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Tuberculosis (TB) infection is a bacterial disease that can involve almost all organs, especially with lung involvement. This disease, which has been known since ancient times, has come to the fore again, especially with the increase in the number of patients receiving immunosuppressive therapy. Biological drugs, which are very popular treatment options today, have revolutionized the treatment of some hematological and autoimmune diseases. This class of drugs includes monoclonal antibodies (adalimumab, infliximab, golimumab) and antibody fragment (certolizumab). Treatment with biological agents such as tumor necrosis factor (TNF) alpha inhibitors is known to be associated with an increased risk of TB. The medical history of the patients who are planned for anti-TNF treatment should be questioned in detail, examined in detail, and chest X-ray should be taken. It should be evaluated for active TB infection or sequelae. TB infection.In this review article, it is aimed to review the current scientific literature., Tüberküloz (TB); özellikle akciğer tutulumu ile giden ancak neredeyse tüm organları tutabilen bakteriyel bir hastalıktır. Eski zamanlardan beri bilinen bu hastalık, özellikle immunsüpresif tedavi alan hasta sayılarının artması ile tekrar gündeme gelmiştir. Günümüzde oldukça popüler tedavi seçeneklerinden olan biyolojik ilaçlar; hematolojik, otoimmün hatta malign hastalıkların tedavisinde devrim yaratmıştır. Bu ilaç sınıfı arasında monoklonal antikorlar (adalimumab, infliximab, golimumab) ve antikor fragmanı (certolizumab) sayılabilir. Tümör nekroz faktör (TNF) alfa inhibitörleri gibi biyolojik ajanlarla tedavinin artmış TB riski ile ilişkisi iyi bilinmektedir. Anti-TNF tedavisi planlanan hastaların tıbbi geçmişleri ayrıntılı bir şekilde sorgulanmalı, ayrıntılı muayene edilmeli ve akciğer grafisi çekilmelidir. Aktif TB enfeksiyonu veya sekel TB enfeksiyonu açısından değerlendirilmelidir. Bu derleme yazısında mevcut bilimsel literatürün gözden geçirilmesi amaçlanmıştır.

Tumor necrosis factor (TNF)-targeted therapies are increasingly used for a rapidly expanding number of rheumatic and autoimmune diseases. With this use and longer follow-up periods of treatment, there are a growing number of reports of the development of autoimmune processes related to anti-TNF agents. Since these drugs are often prescribed to severe rheumatologic patients, there is a controversy about whether the autoimmune diseases that could be related to underlying disease or anti-TNF therapy. We aimed to discuss this subject under the light of literature., Anti-TNF tedavilerin romatolojik ve otoimmün hastalıkların tedavisinde yaygın kullanımı ve uzun dönem takipleri ile birlikte, paradoksal olarak anti-TNF ilişkili otoimmün hastalıklarla ilgili artan sayıda bildiriler olmaktadır. Bu ilaçlar genelde ağır hastalık aktivitesi olan romatolojik hastalarda kullanıldığından, bazı durumlarda bu gelişen hastalıkların altta yatan hastalığa da bağlı olabilmesi ile ilgili çelişkiler bulunmaktadır. Giderek artan vaka serilerinden elde edilen bilgiler ışığında bu konuyu tartışmayı amaçladık

Introduction: Brucella spp. are intracellular bacteria that may cause acute, subacute and chronic infections. Despite optimum antibiotic treatment, relapse of brucellosis occurs in some patients. There is less amount of knowledge about immune response in relapse of brucellosis. Materials and Methods: Twenty patients with acute brucellosis, 16 patients with relapsed brucellosis and as a control group 20 healthy volunteers were enrolled in this study to explore the immune response variation during relapse of brucellosis. The distribution of peripheral blood mononuclear cells was investigated by flow cytometry and level of various cytokines involved in inflammatory and anti-inflammatory response were measured by enzyme-linked immunosorbent assay in serum samples. Results: The most prominent data in phenotyping examination was the significant reduction (1.45 times) in the percentage of activated T cell (CD3+human leukocyte antigen-DR+) population in the relapse group in comparison to the acute brucellosis group. However, percentage of activated T cell population in the relapse group was 2.59 times higher than in healthy controls (p

WOS: 000377870400003, Objective: Currently, tumor necrosis factor-alpha (TNF-alpha) inhibitors are widely used all over the world, especially in the treatment of severe psoriasis. However, multiple sclerosis (MS) and peripheral neuropathy occurrence associated with TNF-a inhibitors have been reported in the treatment of patients with psoriasis. It is not known whether TNF-a inhibitors reveal underlying neurological disorders in patients with psoriasis. The aim of this study was to investigate whether there is an association between psoriasis and MS or peripheral neuropathy. Methods: In this study, 50 psoriasis patients and 25 healthy controls were enrolled. Neurological examination and needle electromyography test were performed. Serum levels of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), S-100 calcium-binding protein (S100B) and neuron specific enolase (NSE), which are involved in neuroinflammatory process, were measured. Results: Serum MMP-9 levels were higher in psoriasis patients compared to healthy controls. Serum MMP-2 and NSE levels were decreased in psoriasis patients compared to healthy controls. There was no significant difference in S100B levels between two groups. All neurophysiological parameters in each individual patient and control were found to be within normal limits and there was no difference between groups. Conclusion: NSE and MMP-9 might play role in the occurrence of MS in psoriasis patients. Especially, we are in the opinion that it might be useful to measure the serum levels of these markers before the administration of TNF-a inhibitors in psoriasis patients with family history of MS.

Chronic obstructive pulmonary disease (COPD) is an inflammatory disease of the lung associated with progressive airflow limitation. The aim of this study is to assess the influence of tiotropium treatment on airway inflammation and symptoms in stable COPD patients. Materials and methods: Inflammatory markers were measured in the expired breath condensate fluid (EBC) before starting tiotropium treatment and at the end of the first month. Results: Twenty-two patients (81% men) with a mean age of 65.4 ± 10.1 years completed the study. The mean nitrotyrosine and 8-isoprostane levels for oxidative stress markers in EBC before and after treatment were 4.5 ± 2.3, 3.5 ± 1.9 pg/mL (P = 0.06) and 7.3 ± 10.8, 8.1 ± 11.7 pg/mL (P = 0.28), respectively. The mean interleukin-6 and tumor necrosis factor-alpha levels for inflammation markers in EBC before and after treatment were 1.03 ± 1.1, 0.77 ± 0.8 pg/mL (P = 0.41) and 27.8 ± 2.6, 29.2 ± 5.7 pg/mL (P = 0.36) respectively. The mean symptom scores decreased significantly with tiotropium and a mean increase of 124.6 ± 0.86 mL was observed in a lung function test (FEV1). Conclusion: Although a 4-week treatment with tiotropium did not modify any of the inflammatory or oxidative stress markers in EBC fluid, tiotropium treatment helps to control symptoms in COPD.

Romatoid Artrit (RA) terimi, ilk olarak 1876 yilinda Sir Alfred Baring Garrod tarafmdan kullanilmakla beraber, hastaligin tanim- lanmasi 1800 yilinda Landre Beauvals'e kadar uzanir. RA teriminin Amerikan Romatizma Cemiyeti (ARA) tarafmdan kabulu ise 1941 yi- lma kadar zaman almistir (15). Romatoid Artrit; kronik ve sistemik bir inflamatuvar hastalik olup, kikirdak erozyonu, kemikte hasar ve eklemlerin fibroz ankilozuna ne- den olabilen kronik bir sinovit ile karakterlidir (23). Bilinmeyen bir antijenik uyari sonrasinda geliserek eklemde harabiyet meydana ge- tiren RA ile postinfeksiyoz olarak gelisen reaktif artrit arasindaki ana patogenetik farklilik bugun tam olarak bilinmemektedir. RA'de has- taligin kronisitesi ve eklemde erozyon gelismesinde sitokinlerin onemli rolu oldugu dusunulmektedir (19). T-hucreleri ve diger immun kom- petan hucreler, antijen ile karsilastiklarinda, cevap olarak bircok im- munolojik aktif madde uretir ve salgilarlar, Bu maddelere sitokin ismi verilmektedir (22). Sitokinler; hucre gelisimini, olgunlasmasini veya fonksiyonlarini etkileyen solubl peptidlerdir. Bu sitokinlerin bir alt gurubuna da interlokin adi verilmektedir. Bir immunopeptidin inter- lokin olarak isimlendirilebilmesi icin su 3 ozellige sahip olmasi gerek- mektedir (7)

Faced with stress and acute instances, brain cells trigger neuroinflammation and increase inflam-mation response and can cause cell damage, cell death and thereby functional insufficiencies, behavioral disorders and autonomic imbalances. Cytokines that play an important role in inflamma-tory processes affect neurotransmitter metabolism, neuroendocrine functions and synaptic plasticity. It has been proven that inflammatory activity increases in depression. Proinflammatory cytokines such as interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-α along with acute phase reactants increase in depression. If the inflammatory response becomes chronic and cannot be balanced, inflammation and cytokines may cause behavioral symptoms and neuropsychiatric disorders such as major depression and anxiety disorders. In this article, the changes that occur in inflammatory processes in depressive disorder will be summarized; the effects of pharmacologic and psychotherapeutic approaches on these changes will be reviewed., Beyin hücreleri stres ve akut olaylar karşısında nöroinflamasyonu tetikleyerek ve inflamasyon yanıtını arttırarak hücre hasarına, ölümüne ve dolayısıyla fonksiyonel yetersizliklere, davranışsal bozukluklara ve otonomik dengesizliklere yol açabilmektedir. İnflamatuvar süreçlerde önemli rol oynayan sitokinler nörotransmitter metabolizması, nöroendokrin işlevler ve sinaptik plastisiteyi etkilemektedir. Depresyonda inflamatuvar aktivitenin artmış olduğu kanıtlanmıştır. Depresyonda interlökin (IL)-1, IL-6 ve tümör nekroz faktör (TNF)-α gibi proinflamatuvar sitokinler ve akut faz reaktanları artmaktadır. Psikososyal stresörlere yanıt olarak ortaya çıkan bu immun değişiklikler geçicidir ve anti-inflamatuvar mekanizmalarla dengelenmektedir. Bununla birlikte, inflamatuvar yanıt kronikleşirse ya da dengelenemezse inflamasyon ve sitokinler davranışsal belirtilere ve major depresyon, anksiyete bozuklukları gibi nöropsikiyatrik hastalıklara yol açabilmektedir. Bu yazıda, major depresif bozuklukta inflamatuvar süreçlerde meydana gelen değişiklikler özetlenecek, farmakolojik ve psikoterapötik yaklaşımların bu değişiklikler üzerine etkileri gözden geçirilmiştir.

WOS: 000314288600004 Objective: Diabetes mellitus is a common metabolic disorder characterized by hyperglycemia. Cytokines induce signal transduction and secondary messenger pathways after binding their specific ligands. In this way, these proteins control and also modulate activity of the target cells. Tumor necrosis factor plays an important role in diabetes and is a member of the family of cytokines. In this study, we aimed to investigate the effect of A252G (TNF-beta NcoI, rs909253) polymorphism in the tumor necrosis factor beta gene on the Type I Diabetes Mellitus in the Turkish population. Materials and Method: Distribution of A252G polymorphism was determined in 96 patients with Type I diabetes and 101 healty individuals by PCR-RFLP. Results: When obtained data was evaluated, the A allele of A252G polymorphism were observed more frequently than G allele in patients and controls. Moreover, G alleles were observed more frequently among patients than in controls. This high frequency of G allele found in patients demonstrates a 1.6 fold increased risk of susceptibility to type I diabetes in Turkish population (P=0.032). However, there was no significant difference between patients and controls in terms of the distribution of genotypes (P=0.132). Conclusion: As a result, although presence of a G allele demonstrated an increased risk of susceptibilty to type I diabetes, TNF-beta A252G polymorphism's genotype distrubution was not associated with type I diabetes in Turkish population. Polymorphisms involved in the development of Type I Diabetes Mellitus results in better understanding of the development and the progression of disease.

AMAÇ: Kesin MS tanılı hastalarla yaptığımız bu çalışmayla, matriks metalloproteinazlar (MMP-9, MMP-2), spesifik inhibitörleri (TIMP-1, TIMP-2) ve tümör nekrozis faktör alfa (TNF?) arasındaki ilişkiyi ortaya koyarak, multipl skleroz hastalığındaki rolünü irdelemeyi amaçladık.MATERYAL ve METOD: Çalışmaya Dicle Üniversitesi nöroloji polikliniğine başvuran en az 1 yıldır immünmodülatör tedavi alan ve en son atağını 1 aydan daha uzun süre önce geçirmiş olan 18-60 yaş arası 41 kadın, 19 erkek toplam 60 MS hastası ile yaş ve cinsiyetle uyumlu 19 kadın, 11 erkek toplam 30 sağlıklı kişi kontrol grubu olarak çalışmaya alınmıştır. ELISA (Enzyme-linked immunosorbent assay) yöntemiyle MMP-2, 9 ve TIMP-1,2; Kemiluminisent (Immulite) yöntemiyle TNF-? plazma düzeyleri saptanmıştır. Hastaların yaş, cinsiyet, hastalık süresi, klinik MS tipi, başlangıç semptomları kaydedilmiştir. EDSS, Kurtzke Genişletilmiş Yetmezlik Durum skoru yardımıyla ölçülmüştür.SONUÇLAR: Gruplar arasında cinsiyet farkı ki kare testi ile analiz edildi.İstatistiksel olarak anlamsız bulundu P>0,05. Gruplar arası yaş dağılımı Anova testi ile analiz edildi.Gruplar arasında farklılık olduğu saptandı. Ancak Post Hoc, Bonferroni düzeltmesi yapılarak gruplar ikili karşılaştırıldığında gruplar arasında farklılığın olmadığı gözlendi (P>0,05).Laboratuar değerleri (MMP-2, 9; TIMP-1,2 ve TNF-?), beş gruba ( ? 5 yıl RRMS, ? 10 yıl RRMS, PPMS, SPMS ve kontrol ) göre Anova testi ile analiz edildi. TNF alfa ve TIMP-1 için yapılan karşılaştırmalarda istatistiksel olarak anlamlı fark bulundu (P0,05). The age distribution between groups was analysed by Anova test. The differences between groups were found significand. However, when the groups were compared in pair using Post Hoc, Bonfrroni correction, the differences were not significand between groups (P>0,05).The laboratuary values (MMP-2, 9; TIMP-1,2 ve TNF-?), were analysed by Anova test according to five groups( ? 5 year RRMS, ? 10 year RRMS, PPMS, SPMS and control ). There was only statistical significance with TNF alpha and TIMP-1. To compare ? 5 year RRMS, ? 10 year RRMS, PPMS, SPMS and control groups in pair, Post Hoc, Bonferroni correction was applied. When comparation ? 5 year RRMS and PPMS with control group, TNF-? plasma level was found statistically significant (P0,05). The age distribution between groups was analysed by Anova test. The differences between groups were found significand. However, when the groups were compared in pair using Post Hoc, Bonfrroni correction, the differences were not significand between groups (P>0,05).The laboratuary values (MMP-2, 9; TIMP-1,2 ve TNF-?), were analysed by Anova test according to five groups( ? 5 year RRMS, ? 10 year RRMS, PPMS, SPMS and control ). There was only statistical significance with TNF alpha and TIMP-1. To compare ? 5 year RRMS, ? 10 year RRMS, PPMS, SPMS and control groups in pair, Post Hoc, Bonferroni correction was applied. When comparation ? 5 year RRMS and PPMS with control group, TNF-? plasma level was found statistically significant (P