The specific associations between antidepressant treatment and alterations in the levels of cytokines remain to be elucidated. In this study, we aimed to explore the role of IL-2, IL-4, IL-12, TNF-α, TGF-β1, and MCP-1 in major depression and to investigate the effects of sertraline therapy. Cytokine and chemokine levels were measured at the time of admission and 8 weeks after sertraline treatment. Our results suggest that the proinflammatory cytokines (IL-2, IL-12, and TNF-α) and MCP-1 were significantly higher, whereas anti-inflammatory cytokines IL-4 and TGF-β1 were significantly lower in patients with major depression than those of healthy controls. It seems likely that the sertraline therapy might have exerted immunomodulatory effects through a decrease in the proinflammatory cytokine IL-12 and an increase in the anti-inflammatory cytokines IL-4 and TGF-β1. In conclusion, our results indicate that Th1-, Th2-, and Th3-type cytokines are altered in the depressed patients and some of them might have been corrected by sertraline treatment.

Our results concerning correlations suggest that disturbances in BMI, body fat, and lipid metabolism may contribute to altered oxidative status in NAFLD, and insulin resistance may be related to decreased antioxidants in NAFLD as well as products of lipid peroxidation. However, although our results suggest interesting correlations, this different mostly "weak" relationships must be taken with caution.

Risk assessment of central nervous system (CNS) infection patients is of key importance in predicting likely pathogens. However, data are lacking on the epidemiology globally. We performed a multicenter study to understand the burden of community-acquired CNS (CA-CNS) infections between 2012 and 2014. A total of 2583 patients with CA-CNS infections were included from 37 referral centers in 20 countries. Of these, 477 (18.5%) patients survived with sequelae and 227 (8.8%) died, and 1879 (72.7%) patients were discharged with complete cure. The most frequent infecting pathogens in this study were Streptococcus pneumoniae (n = 206, 8%) and Mycobacterium tuberculosis (n = 152, 5.9%). Varicella zoster virus and Listeria were other common pathogens in the elderly. Although staphylococci and Listeria resulted in frequent infections in immunocompromised patients, cryptococci were leading pathogens in human immunodeficiency virus (HIV)-positive individuals. Among the patients with any proven etiology, 96 (8.9%) patients presented with clinical features of a chronic CNS disease. Neurosyphilis, neurobrucellosis, neuroborreliosis, and CNS tuberculosis had a predilection to present chronic courses. Listeria monocytogenes, Staphylococcus aureus, M. tuberculosis, and S. pneumoniae were the most fatal forms, while sequelae were significantly higher for herpes simplex virus type 1 (p < 0.05 for all). Tackling the high burden of CNS infections globally can only be achieved with effective pneumococcal immunization and strategies to eliminate tuberculosis, and more must be done to improve diagnostic capacity.

Interleukin (IL)-18 is a proinflammatory cytokine which plays a crucial role in T helper (Th)1 type immune response. The aim of this study is to investigate the relationship of serum levels of IL-18 with disease activity and clinical presentations in patients with Behcet's disease (BD). Sixty patients with BD and 20 healthy controls were included in the study. Patients were grouped as having active or inactive disease according to the Leeds activity score. They were also separated as a systemic involvement or mucocutaneous symptoms only. Patients with systemic involvement were further grouped according to the presence of ocular, articular and vascular involvement. IL-18 levels were significantly higher in all patient subgroups as compared to healthy controls and found to be correlated with the activity score in patients having active disease. In conclusion, this cytokine participates in the pathogenesis of BD and its levels are correlated with the disease activity. Detection of increased levels of IL-18 in patients with inactive disease implies that Th1 activation and subclinical inflammation persist during the inactive period of the disease.

Our results suggest that the high tissue adiponectin levels significantly detected in breast cancer patients and associated with an increased risk for breast cancer.

Objectives: Multiple sclerosis (MS) is a chronic inflammatory disease of the human central nervous system. In the present study, we aimed to determine adiponectin, tumor necrosis factor-α, interleukin (IL)-12p70, and IL-13 levels in the sera of patients with MS and to investigate the effects of interferon (IFN), glatiramer acetate (GA), and immunosuppressive treatment regimens on these parameters. Methods: Fifty-seven patients with MS and 34 healthy controls were enrolled into the study. Serum cytokine levels were measured using enzyme immunoassay. Results: Significantly elevated levels of IL-12p70 and IL-13 were found in the sera of patients with MS, but decreased adiponectin levels were found in patients’ sera compared to healthy controls. The levels of IL-12p70 and IL-13 in the IFN therapy group were higher than those of the healthy controls. However, the IL-12p70 and IL-13 levels in the GA therapy group were not different from those of the healthy controls. There were no differences with regard to adiponectin levels among the subgroups of patients with MS according to therapy regimen and the healthy controls. At the end of a 2-year follow-up period, Expanded Disability Status Scale (EDSS) values were found to be increased in the IFN therapy group but unchanged in the GA therapy group. Conclusions: These findings suggest that adiponectin, IL-12p70, and IL-13 may play a role in the pathogenesis of MS. Additionally, GA therapy regimens in MS are more effective than IFN therapy with respect to decreasing the levels of IL-12p70 and IL-13 and stabilizing the EDSS value.

The objective of this study has been the well established fact that proinflammatory cytokines and metalloproteinases play a crucial role in the pathogenesis of chronic arthritis as well as the development of pannus, with the eventual erosive changes. Among the proinflammatory cytokines, interleukin-18 (IL-18) has been shown to contribute to the pathogenesis of chronic synovitis by increasing the secretion of interleukin-1beta (IL-1beta) and the tumor necrosis factor-alpha (TNF-alpha) and also stimulating angiogenesis. The aim of this study is to investigate the synovial IL-18, IL-1beta, TNF-alpha and matrix metalloproteinase-3 (MMP-3) levels in patients with Behçet's disease (BD), and compare them with the levels of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). 30 patients with BD, 20 with RA, and 20 with OA were included in the study. The synovial levels of IL-18, IL-1beta, TNF-alpha and MMP-3 were detected using the two-step sandwich ELISA method. The synovial IL-18, TNF-alpha and MMP-3 levels were significantly higher in RA patients than patients with BD (P=0.004, 0.019, 0.025, respectively) and with OA (P=0.004, 0.045, 0.032, respectively). There were no differences, with respect to the cytokine levels, when patients with BD were compared with those with OA. Patients with RA and BD had higher IL-1beta levels than patients with OA (P=0.017, 0.013, respectively). However, no such difference was found for IL-1beta between BD and RA patients. Among patients with RA, positive correlations were found between TNF-alpha and MMP-3 (r=0.683, P=0.001). Our results showed that MMP-3 and proinflammatory cytokines, except IL-1beta, were expressed in relatively small quantities in Behçet's synovitis. Detection of the lower levels of these cytokines and metalloproteinases might explain the non-erosive character of Behçet's arthritis. We suggest that IL-1beta may be involved in the pathogenesis of Behçet's synovitis.

SUMMARYAlthough some information is available regarding immune activation in familial Mediterranean fever (FMF), little is known about either peripheral blood T cell activation marker expression or the T cell proliferative response to phytohaemagglutinin (PHA). In the present study, we aimed to investigate the percentages of peripheral blood lymphocyte subsets, T cell expression of cellular activation markers (CD25, CD69, HLA-DR), the T cell response to PHA and serum levels of soluble interleukin-2 receptor (sIL-2R) and interleukin (IL)-10 in patients with FMF. Forty patients with FMF were enrolled into the study. Control groups were sex-and age-matched and consisted of 20 healthy blood donors and 15 patients with inactive Behçet's disease. The patients with FMF in an attack period had higher levels of sIL-2R than those in an attack-free period, and also in comparison with both control groups. The levels of sIL-2R were also found to be higher in patients with FMF in an attack-free period than those in both control groups. The mean levels of IL-10 were found to be lower in patients with FMF in an attack-free period than those in an attack period and were also lower than those in the healthy controls. In an acute attack period, the absolute counts of CD3 CD25+ and CD8 + CD69 + T cells in peripheral blood samples were also higher than those in both control groups. Both the percentages and absolute counts of CD4 + CD69+ T cells in peripheral blood samples of patients with FMF in an attack-free period were slightly but significantly higher than those in the healthy controls. In conclusion, our study indicates that the T cell system is abnormally activated in patients with FMF in both the attack and attack-free period and that decreased IL-10 levels may create a tendency to perpetuate subclinical immune activation in the attack-free period.