| No | 11 (11.00) | 4 (8.00) |
The levels of IL-10 did not differ between the patient and control groups before treatment (P > 0.05), the levels of IL-6 and TNF-α were significantly lower in the control group (P < 0.05). The plasma cytokine levels did not vary between the two groups at the end of the 8-week treatment period (Figure 1).
Before treatment, the levels of IL-10, IL-6, and TNF-α were significantly higher in patients with severe depression compared to those with mild-to-moderate depression (P < 0.05). Table 2 indicates that the concentration of IL-10, IL-6 and TNF-α did not differ significantly (P > 0.05) between the patients with mild to moderate depression and those with severe depression after the 8 weeks of treatment.
| Plasma cytokines (ng/L) | Mild to moderate depression (n = 54) | Severe depression (n = 46) | P value |
| Before treatment | |||
| IL-10 | 0.46 (0.38, 0.55) | 0.71 (0.44, 0.90) | < 0.001 |
| IL-6 | 1.19 (0.90, 1.63) | 2.43 (1.65, 3.51) | < 0.001 |
| TNF-α | 0.87 (0.60, 1.13) | 1.51 (0.98, 1.95) | < 0.001 |
| After treatment | |||
| IL-10 | 0.49 (0.36, 0.57) | 0.40 (0.23, 0.59) | 0.074 |
| IL-6 | 1.02 (0.70, 1.40) | 1.02 (0.75, 1.35) | 0.750 |
| TNF-α | 0.97 (0.70, 1.24) | 0.96 (0.71, 1.23) | 0.793 |
Patients with mild-to-moderate and severe depression recorded an average score of 28.59 ± 4.16 and 52.50 ± 8.71 on HAMD-24 before treatment, respectively. The difference was statistically significant. Whereas, at the end of 8 weeks treatment, the scores were 18.31 ± 4.70 and 25.65 ± 6.18 respectively, and the difference between the groups was statistically significant (Figure 2).
Using “whether the patient had severe depression” as the dependent variable, and IL-6, IL-10, and TNF-α levels as independent variables, stepwise binary logistic regression analysis was performed. The results showed that log-transformed (Lg)IL-6 [odds ratio (OR) = 6.290, 95%CI: 2.708-14.608, P < 0.001], LgIL-10 (OR = 142.175, 95%CI: 5.984-3377.904, P < 0.001), and LgTNF-α (OR = 16.106, 95%CI: 4.057-63.937, P < 0.001) were independent risk factors for severe depression, as shown in Figure 3.
Adolescent depression is a major mental health concern. An increasing number of studies over the past few years have suggested that aberrant stimulation of the immune system is a potential major player in the pathophysiology of depression[22,23]. Patients with depression, especially in their teenage years when the neurological and immune systems are still maturing, exhibit abnormally high levels of proinflammatory mediators in their blood. These agents, such as IL-6 and TNF-α, can cause inflammation in the brain and neurotransmitter imbalances which aggravates the symptoms of depression[24,25]. However, a comprehensive analysis of the features of plasma cytokine alterations in adolescents with first-episode depression and their relationship to the severity of depression remains lacking.
In this study, we found that adolescents with depression diagnosed with a first episode had substantially higher baseline levels of plasma pro-inflammatory cytokines (IL-6 and TNF-α) than the control group (P < 0.05), which is consistent with previous results[26,27]. More importantly, our analysis of the severity subgroups revealed that patients with severe depression exhibited significantly higher baseline levels of IL-6, TNF-α, and even the anti-inflammatory cytokine IL-10, than those with mild-to-moderate depression. This finding suggests a more profound immune dysregulation in severe cases, characterized not only by an exaggerated pro-inflammatory response but also by a potentially com
The significant decrease in HAMD-24 scores and normalization of cytokine levels in the severe group after 8 weeks of SSRI treatment were particularly noteworthy. Post-treatment cytokine levels between the two severity groups were not significantly different, suggesting that effective antidepressant treatment can modulate immune dysregulation. This observation strengthens the hypothesis that these cytokines are state markers that reflect the current clinical condition, rather than fixed traits[30]. This finding is in line with meta-analyses showing that SSRIs such as fluoxetine can reduce pro-inflammatory cytokine levels[31]. The resolution of immune imbalance alongside symptom improvement provides compelling evidence for the intricate link between the inflammatory and psychological systems in adolescent depression[30,32].
Additionally, the small sample size of the study could explain why the difference in the level of IL-10 between the treatment-naive and control groups did not significantly influence the results, even though IL-10 was higher in the former[33]. Besides, IL-6, IL-10 and TNF-α were predicted as independent risk variables of severe depression (P < 0.01) based on the multivariable logistic regression analysis, which offers a potential biological foundation of clinical evaluation[11,34].
This study shows that the severity of adolescent depression is correlated with increased plasma concentrations of IL-6 and TNF-α that may be utilized as a foundation for immunotherapy[25,35]. Plasma cytokines as biomarkers used in future research ought to examine immunological systems to enhance personal diagnosis and treatment of individuals. Therefore, inflammatory modulators may be beneficial auxiliary treatments. However, to enhance therapeutic strategies, a better understanding of immune processes is required, which would necessitate multicenter, large-scale, longitudinal studies.
This study adds to the body of knowledge on the immunological mechanisms that cause depression in adolescents, but has some limitations. First, the cross-sectional nature of the study made it impossible to draw any definite conclusions regarding the existence of a causal relationship between plasma cytokine levels and depression. This observation highlights the need for prospective research to examine how immune markers evolve at various stages of treatment and to confirm their role in the development of illnesses. Second, owing to demographic and geographic heterogeneity, a single-center sample might not be representative of the entire population; therefore, it is better to use multicenter partnerships to make the sample more representative. Third, the levels of cytokines could be confounded by other factors that the study did not consider, including comorbid mental issues, diet, sleep, and stress. Finally, the results cannot be generalized to a larger population because of the small sample size. These results must be further validated by conducting large multicenter randomized controlled trials.
Pro-inflammatory cytokines such as TNF-α and IL-6 were elevated in adolescents with depression. Furthermore, baseline levels of IL-6, TNF-α, and IL-10 were significantly higher in adolescents with severe depression than in those with mild-to-moderate depression, and these differences resolved after successful treatment. Multivariable analysis also identified TNF-α, IL-10, and IL-6 as independent risk variables that add to severity of depression. These findings indicate that immune responses are important in the development of depression in adolescents, and that they may be used as immunological predictors of depression severity in clinical assessments.
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