OBJECTIVE: Immune dysfunction is one of the risk factors which plays an important role in the development of non-Hodgkin lymphoma (NHL), and inflammation may be involved in its etiology. Minimal data is available on the effect of cytokine levels on neurobehavioral function in lymphoma before the initiation of chemotherapy. Therefore, we aimed to explore the risk of NHL by assessment of cytokine and adipokine levels and their correlation with neurobehavioral changes.
METHODS: This case-control study enrolled 62 subjects (age-sex matched: 31 cases and 31 controls). Neurobehavioral assessment was done using Montreal Cognitive Assessment questionnaire (MoCA) and Patient Health Questionnaire (PHQ-9). EORTC Core Quality of Life questionnaire (EORTC QLQ-C30) was used to assess quality of life. Questionnaire assessment and sample collection were done after the patient enrolment and before first cycle of chemotherapy.
RESULTS: Mean age of NHL patients and healthy controls was 51.9 ± 11.8 and 50 ± 10.9 years, respectively. NHL patients showed significantly higher levels of IL-6 (0.77 ± 0.11) and TNF- α (1.47 ± 1.31) than controls (0.55 ± 0.4 and 0.66 ± 0.89, respectively) with p-value<0.005. Also, NHL patients showed significantly lower levels of adiponectin (0.31 ± 0.24) and omentin (0.46 ± 0.1) than controls (0.42 ± 0.13 and 0.53 ± 0.11, respectively) with p-value<0.005. Lower MoCA and EORTC QLQ C-30 scores and higher PHQ-9 scores were observed in NHL patients in comparison to healthy control.
CONCLUSIONS: Our results showed that adiponectin, omentin IL-6 and TNF-α may be used as pre-diagnostic markers of NHL risk. Neurobehavioral changes observed in NHL patients may alter the quality of life.

BACKGROUND: Sarcopenia is a harmful condition common among older adults for which no treatment is available. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and its receptor fibroblast growth factor inducible 14 (FN14) are known to play important roles in the pathogenesis of sarcopenia. This study investigated alterations in methylation in TWEAK and Fn14 to identify potential targets for the managing sarcopenia.
METHODS: Through an epidemiological investigation, we detected methylation of CpG islands (CpGs) in TWEAK and Fn14 in community-dwelling older adult of Xinjiang by bisulfite sequencing. Significant CpGs associated with sarcopenia were selected for detection in 152 older individuals by pyrosequencing. Associations between CpG methylation, plasma inflammatory marker levels, and sarcopenia were analyzed.
RESULTS: Of 38 CpGs in TWEAK and 30 CpGs in Fn14 detected in 60 individuals, 6 CpGs showed lower methylation in sarcopenia patients compared with control individuals. In 152 older adults, covariance analysis with adjustment for age, gender, triglyceride level, obesity, diabetes, and hypertension showed that the methylation levels of 6 CpGs (CpG8, CpG12, CpG13, CpG20 and CpG21of TWEAK, and CpG24 of Fn14) were significantly lower in sarcopenia patients than in control individuals. With adjustment for additional confounding factors, covariate variance analysis showed that plasma TWEAK, TNF-α and IL-10 levels in the sarcopenia group were significant higher than those in the control group (P = 0.007, P < 0.001, P = 0.003). Multivariate logistic regression analysis showed that CpG8, CpG13, CpG21, and total methylation of TWEAK (OR = 0.767, 95 % CI = 0.622-0.947; OR = 0.740, 95 % CI = 0.583-0.941; OR = 0.734, 95 % CI = 0.561-0.958; OR = 0.883, 95 % CI = 0.795-0.980) as well as CpG22 and total methylation of Fn14 were significantly associated with sarcopenia (OR = 826, 95 % CI = 0.704-0.968; OR = 0.918, 95 % CI = 0.852-0.989). From partial correlation analysis, plasma TWEAK was correlated with plasma TNF-α (r = 0.172, P = 0.042).
CONCLUSIONS: Sarcopenia is associated with hypomethylation of TWEAK and increased plasma levels of TWEAK and its downstream inflammatory factor TNF-α in a community-dwelling population of older adults in Xinjiang.

OBJECTIVE: We focused our study on examining the genotype and allele frequency of IL-6 (rs1800795), TNF-α (rs1800629) and IL-10 (rs1800872) single nucleotide polymorphisms (SNP) on preeclampsia (PE) diagnosed Mexican pregnant women.
METHODS: A case-control study was designed including 86 preeclampsia patients and 100 normotensives pregnancies from Women\'s Hospital of Culiacan, Mexico. Genotyping of IL-6, TNF-α and IL-10 was performed using TaqMan SNP Genotyping.
RESULTS: Not significant association was found between development of PE and genotypic (p > 0.05) and allelic (p > 0.05) frequencies of IL-6, TNF-α and IL-10 SNPs. Genotype distributions of IL-6 (p = 0.599), TNF-α (p = 0.721) and IL-10 (p = 0.761) polymorphisms in the two groups were in agreement with Hardy-Weinberg equilibrium.
CONCLUSIONS: According to the findings, the IL-6, TNF-α and IL-10 SNPs are not exponents of susceptibility to developing PE.

The cytokine storm is a complication related to SARS-CoV-2 infection worldwide. This study aimed to address the level of three cytokines which were interleukin-1-beta (IL-1β), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α), with different blood parameters to the formation of cytokine storm or any complication among COVID-19 patients.
UNASSIGNED: A total of 104 serum samples were included for this purpose, and they were divided into three categories the healthy control group (n=30), mild COVID-19 patients (n=23), and severe cases of COVID-19 patients (n=51). The cytokine concentration was measured by enzyme-linked immunosorbent assays (ELISA). Serum ferritin, C-reactive protein (CRP) levels, and erythrocyte sedimentation rate were also evaluated and compared with the concentration of the proinflammatory cytokines.
UNASSIGNED: The data analysis showed a significant relationship between the serum IL-6 level with serum ferritin and CRP and the progression to the severity of SARS-CoV-2 infection. The IL-6 level was increased in mild COVID-19 patients and was significantly elevated in severe COVID-19 patients. Patients in the severe group had significantly higher serum ferritin, CRP, and erythrocyte sedimentation rate levels than those in the mild and healthy groups. The IL-1β and TNF-α were not significantly different in the groups compared with the healthy control group.
UNASSIGNED: This study revealed that the proinflammatory cytokines and biochemical laboratory tests are promising biomarkers for detecting the severity of COVID-19 cases.

BACKGROUND: Psoriasis (PsO) is a systemic autoimmune disease. Many pro-inflammatory and anti-inflammatory biomarkers have been associated with the pathogenetic process of psoriasis. IL-35 act as an anti-inflammatory cytokine through downregulation of TH-17 cell development and cytokine production. So, IL-35 might be utilized as potential future therapeutic agent for psoriasis.
OBJECTIVE: To investigate the association between inflammatory (IL-17, TNF-α, IFN-γ) and anti-inflammatory cytokines (IL-35, TGF-β) in psoriasis patients.
METHODS: A case-control study enrolled two groups: (Group I: 40 patients with psoriasis) and (Group II: 40 healthy age and sex-matched subjects). Full history was taken from all cases along with full dermatologic examination. The assessment of psoriasis severity was conducted by using PASI score. Assessment of inflammatory (IL-17, TNF-α, IFN-γ) and anti-inflammatory cytokines (IL-35, TGF-β) was performed by using ELISA technique.
RESULTS: There was a statistically significant increase of mean level of TNF-α, IL-17, and IFN-γ among psoriasis cases in comparison with controls. The mean level of TGF-β and IL-35 was statistically significantly reduced among the psoriasis cases in comparison with controls. TNF-α, IL-17, and IFN-γ showed a significant strong positive association in between and statistically significant strong negative relationship with IL-35 and TGF-β.
CONCLUSIONS: IL-35 has a significant role in the pathogenetic process of PsO, and it serves as a potential future therapeutic agent for psoriasis. The current results could be used as a clue for the utilization of inflammatory (IL-17, TNF-α, IFN-γ) versus anti-inflammatory cytokines (IL-35, TGF-β) in psoriasis patients as a diagnostic biomarker for severity of cases with psoriasis.

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder with significant morbidity and impairment of life quality. Prevalence is increasing around the world; therefore, intensive research is ongoing to understand the mechanisms of development of AD and offer new treatment options for AD patients.
OBJECTIVE: To investigate the association between Inflammatory (IL-17, TNF-α, IFN-γ) versus anti-Inflammatory Cytokines (IL-35, TGF-β) in AD patients.
METHODS: A case control study included 40 AD patients and 20 age- and sex-matched healthy subjects. Cases were subjected to full history taking and full dermatological examination. The assessment of disease severity was conducted by using SCORAD score. Assessment of inflammatory (IL-17, TNF-α, IFN-γ) and anti-Inflammatory Cytokines (IL-35, TGF-β) was performed by using ELISA technique.
RESULTS: The mean level of TNF-α, IL-17 was statistically significantly higher in the AD cases as compared with the control group. The mean level of TGF-β, Il-35, and IFN-γ was statistically significantly lower in the Atopic dermatitis cases as compared with the control group. There was statistically significant strong positive correlation between TNF-α with SCORAD score and IL-17 while there was statistically significant strong negative correlation between TNF-α with TGF-β and IL-35. There was statistically significant strong positive correlation between IL-17 with SCORAD score and TNF-α while there was statistically significant strong negative correlation between IL-17 with TGF-β and IL-35.
CONCLUSIONS: The current results could be used as a clue for the utilization of inflammatory (IL-17, TNF-α, IFN-γ) versus anti-inflammatory Cytokines (IL-35, TGF-β) in AD as a diagnostic biomarker for severity of cases with Atopic dermatitis. IL-17 plays an important role in the pathogenesis of AD, and IL-17 blocker may be used as a potential future treatment of AD.

Incontinentia pigmenti is a rare genetic disease affecting the skin, microvasculature, and central nervous system, in which a hyperactive inflammatory response is observed. Due to the inflammatory phase of COVID-19 and associated cytokine storm, infection with SARS-CoV-2 in individuals with incontinentia pigmenti is a concern. Furthermore, type I interferon autoantibodies are found in life-threatening COVID-19 pneumonia and in 25% of individuals with incontinentia pigmenti. The present case report describes a 31-year-old Caucasian woman with incontinentia pigmenti and severe COVID-19. She was hospitalized for oxygen therapy, intravenous antibiotics, and corticosteroids. Eight months later, she is still symptomatic. To our knowledge, she is the first reported case of long COVID in incontinentia pigmenti. Increased autoimmunity may be implicated in both incontinentia pigmenti and long COVID. Pending evidence-based guidelines, COVID-protective measures including vaccination should be recommended to all patients with incontinentia pigmenti. Specific interferon therapy may be considered along with usual COVID treatment.

To describe the relationship between the severity of lung damage and cytokine levels in sputum, bronchoalveolar lavage fluid (BALF), serum.
Eight severe patients infected with coronavirus disease 2019 (COVID-19) were admitted and their cytokines and chest computed tomography (CT) were analyzed.
Compared with in serum, IL-6 and TNF-α in sputum and in BALF show more directly reflect the severity of COVID-19 critical patients. The gradient ratio of IL-6 levels may predict the prognosis of severe patients.
Cytokine levels in the sputum may be more helpful for indicating lung damage. Local intervention through the respiratory tract is expected to benefit patients with severe COVID-19.

BACKGROUND: High levels of the tumor necrosis factor alpha (TNF-α) induce apoptosis and pro-inflammatory effects for primary degeneration of tendon and development of tendinopathy. The aim of this study was to investigate the association between the TNF-α polymorphisms and tendinopathy in athletes.
METHODS: Two hundred and seventy athletes (135 tendinopathy cases and 135 controls) were included and genotyped (TNF-α -1031T > C; -857 C > T; -308G > A) using TaqMan validated assays. The association of the polymorphisms with tendinopathy was evaluated by a multivariate logistic regression model, using odds ratios (OR) and 95 % confidence intervals (CI).
RESULTS: The variant allele - 308 A was significantly associated with patellar (OR: 1.9; 95 % CI: 1.01-3.6) or Achilles tendinopathies (OR: 2.7; 95 % CI: 1.1-6.7). No significant differences were found in allele or genotype distributions of the - 1031T > C and - 857 C > T polymorphisms between cases and controls. TNF-α TCA haplotype was associated with increased tendinopathies risk, either considering all cases (OR: 2.6, 95 % CI: 1.3-5.3), patellar (OR: 3.3, 95 % CI: 1.5-7.3), rotator cuff (OR: 3.1, 95 % CI: 1.4-7.2) or Achilles tendinopathies (OR: 3.8, 95 % CI: 1.1-12.7).
CONCLUSIONS: These results suggest that the TNF-α polymorphisms could influence the susceptibility to developing tendinopathy among athletes. Knowledge of the TNF-α polymorphisms associated to tendinopathy in athletes can further understanding of the inflammatory role in the early stages of the disease and contribute for sports injury surveillance programmes, in which athletes with TNF-α TCA haplotype could be early subjected to cryotherapy after training and competition to avoid tendinopathy development.

Eosinophilic gastroenteritis (EGE) is a chronic allergic disorder characterized by infiltration of eosinophils in the gastrointestinal (GI) tract and hypereosinophilia. Although T helper type 2 (Th2) responses play pathogenic roles in EGE, roles of innate immunity cytokines including IL-6 and TNF-α have been poorly defined. Here, we describe a case of EGE exhibiting accumulation of eosinophils in the upper GI mucosa and hypereosinophilia. Induction of remission by prednisolone reduced expression levels not only of Th2 cytokines but also of IL-6 and TNF-α in the GI mucosa. Moreover, induction of remission was accompanied by a marked reduction in serum levels of chemokine C-C motif ligand 17 (CCL17, TARC), IL-6 and TNF-α, implicating that both Th2 and innate immune responses were involved in the development of EGE in this case. Collectively, this case suggests possible involvement of IL-6 and TNF-α in the development of EGE.