Kronik obstrüktif akciğer hastalığınıda atak sırasında serum interlökin-6, interlökin-8 ve tümör nekrozis faktör-α düzeylerinin değerlendirilmesi
Loading...
Date
2004
Authors
Şahin, Fulya Gürkan
Journal Title
Journal ISSN
Volume Title
Publisher
Uludağ Üniversitesi
Abstract
Kronik obstrüktif akciğer hastalığı (KOAH); alveoler duvarların kaybı ve mukus hipersekresyonu ile birlikte goblet hücre metaplazisini içeren kronik havayolu enflamasyonu ve yapısal yenilenme ile ilişkilidir. Enflamatuar hücreler, proteazların, fibrotik veya mitojenik büyüme faktörlerinin ve sitokinlerin sekresyonu yoluyla havayollarının yeniden yapılanmasında etkili olurlar. Makrofajlar ve nötrofiller KOAH'ta başlıca enflamatuar hücrelerdir. Bu enflamatuar hücreler KOAH atağı sırasında artmaktadırlar. Enflamatuar hücrelerin migrasyonu ve aktivasyonu sitokinler ve kemokinler tarafından düzenlenir. Sitokinler ekstrasellüler sinyal proteinlerdir. KOAH'la ilişkili başlıca sitokinler interlökin (IL)-6, IL-8 ve tümör nekrozis faktör (TNF)-α 'dır. TNF-α ; makrofajlar, T hücreleri, mast hücreleri ve epitel hücrelerini içeren birçok hücreden üretilir, fakat başlıca kaynağı makrofajlardır. TNF- α adhesyon moleküllerinin ekspresyonunu arttırır. KOAH akut atağında TNF-α 'nın konsantrasyonunun artışı lökositlerin bronş mukozasına adhezyonunu ve migrasyonunu arttırır. IL-8; alveoler makrofajlardan, lenfositlerden, epitel hücrelerinden ve nötrofillerden üretilen kemotaktik bir sitokindir. IL-8, nötrofilleri bir araya toplar ve aktive eder. IL-6, proenflamatuar bir sitokin ve endojen bir pirojendir. IL-6 adhezyon moleküllerinin ekspresyonunu indükler, nötrofilierin ve eozinofillerin vasküler endotele ve respiratuar epitele adhezyonunu arttırır. Araştirmamızda KOAH atağındaki hastalarda serum IL-6, IL-8 ve TNF-α düzeylerini, tedavi sonrası stabil KOAH'li hastaların düzeyleriyle ve sağlıklı kontrol grubuyla karşılaştırmayı amaçladık. Ayrıca serum reaktif protein (CRP), zorlu ekspiratuar volüm 1. saniye (FEV1) değeri ve nötrofil sayısı ile serum IL-6, IL-8 ve tnf- arasında ilişki olup olmadığını ortaya koymayı hedefledik. KOAH atağındaki hastalar 30, tedavi sonrası stabil KOAH hastaları 30 ve sağlıklı kontrol grubu 18 olgudan oluşuyordu. Serum IL-6, SL-8 ve TNF-α düzeyleri ELISA yöntemi kullanılarak ölçüldü. Serum ömeklerinde IL-6, IL-8 ve TNF-α düzeyleri sağlıklı kontrol grubuyla karşılaştırıldığında, KOAH atağı sırasındaki hastalarda serum IL-6, IL-8 ve TNF-α düzeyleri istatistiksel olarak anlamlı düzeyde yüksek bulundu (p[0.05). KOAH atağındaki hastaların serum IL-6, İL-8 ve TNF-α düzeyleri atak sonrası stabil KOAH'lı hastaların düzeylerinden istatistiksel olarak anlamlı düzeyde daha yüksek bulundu (p[0.05). KOAH atağındaki hastaların serum IL-6 ile IL-8, IL-6 ile TNF-α ve İL-8 ile TNF-α düzeyleri arasında pozitif korelasyon saptandı (p[0.05). KOAH atağındaki hastaların nötrofil sayısı tedavi sonrası stabil KOAH'lı hastaların nötrofil sayısından istatistiksel olarak artmış saptandı. KOAH atağındaki hastaların notrofil sayısı ile serum IL-6, IL-8 ve TNF-α arasında ve tedavi sonrası stabil KOAH'lı hastaların notrofil sayısı ile serum IL-6, IL-8 ve TNF-α arasında korelasyon saptanmadı. KOAH atağındaki hastaların serum IL-6, IL-8 ve TNF-α düzeyleri ile CRP düzeyleri ve FEV1 değerleri arasında ilişki saptanmadı. Sonuç olarak; serum IL-6, IL-8 ve TNF-α 'nın akut ataktaki düzeylerinin, tedavi sonrası düzeylerinden ve sağlıklı olguların düzeylerinden yüksek saptanması alışılmışın dışında orijinal tedavilere yol göstermektedir.
Chronic obstructive pulmonary disease (COPD); is associated with chronic airways inflammation and structural remodeling, including loss of alveolar walls, and goblet cell metaplasia with mucus hypersecretion. Inflammatory cells may contribute to the airway remodeling via secretion of proteases, fibrotic or mitogenic growth factors, and cytocines. Neutrophils and macrophages are the predominant inflammatory cells in COPD. These inflammatory cells increase during COPD exacerbation. Migration and activation of inflammatory cells is regulated by cytokines and chemokines. Cytocines are extracellular signalling proteins. The principle cytokines associated with COPD are IL-6, IL-8 and TNF-α. TNF-α is produced by many cells including macrophages, T-cells, mast cells and epithelial cells, but the principle source is the macroptiage. TNF-α increases expression of the adhesion molecule. The increased concentrations of TNF-α at the time of COPD exacerbations is increased to adhesion and migration of leukocytes into the bronchial mucosa. IL-8 is a chemotactic cytokine produced by alveolar macrophages, lymphocytes, epithelial cells, and neutrophils. IL-8 is recruited and activated by neutrophils. IL-6 is a proinflammatory cytokine and an endogenous pyrogen. IL-6 induces expression of the adhesion molecules, increased adhesion of neutrophils and eosinophils to the vascular endothelium and respiratory epithelium. In our study, we investigated the serum IL-6, IL-8 and TNF-α levels from during acute exacerbation of COPD patients and compared with after treatment from stable COPD patients and healthy control group. We also tried to determine the relationship between serum reactive protein (CRP), force expiratuar volume first second (FEV1) and neutrophils count with serum IL-6, IL-8 and TNF-α levels. Study population was consisted of 30 patients with COPD exacerbation, 30 patients after the treatment of stable COPD patients and 18 healthy control subjects. Levels of IL-6, IL-8 and TNF-α levels in serum measured with ELISA method. In serum specimens IL-6, IL-8 and TNF-α levels were significantly higher during acute exacerbation of COPD patients, compared with the healthy control group (p<0.05). During acute exacerbation of COPD patients serum IL-6, IL-8 and TNF-α levels were statistically significantly higher than stable COPD patients (p<0.05). We observed pozitive correlation between serum IL-6 levels with serum IL-8, between serum IL-6 levels with TNF-α levels and between serum IL-8 levels with serum TNF-α levels during acute COPD exacerbation. During acute exacerbation of COPD patients neutrophils count were statistically significantly higher than after treatment of stable COPD patients (p<0.05). There was no relation between neutrophils with serum IL-6, IL-8 and TNF-α levels during acute COPD exacerbation and between neutrophils with serum IL-6, IL-8 and TNF-α levels after treatment of stable COPD patients. We observed no relation between serum IL-6, IL-8 and TNF-α levels with serum CRP levels and FEV1 levels during acute COPD exacerbation. Conclusion; serum IL-6, IL-8 and TNF-α levels are higher during acute COPD exacerbation compared to after treatment and healthy subjects, they may represent targets for novel therapies.
Chronic obstructive pulmonary disease (COPD); is associated with chronic airways inflammation and structural remodeling, including loss of alveolar walls, and goblet cell metaplasia with mucus hypersecretion. Inflammatory cells may contribute to the airway remodeling via secretion of proteases, fibrotic or mitogenic growth factors, and cytocines. Neutrophils and macrophages are the predominant inflammatory cells in COPD. These inflammatory cells increase during COPD exacerbation. Migration and activation of inflammatory cells is regulated by cytokines and chemokines. Cytocines are extracellular signalling proteins. The principle cytokines associated with COPD are IL-6, IL-8 and TNF-α. TNF-α is produced by many cells including macrophages, T-cells, mast cells and epithelial cells, but the principle source is the macroptiage. TNF-α increases expression of the adhesion molecule. The increased concentrations of TNF-α at the time of COPD exacerbations is increased to adhesion and migration of leukocytes into the bronchial mucosa. IL-8 is a chemotactic cytokine produced by alveolar macrophages, lymphocytes, epithelial cells, and neutrophils. IL-8 is recruited and activated by neutrophils. IL-6 is a proinflammatory cytokine and an endogenous pyrogen. IL-6 induces expression of the adhesion molecules, increased adhesion of neutrophils and eosinophils to the vascular endothelium and respiratory epithelium. In our study, we investigated the serum IL-6, IL-8 and TNF-α levels from during acute exacerbation of COPD patients and compared with after treatment from stable COPD patients and healthy control group. We also tried to determine the relationship between serum reactive protein (CRP), force expiratuar volume first second (FEV1) and neutrophils count with serum IL-6, IL-8 and TNF-α levels. Study population was consisted of 30 patients with COPD exacerbation, 30 patients after the treatment of stable COPD patients and 18 healthy control subjects. Levels of IL-6, IL-8 and TNF-α levels in serum measured with ELISA method. In serum specimens IL-6, IL-8 and TNF-α levels were significantly higher during acute exacerbation of COPD patients, compared with the healthy control group (p<0.05). During acute exacerbation of COPD patients serum IL-6, IL-8 and TNF-α levels were statistically significantly higher than stable COPD patients (p<0.05). We observed pozitive correlation between serum IL-6 levels with serum IL-8, between serum IL-6 levels with TNF-α levels and between serum IL-8 levels with serum TNF-α levels during acute COPD exacerbation. During acute exacerbation of COPD patients neutrophils count were statistically significantly higher than after treatment of stable COPD patients (p<0.05). There was no relation between neutrophils with serum IL-6, IL-8 and TNF-α levels during acute COPD exacerbation and between neutrophils with serum IL-6, IL-8 and TNF-α levels after treatment of stable COPD patients. We observed no relation between serum IL-6, IL-8 and TNF-α levels with serum CRP levels and FEV1 levels during acute COPD exacerbation. Conclusion; serum IL-6, IL-8 and TNF-α levels are higher during acute COPD exacerbation compared to after treatment and healthy subjects, they may represent targets for novel therapies.
Description
Keywords
Kronik obstrüktif akciğer hastalığı (KOAH), Sitokin, İnterlökin-6 (IL-6), İnterlökin-8 (IL-8), Tümör nekroz faktör-α (TNF-α), Chronic obstructive lung disease (COPD), Cytokine, Interleukin-6 (iL-6), Interleukin-8 (IL-8), Tumor necrosis factor-alpha (TNF-α)
Citation
Şahin, F. G. (2004). Kronik obstrüktif akciğer hastalığında atak sırasında serum interlökin-6, interlökin-8 ve tümör nekrozis faktör-α düzeylerinin değerlendirilmesi. Yayınlanmamış tıpta uzmanlık tezi. Uludağ Üniversitesi Tıp Fakültesi.