Increased serum resistin but not G-CSF levels are associated in the pathophysiology of major depressive disorder: Findings from a case-control study

Abstract

Background Many studies have predicted major depressive disorder (MDD) as the leading cause of global health by 2030 due to its high prevalence, disability, and illness. However, the actual pathophysiological mechanism behind depression is unknown. Scientists consider alterations in cytokines might be tools for understanding the pathogenesis and treatment of MDD. Several past studies on several inflammatory cytokine expressions in MDD reveal that an inflammatory process is activated, although the precise causes of that changes in cytokine levels are unclear. Therefore, we aimed to investigate resistin and G-CSF in MDD patients and controls to explore their role in the pathogenesis and development of depression. Methods We included 220 participants in this study. Among them, 108 MDD patients and 112 age-sex matched healthy control (HCs). We used DSM-5 to evaluate study participants. Also, we applied the Ham-D rating scale to assess the severity of patients. Serum resistin and G-CSF levels were measured using ELISA kits (BosterBio, USA). Results The present study observed increased serum resistin levels in MDD patients compared to HCs (13.82 ± 1.24ng/mL and 6.35 ± 0.51ng/mL, p <0.001). However, we did not find such changes for serum G-CSF levels between the groups. Ham-D scores showed a significant correlation with serum resistin levels but not G-CSF levels in the patient group. Furthermore, ROC analysis showed a fairly predictive performance of serum resistin levels in major depression (AUC = 0.746). Conclusion The present study findings suggest higher serum resistin levels are associated with the pathophysiology of MDD. This elevated serum resistin level may serve as an early risk assessment indicator for MDD. However, the role of serum G-CSF in the development of MDD is still unclear despite its neuroprotective and anti-inflammatory effects.

Relationship of herpesvirus (HSV1, EBV, CMV, HHV6) seropositivity with depressive disorder and its clinical aspects: The first study in children

“…29 The relationship between depressive disorder and inflammation has been identified in several studies. [30][31][32][33][34][35][36] Whether infections trigger depression or depression predisposes individuals to infections is an important question. One study found that the expression of inflammation-related genes was increased and that the expression of antiviral-related genes was decreased in adolescents with clinically significant levels of depressive symptoms compared with their peers with lower levels of depressive symptoms.…”

“…The relationship between depressive disorder and inflammation has been identified in several studies 30–36 . Whether infections trigger depression or depression predisposes individuals to infections is an important question.…”

Higher IL-6 and IL-4 plasma levels in depressed elderly women are influenced by diabetes mellitus

“…Since the early 1990s, depressive disorders have been associated with altered circulating levels of inflammatory markers, such as interleukin (IL) -6 and tumor necrosis factor (TNF) (1)(2)(3) . This is a matter still on debate with recent findings confirming the association of altered cytokine levels and MDD (4)(5)(6) . There is also evidence of T helper (Th) 1/Th2 cytokine imbalance (7)(8)(9)(10) , with higher Th1/Th2 ratios in depressed patients when compared to controls.…”

Evaluation of serum interleukin‐1 receptor antagonist levels in major depressive disorder: A case‐control study

“…It is thought to be complex and multifactorial, with several biological, genetic, environmental, and psychological factors contributing to the development of depression. 12 , 13 , 14 , 15 , 16 Based on several studies, 17 , 18 depression is associated with cell‐mediated immunity activation and a persistent low‐grade inflammatory response. It has been hypothesized that the release of cytokines in response to immune system activation could be a possible cause of depression.…”

“… 17 , 35 Thus, major depression has been correlated with a CIRS that suppresses the immune‐inflammatory reaction, that in turn results in sickness behavior, which is the outcome of a CIRS for acute inflammation. 19 A decrease in adrenocortical activity and a decrease in hippocampal neurogenesis has demonstrated the significance of IL‐1RA in the progression of depression. 36 , 37 However, a little work has been done so far, with varied outcomes.…”