Journals / Turkish Journal of Medical Sciences / 2011 / Cilt: 41 - Sayı: 2

Immunomodulatory role of leptin treatment in experimental sepsis caused by gram negative bacteria

Pages
251–258
Publication Date
2022-11-05
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: According to our results, leptin has a profound influence on sepsis, and to some extent it restricts the inflammatory events in sepsis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:To investigate the effect of leptin treatment on circulating inflammatory cytokines and on tissue damage in experimental rat model of gram-negative sepsis.
📊
Key Findings & Data:Materials and methods: Adult male Wistar rats, 28 in total, were randomly divided into 4 groups (n = 7): sham, leptin, sepsis, and sepsis group treated with leptin (sepsis+leptin).
💡
Conclusion & Impact:Conclusion: According to our results, leptin has a profound influence on sepsis, and to some extent it restricts the inflammatory events in sepsis.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Key words: Cytokines · leptin · myeloperoxidase

Abstract

To investigate the effect of leptin treatment on circulating inflammatory cytokines and on tissue damage in experimental rat model of gram-negative sepsis. Materials and methods: Adult male Wistar rats, 28 in total, were randomly divided into 4 groups (n = 7): sham, leptin, sepsis, and sepsis group treated with leptin (sepsis+leptin). Sepsis was induced by intraperitoneal (ip) injection of 2 × 1010 CFU of Escherichia coli ATCC 25922. Leptin and sepsis+leptin groups received a single dose ip 0.1 mg/kg leptin, while sham group received 1 mL of ip saline. Rats were sacrificed 24 h after the induction of sepsis. Blood samples, lung, and kidney tissues were collected for analysis. Results: The sepsis group had significantly higher serum TNF-a, IL-6, and endothelin levels than the sham group (P = 0.05, P < 0.001, P = 0.003, respectively). The sepsis+leptin group had significantly lower IL-6 and endothelin levels (P = 0.001 and P = 0.020, respectively), and higher lung and kidney tissue myeloperoxidase activities when compared with the sepsis group (P = 0.039, P = 0.033, respectively). Conclusion: According to our results, leptin has a profound influence on sepsis, and to some extent it restricts the inflammatory events in sepsis.

Özet

To investigate the effect of leptin treatment on circulating inflammatory cytokines and on tissue damage in experimental rat model of gram-negative sepsis. Materials and methods: Adult male Wistar rats, 28 in total, were randomly divided into 4 groups (n = 7): sham, leptin, sepsis, and sepsis group treated with leptin (sepsis+leptin). Sepsis was induced by intraperitoneal (ip) injection of 2 × 1010 CFU of Escherichia coli ATCC 25922. Leptin and sepsis+leptin groups received a single dose ip 0.1 mg/kg leptin, while sham group received 1 mL of ip saline. Rats were sacrificed 24 h after the induction of sepsis. Blood samples, lung, and kidney tissues were collected for analysis. Results: The sepsis group had significantly higher serum TNF-a, IL-6, and endothelin levels than the sham group (P = 0.05, P < 0.001, P = 0.003, respectively). The sepsis+leptin group had significantly lower IL-6 and endothelin levels (P = 0.001 and P = 0.020, respectively), and higher lung and kidney tissue myeloperoxidase activities when compared with the sepsis group (P = 0.039, P = 0.033, respectively). Conclusion: According to our results, leptin has a profound influence on sepsis, and to some extent it restricts the inflammatory events in sepsis.

🔖

Cite This Article

ALICI, Ö., KAVAKLI, H. Ş., KOCA, C. (2022). Immunomodulatory role of leptin treatment in experimental sepsis caused by gram negative bacteria. Turkish Journal of Medical Sciences, Cilt: 41 - Sayı: 2, 251–258. https://ajindex.com/articles/611277

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Hotchkiss RS, Karl IE. Cytokine blockade in sepsis—Are two better than one? Crit Care Med 2001; 29: 671-2.
  2. Kellum JA, Kong L, Fink MP, Weissfeld LA, Yealy DM, Pinsky MR et al. Understanding the infl ammatory cytokine response in pneumonia and sepsis: results of the Genetic and Infl ammatory Markers of Sepsis (GenIMS) Study. Arch Intern Med 2007; 167: 1655-63. 3. Zhang Y, Proenca R, Maff ei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature 1994; 372: 425-32.
  3. Otero M, Lago R, Lago F, Casanueva FF, Dieguez C, Gómez- Reino JJ et al. Leptin, from fat to infl ammation: old questions and new insights. FEBS Lett 2005; 579: 295-301.
  4. Fantuzzi G, Faggioni R. Leptin in the regulation of immunity, infl ammation, and hematopoiesis. J Leukoc Biol 2000; 68: 437- 46. Tschöp J, Nogueiras R, Haas-Lockie S, Kasten KR, Castañeda TR, Huber N et al. CNS leptin action modulates immune response and survival in sepsis. J Neurosci 2010; 30: 6036-47.
  5. Gultekin FA, Kerem M, Tatlicioglu E, Aricioglu A, Unsal C, Bukan N. Leptin treatment ameliorates acute lung injury in rats with cerulein-induced acute pancreatitis. World J Gastroenterol 2007; 13: 2932-38.
  6. Hacioglu A, Algin C, Pasaoglu O, Pasaoglu E, Kanbak G. Protective eff ect of leptin against ischemia-reperfusion injury in the rat small intestine. BMC Gastroenterol 2005; 5: 37. Gülen S, Dinçer S. Eff ects of leptin on oxidative stress in healthy and Streptozotocin-induced diabetic rats. Mol Cell Biochem 2007; 302: 59-65.
  7. Giacometti A, Ghiselli R, Cirioni O, Mocchegiani F, D’Amato G, Orlando F et al. Th erapeutic effi cacy of the magainin analogue MSI-78 in diff erent intra-abdominal sepsis rat models. J Antimicrob Chemother 2004; 54: 654-60.
  8. Koike K, Moore EE, Moore FA, Read RA, Carl VS, Banerjee A. Gut ischemia/reperfusion produces lung injury independent of endotoxin. Crit Care Med 1994; 22: 1438-44.
  9. Faggioni R, Feingold KR and Grunfeld C. Leptin regulation of the immune response and the immunodefi ciency of malnutrition. FASEB J 2001; 14: 2565–71.
  10. Cano V, Merino B, L Ezquerra L, Somoza B and Ruiz-Gayo M. A cholecystokinin-1 receptor agonist (CCK-8) mediates increased permeability of brain barriers to leptin British Journal of Pharmacology 2008; 154: 1009-15.
  11. Siegmund B, Lear-Kaul KC, Faggioni R, Fantuzzi G. Leptin defi ciency, not obesity, protects mice from Con A-induced hepatitis. Eur J Immunol 2002; 32: 552-60.
  12. Faggioni R, Fantuzzi G, Gabay C, Moser A, Dinarello CA,