Inflammation In People Research Articles

Abdominal Adipose Tissue Is Associated With Alterations in Tryptophan-Kynurenine Metabolism and Markers of Systemic Inflammation in People With Human Immunodeficiency Virus.

While both adipose tissue accumulation and tryptophan metabolism alterations are features of human immunodeficiency virus (HIV) infection, their interplay is unclear. We investigated associations between abdominal adipose tissue, alterations in kynurenine pathway of tryptophan metabolism, and systemic inflammation in people with HIV (PWH). Eight hundred sixty-four PWH and 75 uninfected controls were included. Plasma samples were collected and analyzed for kynurenine metabolites, neopterin, high-sensitivity C-reactive protein (hs-CRP), and lipids. Regression models were used to test associations in PWH. PWH had higher kynurenine-to-tryptophan ratio than uninfected individuals (P < .001). In PWH, increase in waist-to-hip ratio was associated with higher kynurenine-to-tryptophan ratio (P = .009) and quinolinic-to-kynurenic acid ratio (P = .006) and lower kynurenic acid concentration (P = .019). Quinolinic-to-kynurenic acid ratio was associated with higher hs-CRP (P < .001) and neopterin concentrations (P < .001), while kynurenic acid was associated with lower hs-CRP (P = .025) and neopterin concentrations (P = .034). In PWH, increase in abdominal adipose tissue was associated with increased quinolinic-to-kynurenic acid ratio, suggesting activation of proinflammatory pathway of kynurenine metabolism, with reduction of anti-inflammatory molecules and increase in systemic inflammation. Our results suggest dysregulation of kynurenine metabolism associated with abdominal fat accumulation to be a potential source of inflammation in HIV infection.

Sex Differences in the Association of Fat and Inflammation Among People with Treated HIV Infection.

Introduction:Ectopic fat deposition may contribute to chronic inflammation in people with HIV (PWH). To provide information for future mechanistic studies of metabolic risk in this population, we sought to determine which fat measures relate more strongly to inflammation and whether the fat-inflammation relationship is modified by sex or HIV status.Methods:We conducted a cross-sectional study of 105 PWH and 20 age- and sex-matched HIV-negative controls. Interleukin-6 (IL-6) and high-sensitivity C reactive protein (hs-CRP) levels were measured from plasma. Pericardial fat (PCF) and thoracic periaortic adipose tissue (TAT) volumes and peri-right coronary artery (RCA), left atrium (LA) roof, and liver densities were measured from cardiac CT scans. Unadjusted and multivariate adjusted linear regression models were used to determine the relationship between ectopic fat measures and inflammation biomarkers.Results:Forty participants had BMI < 25, 33 had BMI 25 to 30, and 52 had BMI > 30. Systolic blood pressure and insulin resistance increased with BMI. Participants with higher BMI had a higher CD4+ count. In models adjusted for demographics, HIV status, and metabolic risk factors, BMI was positively associated with IL-6 and hs-CRP. Ectopic PCF and TAT volumes were positively associated with IL-6 and hs-CRP; however, these relationships were somewhat attenuated in adjusted models. LA roof (but not peri-RCA) fat radiodensity was inversely associated with hs-CRP in fully adjusted models, and the association with IL-6 was borderline statistically signifi-cant (P = 0.054). IL-6 was more strongly associated with BMI and LA roof density in women than in men (P for interaction = 0.05).Conclusions:Among PWH receiving antiretroviral therapy, higher BMI and excessive ectopic fat burden were associated with circulating markers of systemic inflammation. Because these measures appear to be more strongly related to inflammation among women than men, future clinical studies of metabolic risk and inflammation among PWH should include sex-stratified analyses.

Lung Injury on Antiretroviral Therapy in Adults With Human Immunodeficiency Virus/Tuberculosis.

Immune restoration on antiretroviral therapy (ART) can drive inflammation in people living with human immunodeficiency virus (HIV) who have pulmonary tuberculosis (TB), but its effects on the lungs have not been assessed. We evaluated associations between pulmonary inflammation, recovery of pathogen-specific CD4 T-cell function, and lung injury prior to and after ART initiation in adults with HIV and pulmonary TB. This was a prospective cohort study in South Africa, following adults with HIV and pulmonary TB prior to and up to 48 weeks after ART initiation. Pulmonary-specific inflammation was defined as total glycolytic activity (TGA) on [18]F-fluorodeoxyglucose (FDG) positron emission tomography-computed tomography (PET-CT) at baseline and 4 weeks after ART initiation. Spirometry, respiratory symptom tests, and flow cytometry were performed at the same times to assess lung involvement and the frequency of mycobacteria-specific CD4 T-cells. In addition, we evaluated lung function longitudinally up to 48 weeks after ART initiation. Greater lung TGA on FDG PET-CT was associated with worse lung function and respiratory symptoms prior to ART initiation, and nearly half of subjects experienced worsening lung inflammation and lung function at Week 4 of ART. Worsening Week 4 lung inflammation and pulmonary function were both associated with greater increases in pathogen-specific functional CD4 T-cell responses on ART, and early decreases in lung function were independently associated with persistently lower lung function months after TB treatment completion. Increases in pulmonary inflammation and decreases in lung function are common on ART, relate to greater ART-mediated CD4 T-cell restoration, and are associated with the persistent impairment of lung function in individuals with HIV/TB.

Oral hygiene interventions for people with intellectual disabilities.

Oral hygiene interventions for people with intellectual disabilities.

Why Treating Chronic Low-Grade Inflammation in People with the Risk Gene for Alzheimer's Disease Could Be a Viable Therapeutic Option

Why Treating Chronic Low-Grade Inflammation in People with the Risk Gene for Alzheimer's Disease Could Be a Viable Therapeutic Option

Interventions for reducing inflammation in familial Mediterranean fever.

Interventions for reducing inflammation in familial Mediterranean fever.

New asthma testing enhances the care of respiratory patients

New asthma testing enhances the care of respiratory patients

Impact of exercise therapy on molecular biomarkers related to articular cartilage and inflammation in people at risk of, or with established, knee osteoarthritis: a systematic review and meta-analysis of randomized controlled trials

Impact of exercise therapy on molecular biomarkers related to articular cartilage and inflammation in people at risk of, or with established, knee osteoarthritis: a systematic review and meta-analysis of randomized controlled trials

Physical Activity and Exercise Capacity in Severe Asthma: Key Clinical Associations

Physical inactivity and sedentary time are distinct behaviors that may be more prevalent in severe asthma, contributing to poor disease outcomes. Physical activity and sedentary time in severe asthma however have not been extensively examined. We aimed to objectively measure physical activity and sedentary time in people with severe asthma compared with age-matched control participants, describing the associations of these behaviors with clinical and biological outcomes. We hypothesized that people with severe asthma would be less active and more sedentary. In addition, more activity and less sedentary time would be associated with better clinical outcomes and markers of systemic and airway inflammation in people with severe asthma. Adults with severe asthma (n= 61) and sex- and age-matched controls (n= 61) underwent measurement of lung function, exercise capacity, asthma control, health status, and airway and systemic inflammation. Physical activity and sedentary time were measured using an accelerometer. The severe asthma and control groups were matched in terms of age and sex (32 [53%] females in each group). Individuals with severe asthma accumulated less minutes per day in moderate and higher intensity activity, median (IQR) 21.9 (12.9-36.0) versus 41.7 (29.5-65.2) (P < .0001) and accumulated 2,232 fewer steps per day (P= .0002). However, they engaged in more light-intensity physical activity. No differences were found for sedentary time. In a multivariate regression model, steps per day were strongly and independently associated with better exercise capacity in participants with severe asthma (coefficient, 0.0169; 95% CI, 0.008-0.025; P < .001). People with severe asthma perform less moderate and vigorous activity than do controls. Higher levels of activity and lower levels of sedentary time are associated with better exercise capacity, asthma control, and lower levels of systemic inflammation.

Restoring Cystic Fibrosis Transmembrane Conductance Regulator Function Reduces Airway Bacteria and Inflammation in People with Cystic Fibrosis and Chronic Lung Infections.

Previous work indicates that ivacaftor improves cystic fibrosis transmembrane conductance regulator (CFTR) activity and lung function in people with cystic fibrosis and G551D-CFTR mutations but does not reduce density of bacteria or markers of inflammation in the airway. These findings raise the possibility that infection and inflammation may progress independently of CFTR activity once cystic fibrosis lung disease is established. To better understand the relationship between CFTR activity, airway microbiology and inflammation, and lung function in subjects with cystic fibrosis and chronic airway infections. We studied 12 subjects with G551D-CFTR mutations and chronic airway infections before and after ivacaftor. We measured lung function, sputum bacterial content, and inflammation, and obtained chest computed tomography scans. Ivacaftor produced rapid decreases in sputum Pseudomonas aeruginosa density that began within 48 hours and continued in the first year of treatment. However, no subject eradicated their infecting P. aeruginosa strain, and after the first year P. aeruginosa densities rebounded. Sputum total bacterial concentrations also decreased, but less than P. aeruginosa. Sputum inflammatory measures decreased significantly in the first week of treatment and continued to decline over 2 years. Computed tomography scans obtained before and 1 year after ivacaftor treatment revealed that ivacaftor decreased airway mucous plugging. Ivacaftor caused marked reductions in sputum P. aeruginosa density and airway inflammation and produced modest improvements in radiographic lung disease in subjects with G551D-CFTR mutations. However, P. aeruginosa airway infection persisted. Thus, measures that control infection may be required to realize the full benefits of CFTR-targeting treatments.

Arterial Stiffness Is Positively Associated With 18F-fluorodeoxyglucose Positron Emission Tomography-Assessed Subclinical Vascular Inflammation in People With Early Type 2 Diabetes.

Type 2 diabetes is accompanied by premature atherosclerosis and arterial stiffness. The underlying association remains incompletely understood. The possible relationship between subclinical arterial inflammation assessed by (18)F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) and arterial stiffness was investigated in patients with early type 2 diabetes. Patients with type 2 diabetes (n = 44), without cardiovascular disease and any type of antidiabetic medication, were studied (median age 63 years [interquartile range 54-66], men:women 27:17). Arterial inflammation was quantified as the FDG uptake maximal standardized uptake value (SUVmax). SUVmax was corrected for the prescan glucose level. A target-to-background ratio (TBR) was calculated by dividing the SUVmax of the arteries by the SUVmean of the caval veins (blood pool). TBRs were calculated for four individual segments (carotid arteries, ascending aorta and aortic arch, descending and abdominal aorta, and iliac and femoral arteries) and averaged for the total aortic tree (meanTBR). Arterial stiffness was assessed as central systolic blood pressure (cSBP), carotid-femoral pulse wave velocity (PWV), and augmentation index (AIx). The meanTBR was significantly associated with PWV (R = 0.47, P = 0.001) and cSBP (R = 0.45, P = 0.003) but not with AIx. TBR of each separate segment was also significantly associated with PWV and cSBP. In a multiple linear regression model including age, sex, BMI, hemoglobin A1c (HbA1c), hs-CRP, cholesterol, cSBP, and PWV, PWV was the strongest determinant of meanTBR. In patients with type 2 diabetes, FDG-PET/CT-imaged subclinical arterial inflammation is positively associated with determinants of arterial stiffness.

Does systemic inflammation and immune activation contribute to fracture risk in HIV?

There is increasing evidence pointing toward an important role of heightened immune activation and inflammation in people living with HIV contributing to the development of non-AIDS comorbidities. This review aims to explore low bone mineral density (BMD) in HIV with a focus on the underlying mechanisms and relationships between the immune and skeletal systems. Baseline immune activation and inflammation negatively impact BMD at antiretroviral therapy (ART) initiation. B- and T-cell alterations in HIV lead to an imbalance in the osteoblastic osteoprotegerin (OPG) and osteoclastic receptor activator of NF-κB ligand (RANKL) cytokines which favours osteoclastogenesis and bone resorption. These findings suggest an important role for immune-mediated mechanisms in the pathogenesis of low BMD in HIV. Bone homeostasis is in part regulated by cells of the immune system through complex interactions with the RANK/RANKL/OPG axis. Disturbances in the normal functioning of T, B cells, and monocytes in HIV and the resulting proinflammatory state may contribute to dysregulation of this finely controlled balance leading to increased bone loss. Pre-ART levels of immune activation and inflammation have a consistently negative effect on BMD and further suggest the immunocentric basis of bone loss in HIV alongside supporting the benefits of earlier ART initiation. Further longitudinal studies will help determine the effect this will have on fracture risk in people living with HIV.

Oral aspirin for treating venous leg ulcers.

Oral aspirin for treating venous leg ulcers.

Effect of N-acetylcysteine supplementation on oxidative stress status and alveolar inflammation in people exposed to asbestos: a double-blind, randomized clinical trial.

Many of the pathological consequences in the lung following inhalation of asbestos fibres arise as a consequence of persistent oxidative stress and inflammation. Inflammatory responses can be observed in asymptomatic asbestos-exposed individuals. There are currently no interventions to reduce inflammatory or oxidative responses to asbestos before disease develops. We investigated the effects of oral N-acetylcysteine (NAC) on indicators of inflammation or oxidative stress in asymptomatic people previously exposed to asbestos. A double-blind, randomized, placebo-controlled study was conducted to assess the effectiveness and safety of 1800 mg of NAC given orally over a period of 4 months. This was a proof of principle study. Effectiveness was assessed using indicators of inflammation or oxidation as primary end-points. Serum levels of total combined thiols (cysteine, cysteinylglycine, glutathione and homocysteine) were used to monitor the NAC supplementation. Thirty-four subjects were randomly allocated to NAC and 32 to placebo. Serum levels of total combined thiols were similar between the groups after intervention. There were no differences in levels of inflammatory or oxidative stress end-points between the groups. No adverse effects were identified. No evidence was found that NAC supplementation replenishes total combined thiols in the blood of healthy subjects with a history of asbestos exposure. There was also no evidence of reduced indicators of inflammation or oxidative stress. Further studies should determine the conditions required to increase levels of total anti-oxidant capacity in the blood and in the lungs of subjects with either asbestos-related diseases or subclinical lung inflammation.

Effects of dietary N-3 fatty acid and/or polyphenols on subclinical inflammation in people at high cardiovascular risk: the etherpaths project

Effects of dietary N-3 fatty acid and/or polyphenols on subclinical inflammation in people at high cardiovascular risk: the etherpaths project

Haemophilus influenzae responds to glucocorticoids used in asthma therapy by modulation of biofilm formation and antibiotic resistance.

Glucocorticosteroids are used as a main treatment to reduce airway inflammation in people with asthma who suffer from neutrophilic airway inflammation, a condition frequently associated with Haemophilus influenzae colonization. Here we show that glucocorticosteroids have a direct influence on the behavior of H. influenzae that may account for associated difficulties with therapy. Using a mouse model of infection, we show that corticosteroid treatment promotes H. influenzae persistence. Transcriptomic analysis of bacteria either isolated from infected mouse airway or grown in laboratory medium identified a number of genes encoding regulatory factors whose expression responded to the presence of glucocorticosteroids. Importantly, a number of these corticosteroid-responsive genes also showed elevated expression in H. influenzae within sputum from asthma patients undergoing steroid treatment. Addition of corticosteroid to H. influenzae led to alteration in biofilm formation and enhanced resistance to azithromycin, and promoted azithromycin resistance in an animal model of respiratory infection. Taken together, these data strongly suggest that H. influenzae can respond directly to corticosteroid treatment in the airway potentially influencing biofilm formation, persistence and the efficacy of antibiotic treatment.

Interventions for reducing inflammation in familial Mediterranean fever.

Familial Mediterranean fever, a hereditary auto-inflammatory disease, mainly affects ethnic groups living in the Mediterranean region. Early studies reported colchicine as a potential drug for preventing attacks of familial Mediterranean fever. For those people who are colchicine-resistant or intolerant, drugs such as rilonacept, anakinra, etanercept, infliximab, thalidomide and interferon-alpha might be beneficial. To evaluate the efficacy and safety of interventions for reducing inflammation in people with familial Mediterranean fever. We used detailed search strategies to search the following databases: CENTRAL; MEDLINE; Embase; Chinese Biomedical Literature Database (CBM), China National Knowledge Infrastructure Database (CNKI); Wan Fang; and VIP. In addition, we also searched the clinical trials registries including ClinicalTrials.gov, the International Standard Randomized Controlled Trial Number Register, the WHO International Clinical Trials Registry Platform and the Chinese Clinical Trial Registry, as well as references listed in relevant reports.Date of last search: 21 May 2014. Randomized controlled studies of people with diagnosis of familial Mediterranean fever, comparing active interventions (including colchicine, anakinra, rilonacept, etanercept, infliximab, thalidomide, interferon-alpha, ImmunoGuard™ (a herbal dietary supplement) and non-steroidal anti-inflammatory drugs) with placebo or no treatment, or comparing active drugs to each other. The authors independently selected studies, extracted data and assessed risk of bias. We pooled data to present the risk ratio or mean difference with their 95% confidence intervals. We assessed overall evidence quality according to the GRADE approach. We included four randomized placebo-controlled studies with a total of 75 participants (aged three to 53 years); three were of cross-over and one of parallel design. Two studies used the active intervention of oral colchicine (0.6 mg three times daily or 0.5 mg twice daily), one study used oral ImmunoGuard™ and the fourth used rilonacept as a subcutaneous injection. The duration of each study arm ranged from one to three months.The two most recent studies were generally well-designed, except for an unclear risk of detection bias in one of these. However, some inadequacy existed in the other two older studies, where each had an unclear risk of selection bias, a high risk of attrition bias, an unclear risk of reporting bias and a high risk of other potential bias (baseline characteristics such as mutation status and disease severity were not described); one of these studies additionally had an unclear risk of detection bias.We aimed to report on the number of participants experiencing an attack, the timing of attacks, any adverse drug reactions and the response of a number of biochemical markers from the acute phase of an attack, but data were not available for all outcomes across all comparisons.Based on one study (15 participants), there was a significant reduction in the number of people experiencing attacks at three months when colchicine was administered at a dose of 0.6 mg three times daily (14% versus 100%), risk ratio 0.21 (95% confidence interval 0.05 to 0.95); however, the GRADE evidence quality was low. Based on two further studies, there was no significant reduction in the number of participants experiencing attacks at two months when colchicine was administered at a dose of 0.5 mg twice daily (22 participants) in people with familial Mediterranean fever, or at three months when rilonacept was used in individuals who were colchicine-resistant or colchicine-intolerant (14 participants). In the ImmunoGuard™ study (24 participants) acute phase response indicators (including erythrocyte sedimentation rate, white blood cell count and C-reactive protein) were not reduced after one month treatment. There were limited randomized controlled studies assessing interventions for people with familial Mediterranean fever. Based on the evidence, colchicine appears to reduce the number of people experiencing attacks; however, only a few low-quality randomized controlled studies contributed data for analysis. Further randomized controlled studies examining active interventions, not only colchicine, are necessary before a comprehensive conclusion regarding the efficacy and safety of interventions for reducing inflammation in familial Mediterranean fever can be drawn.

A clearer view of type 1 diabetes

Medical Imaging![Figure][1] Nanoparticles help to visualize pancreatic inflammation in people with type 1 diabetes PHOTO: J. L. GAGLIA ET AL., PNAS 112 , 7 (17 FEBRUARY 2015) © NATIONAL ACADEMY OF SCIENCES Pancreatic beta cells keep blood glucose levels in check by secreting insulin, which removes glucose from blood. In type 1 diabetes, beta cells stop functioning because the immune system destroys them. Noninvasive imaging of pancreatic inflammation—an early sign of this immune attack—could provide scientists with new insights into how the disease begins and progresses. In a pilot study, Gaglia et al. used magnetic resonance imaging to generate three-dimensional high-resolution maps of pancreatic inflammation in patients with recent-onset type 1 diabetes. Key to their success was an imaging agent called ferumoxytol, a clinically approved magnetic nanoparticle taken up by macrophages. Proc. Natl. Acad. Sci. U.S.A. 112 , 2139 (2015). [1]: pending:yes

The neuroendocrine regulation's features of the inflammatory process in bronchial asthma

Event Abstract Back to Event The neuroendocrine regulation's features of the inflammatory process in bronchial asthma Alexandr V. Zhukov1 and Anatoliy P. Godovalov1* 1 Acad. E.A. Wagner Perm State Medical University, immunology, Russia Chronic inflammation is a key factor of pathogenesis of many diseases. It is known that the autonomic nervous system (ANS) takes part in an inflammatory process by the regulation of effector cells functions and redistribution of energy in the immune system. Patients with autoimmune, infectious and other diseases have a dysfunction of ANS. This could be primary dysfunction because it leads to overproduction of proinflammatory cytokines in response to the specific antigens [2]. It is considered that the sympathetic nervous system's (SNS) activity increases during inflammation what is necessary for the energy supply of the immune system. On the other hand a parasympathetic dysfunction leads to reduction of Th1-response which is necessary for an adequate inflammatory process and elimination of the pathogen [4]. This is realized by the interaction between nervous and immune systems. It is known that immune cells have got receptors to neuropeptides: acetylcholine, dopamine, enkephalins and endorphins. At the same time immune cells can synthesize neuropeptides and respond to most of substances from this group. Nervous cells can synthesize some cytokines and respond to them. That's why this systems can be considered to use the same number of signal molecules or they've got intersecting signal ways for intersystem communication.In this connection the research of features and activity of inflammation in people with different types of ANS during diseases is interesting. The purpose of research is the study of leukocytes structure and biochemical parameters of peripheral blood in patient with asthma depending on ANS type. Materials and methods. There were 15 patients with asthma. We counted leukocytes, glucose concentration, proteins, C-reactive protein and transaminases in peripheral blood. ANS type was determined by Vein's method [1]. Statistical analysis was performed with using Student's t-test. Results. Studies revealed that patients with sympathetic type of ANS were treated in hospital for 17.0±1.6 days but patients with parasympathetic type of ANS were treated for 21.0±2.0 days (p<0.05). The leukocytes structure in peripheral blood doesn't differ in patients with different types of ANS. Erythrocytes sedimentation rate was higher in patients with parasympathetic type – 20.5±2.5 mm/h (in patients with sympathetic type – 12.1±3.4 mm/h; p<0.05). C-reactive protein was higher in patients with parasympathetic type – 22.2±1.8 mg/l (in patients with sympathetic type – 9.3±3.3 mg/l; p<0.05). Discussion. The research has shown that patients with the parasympathetic type of ANS have got more expressed signs than patients with the sympathetic type. It is shown that the products of activated proinflammatory cells could stimulate neuronal synapses what causes long-term neuronal activity's changes and this leads to changes in endocrine activity of ANS [7]. The number of sympathetic fibres is reduced in inflamed tissue it leads to proinflammatory signals reduction and with production of neuropeptides from sensitive neural fibres this leads to local inflammation. In case of an acute inflammation this configuration promotes antigen releasing. But in case of chronic process these changes leads to constant redistribution of energy and continuous local destruction[5]. Lujan H.L. and co-authors have shown in their research that increas of parasympathetic activity may be used as therapeutic strategy for inhibition and prevention of a chronic inflammation [3]. Activation of the cholinergic anti-inflammatory signaling pathway contributes to a significant improvement in case of such cytokine-mediated diseases as sepsis, colitis, pancreatitis etc [6]. Conclusion. Thus our research has revealed that inflammatory activity depends on the type of ASN. The changes of activity of ANS may be a perspective therapeutic method treating of inflammatory processes.

The association between depressive symptoms and systemic inflammation in people with type 2 diabetes: findings from the South London Diabetes Study.

The prevalence of depression and depressive symptoms is increased twofold in people with type 2 diabetes compared with the general population and is associated with worse biomedical outcomes and increased mortality. Type 2 diabetes, cardiovascular disease, and depression in nondiabetes subjects are independently associated with raised concentrations of circulating inflammatory markers, but it is not known if a similar association is observed in type 2 diabetes. We tested the hypothesis that higher depressive symptom scores in newly diagnosed type 2 diabetes patients were associated with higher concentrations of inflammatory markers. Depressive symptoms in adults with newly diagnosed type 2 diabetes recruited from primary care were assessed using the Patient Health Questionnaire-9. Twelve markers of inflammation (C-reactive protein [hs-CRP], interleukin-4 [IL-4], IL-6, IL-10, vascular endothelial growth factor [VEGF], tumor necrosis factor-α [TNF-α], IL-1β, IL-1 receptor antagonist [IL-1RA], monocyte chemotactic protein-1 [MCP-1], white blood cell count [WBC], adiponectin, and triglyceride [TG]) were measured. Covariates included sociodemographic factors, adiposity, macrovascular disease, HbA1c, and prescribed medication. The association between each inflammatory marker and depressive symptom score was estimated by multiple linear regression. The baseline cohort consisted of 1,790 participants. After adjusting for covariates, CRP (B = 0.13, P < 0.001), IL-1β (B = 0.06, P = 0.047), IL-1RA (B = 0.13, P < 0.001), MCP-1 (B = 0.11, P = 0.001), WBC (B = 0.13, P < 0.001), and TG (B = 0.10, P < 0.001) were associated with depressive symptoms. Increased inflammation may be involved in the pathogenesis of depressive symptoms in type 2 diabetes and contribute to the increased risk of complications and mortality in this group.