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mRNA expressions of SOCS3 gene in meningitis patients

Year 2011, Volume: 17 Issue: 1, 29 - 32, 01.02.2011

Abstract

Meningitis is an inflammatory disease caused by microorganisms and viruses with various clinical symptoms, which damages the brain tissue and membranes, and which induces biochemical and cellular changes in cerebrospinal fluid (CSF). Meningitis is an infectious disease with higher rates of mortality and morbidity. The possibility of death or permanent damage to patient is considerable, mortality rate is one in ten patients and permanent damages like deafness or various brain damages are one in seven patients. Experimental animal meningitis revealed that the leukocytes infiltrated in CSF due to bacterial dissemination contributed to damage progression in brain tissue, increased brain edema and intracranial pressure. The association between gene expression of SOCS3 which is effective in repressing the JAK/STAT signal transduction pathway and meningitis disease were investigated in this study. Gene expression levels of SOCS3 in leukocytes leaked to CSF were investigated by using real-time PCR method in this study. As a result of our study, there was no difference in blood SOCS3 gene expression levels between meningitis patients and healthy controls (p>0.05). Additionally, there was no meaningful difference between SOC3 gene expression of blood and CSF samples in meningitis patients (p>0.05). Our data suggests that further molecular studies are needed and important in meningitis disease diagnosis and treatment, and in the other genes responsible for repressing of inflammatory development.

References

  • 1. Oktar M, Kliniğimizde Son Altı Yıldır İzlenen Menenjit Olgularının Değerlendirilmesi. Sağlık Bakanlığı Şişli Etfal Eğitim ve Araştırma Hastanesi Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Kliniği, Uzmanlık tezi, İstanbul. 2006.
  • 2. Kanra G, Ceyhan M, Kara A. Menenjit I etiyopatogenez. Çocuk Sağlığı ve Hastalıkları Dergisi 2003;46:57-66.
  • 3. Nicola NA. Guidebook to Cytokines and Their Receptors. Oxford: Oxford University Press, 1994.
  • 4. Ihle JN. Cytokine receptor signaling. Nature 1995;377:591-4. 5. Yasukawa H, Sasaki A, Yoshimura A. Negative regulation of cytokine signaling pathways. Annu Rev Immunol 2000;18:143- 64.
  • 6. Alexander WS. Suppressors of cytokine signalling (SOCS) in the immune system. Nat Rev Immunol 2002;2:410-6.
  • 7. Dalpke A, Heeg K, Bartz H, Baetz A. Regulation of innate immunity by suppressor of cytokine signaling (SOCS) proteins. Immunobiology 2008;213(3-4):225-35.
  • 8. Yoshimura A, Nishinakamura H, Matsumura Y, Hanada T. Negative regulation of cytokine signaling and immune responses by SOCS proteins. Arthritis Res Ther 2005;7:100-10.
  • 9. Egan PJ, Lawlor KE, Alexander WS, Wicks IP. Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation. J Clin Invest 2003;111:915-24.
  • 10. Alexander WS, Hilton DJ. The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response. Annu Rev Immunol 2004; 22:503-29.
  • 11. Bellou A, Schaub B, Ting L, Finn PW. Toll receptors modulate allergic responses: interaction with dendritic cells, T cells and mast cells. Curr Opin Allergy Clin Immunol 2003;3(6):487-94.
  • 12. Ji KA, Yang MS, Jou I, Shong MH, Joe EH. Thrombin induces expression of cytokine-induced SH2 protein (CIS) in rat brain astrocytes: involvement of phospholipase A2, cyclooxygenase, and lipoxygenase. Glia 2004;48:102-11.
  • 13. Alexander WS, Starr R, Fenner JE, Scott CL, Handman E, Sprigg NS, et al. SOCS1 is a critical inhibitor of interferon gamma signaling and prevents the potentially fatal neonatal actions of this cytokine. Cell 1999;98:597-608.
  • 14. Gatto L, Berlato C, Poli V, Tininini S, Kinjyo I, Yoshimura A, et al. Analysis of SOCS-3 promoter responses to interferon gamma. J Biol Chem 2004;279:13746-54.
  • 15. Dalpke AH, Opper S, Zimmermann S, Heeg K. Suppressors of cytokine signaling (SOCS)-1 and SOCS-3 are induced by CpGDNA and modulate cytokine responses in APCs. J Immunol 2001;166:7082-9.
  • 16. Crespo A, Filla MB, Russell SW, Murphy WJ. Indirect induction of suppressor of cytokine signalling-1 in macrophages stimulated with bacterial lipopolysaccharide: partial role of autocrine/paracrine interferon-alpha/beta. Biochem J 2000;349:99-104.
  • 17. Yang M, Min K, Joe E. Multiple mechanisms that prevent excessive brain inflammation. J Neurosci Res 2007;85:2298- 305.
  • 18. Min KJ, Pyo HK, Yang MS, Ji KA, Jou I, Joe EH. Gangliosides activate microglia via protein kinase C and NADPH oxidase. Glia 2004; 48:197-206.

Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi

Year 2011, Volume: 17 Issue: 1, 29 - 32, 01.02.2011

Abstract

Menenjit, çeşitli mikroorganizma ve virüslerin neden olduğu, beyin zarlarını ve beyin dokusunu zedeleyen, beyin omurilik sıvısında (BOS) hücresel ve biyokimyasal değişikliklere sebep olan, klinikte çeşitli nörolojik bulgular gösteren iltihabi bir hastalıktır. Menenjit mortalitesi ve morbiditesi yüksek bir enfeksiyon hastalığıdır. Hastalığın seyrinde ölüm ve tedavi sonrası kalıcı hasar olasılığı yüksektir. Her on hastadan biri kaybedilmekte ve yedi olgudan birinde sağırlık veya çeşitli beyin zedelenmeleri sonucu kalıcı hasarlara yol açmaktadır. Hayvan deneyleri ile geliştirilen menenjitlerde, bakterilerin sebep olduğu iltihap nedeni ile beyin omurilik sıvısına sızan lökositlerin, beyin dokusunda zedelenme gelişimine katkıda bulunduğu, beyin ödemini ve kafa içi basıncı arttırdığı gösterilmiştir. Bu çalışmada JAK/STAT sinyal ileti yolağının baskılamada etkili bir gen olan ve iltihabın önemli negatif düzenleyicilerinden olan SOCS3 geni ifadesinin menenjit hastalığı ile ilişkisi araştırıldı. Yaptığımız çalışmada insan beyin omurilik sıvısına sızan lökositlerin SOCS3 gen ifade düzeyleri real time PCR yöntemi ile araştırıldı. Bu çalışma sonuçlarına göre menenjitli hastalardaki kan SOCS3 gen ifadesi sağlıklı kontrol grubuna göre farklılık göstermedi (p>0,05). Ayrıca hastaların kan SOCS3 gen ifadesi ile beyin omurilik sıvısına sızan lökositlerdeki SOCS3 gen ifadesi arasında anlamlı bir fark bulunamadı (p>0.05). Bu bulgular menenjit tedavi ve tanısında daha ileri moleküler çalışmaların devamının gerekliliği ve iltihabi gelişimin baskılanmasında görevli diğer genlerin araştırılmasının önemli olacağı düşünülmektedir.

References

  • 1. Oktar M, Kliniğimizde Son Altı Yıldır İzlenen Menenjit Olgularının Değerlendirilmesi. Sağlık Bakanlığı Şişli Etfal Eğitim ve Araştırma Hastanesi Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Kliniği, Uzmanlık tezi, İstanbul. 2006.
  • 2. Kanra G, Ceyhan M, Kara A. Menenjit I etiyopatogenez. Çocuk Sağlığı ve Hastalıkları Dergisi 2003;46:57-66.
  • 3. Nicola NA. Guidebook to Cytokines and Their Receptors. Oxford: Oxford University Press, 1994.
  • 4. Ihle JN. Cytokine receptor signaling. Nature 1995;377:591-4. 5. Yasukawa H, Sasaki A, Yoshimura A. Negative regulation of cytokine signaling pathways. Annu Rev Immunol 2000;18:143- 64.
  • 6. Alexander WS. Suppressors of cytokine signalling (SOCS) in the immune system. Nat Rev Immunol 2002;2:410-6.
  • 7. Dalpke A, Heeg K, Bartz H, Baetz A. Regulation of innate immunity by suppressor of cytokine signaling (SOCS) proteins. Immunobiology 2008;213(3-4):225-35.
  • 8. Yoshimura A, Nishinakamura H, Matsumura Y, Hanada T. Negative regulation of cytokine signaling and immune responses by SOCS proteins. Arthritis Res Ther 2005;7:100-10.
  • 9. Egan PJ, Lawlor KE, Alexander WS, Wicks IP. Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation. J Clin Invest 2003;111:915-24.
  • 10. Alexander WS, Hilton DJ. The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response. Annu Rev Immunol 2004; 22:503-29.
  • 11. Bellou A, Schaub B, Ting L, Finn PW. Toll receptors modulate allergic responses: interaction with dendritic cells, T cells and mast cells. Curr Opin Allergy Clin Immunol 2003;3(6):487-94.
  • 12. Ji KA, Yang MS, Jou I, Shong MH, Joe EH. Thrombin induces expression of cytokine-induced SH2 protein (CIS) in rat brain astrocytes: involvement of phospholipase A2, cyclooxygenase, and lipoxygenase. Glia 2004;48:102-11.
  • 13. Alexander WS, Starr R, Fenner JE, Scott CL, Handman E, Sprigg NS, et al. SOCS1 is a critical inhibitor of interferon gamma signaling and prevents the potentially fatal neonatal actions of this cytokine. Cell 1999;98:597-608.
  • 14. Gatto L, Berlato C, Poli V, Tininini S, Kinjyo I, Yoshimura A, et al. Analysis of SOCS-3 promoter responses to interferon gamma. J Biol Chem 2004;279:13746-54.
  • 15. Dalpke AH, Opper S, Zimmermann S, Heeg K. Suppressors of cytokine signaling (SOCS)-1 and SOCS-3 are induced by CpGDNA and modulate cytokine responses in APCs. J Immunol 2001;166:7082-9.
  • 16. Crespo A, Filla MB, Russell SW, Murphy WJ. Indirect induction of suppressor of cytokine signalling-1 in macrophages stimulated with bacterial lipopolysaccharide: partial role of autocrine/paracrine interferon-alpha/beta. Biochem J 2000;349:99-104.
  • 17. Yang M, Min K, Joe E. Multiple mechanisms that prevent excessive brain inflammation. J Neurosci Res 2007;85:2298- 305.
  • 18. Min KJ, Pyo HK, Yang MS, Ji KA, Jou I, Joe EH. Gangliosides activate microglia via protein kinase C and NADPH oxidase. Glia 2004; 48:197-206.
There are 17 citations in total.

Details

Primary Language Turkish
Journal Section Articles
Authors

Serdar Öztuzcu This is me

Ahmet Arslan This is me

Ercan Sivaslı This is me

Mustafa Namıduru This is me

Yusuf Ziya İğci This is me

Esma Özkara This is me

Mehri İğci This is me

Zeynep Eşlik This is me

Recep Bayraktar This is me

Ecir Ali Çakmak This is me

Mehmet Yavuz Coşkun This is me

Publication Date February 1, 2011
Published in Issue Year 2011 Volume: 17 Issue: 1

Cite

APA Öztuzcu, S., Arslan, A., Sivaslı, E., Namıduru, M., et al. (2011). Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi. Gaziantep Medical Journal, 17(1), 29-32.
AMA Öztuzcu S, Arslan A, Sivaslı E, Namıduru M, İğci YZ, Özkara E, İğci M, Eşlik Z, Bayraktar R, Çakmak EA, Coşkun MY. Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi. Gaziantep Medical Journal. February 2011;17(1):29-32.
Chicago Öztuzcu, Serdar, Ahmet Arslan, Ercan Sivaslı, Mustafa Namıduru, Yusuf Ziya İğci, Esma Özkara, Mehri İğci, Zeynep Eşlik, Recep Bayraktar, Ecir Ali Çakmak, and Mehmet Yavuz Coşkun. “Menenjitli Hastalarda SOCS3 Geninin MRNA düzeyinde Ifadesi”. Gaziantep Medical Journal 17, no. 1 (February 2011): 29-32.
EndNote Öztuzcu S, Arslan A, Sivaslı E, Namıduru M, İğci YZ, Özkara E, İğci M, Eşlik Z, Bayraktar R, Çakmak EA, Coşkun MY (February 1, 2011) Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi. Gaziantep Medical Journal 17 1 29–32.
IEEE S. Öztuzcu, “Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi”, Gaziantep Medical Journal, vol. 17, no. 1, pp. 29–32, 2011.
ISNAD Öztuzcu, Serdar et al. “Menenjitli Hastalarda SOCS3 Geninin MRNA düzeyinde Ifadesi”. Gaziantep Medical Journal 17/1 (February 2011), 29-32.
JAMA Öztuzcu S, Arslan A, Sivaslı E, Namıduru M, İğci YZ, Özkara E, İğci M, Eşlik Z, Bayraktar R, Çakmak EA, Coşkun MY. Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi. Gaziantep Medical Journal. 2011;17:29–32.
MLA Öztuzcu, Serdar et al. “Menenjitli Hastalarda SOCS3 Geninin MRNA düzeyinde Ifadesi”. Gaziantep Medical Journal, vol. 17, no. 1, 2011, pp. 29-32.
Vancouver Öztuzcu S, Arslan A, Sivaslı E, Namıduru M, İğci YZ, Özkara E, İğci M, Eşlik Z, Bayraktar R, Çakmak EA, Coşkun MY. Menenjitli hastalarda SOCS3 geninin mRNA düzeyinde ifadesi. Gaziantep Medical Journal. 2011;17(1):29-32.