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Journals / Dicle Üniversitesi Veteriner Fakültesi Dergisi / 2026 / Cilt: 19 Sayı: 1

Effects of Acute Inflammation Induced by Lipopolysaccharide (LPS) and Pam3csk4 (TLR2/1 Agonist) on Anti-Müllerian Hormone (AMH) Expression and Serum Levels in the Mouse Ovary

Lipopolisakkarit (LPS) ve Pam3csk4 (TlR2/1 Agonisti) Tarafından İndüklenen Akut İnflamasyonun Fare Ovaryumunda Anti-Müllerian Hormon (Amh) Ekspresyonu ve Serum Düzeyleri Üzerindeki Etkileri

Duygu Yaman Gram(ERCİYES ÜNİVERSİTESİ)0000-0003-2404-0384
Gökhan Uyanık(Hatay Mustafa Kemal University)0000-0003-4488-3055
Murat Abay(ERCİYES ÜNİVERSİTESİ)0000-0003-2457-1919
Pages
70–77
Publication Date
2026-06-30
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AI Summary & Key Takeaways

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

In conclusion, LPS altered serum AMH levels, whereas neither PAMP changed the qualitative ovarian localization of AMH within the 24-hour observation period.

📌 3 Key Takeaways

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Objective & Hypothesis:This study aimed to investigate the effects of acute inflammation induced by lipopolysaccharide (LPS) and Pam3CSK4 (TLR2/1 agonist) during the follicular phase on ovarian and serum anti-Müllerian hormone (AMH) responses in mice.
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Key Findings & Data:A total of 30 female BALB/c mice aged 6-8 weeks were divided into three groups: control (n = 10), Pam3CSK4 (n = 10), and lipopolysaccharide (LPS) (n = 10).
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Conclusion & Impact:In conclusion, LPS altered serum AMH levels, whereas neither PAMP changed the qualitative ovarian localization of AMH within the 24-hour observation period.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:AMH · LPS · Ovaryum

Abstract

This study aimed to investigate the effects of acute inflammation induced by lipopolysaccharide (LPS) and Pam3CSK4 (TLR2/1 agonist) during the follicular phase on ovarian and serum anti-Müllerian hormone (AMH) responses in mice. A total of 30 female BALB/c mice aged 6-8 weeks were divided into three groups: control (n = 10), Pam3CSK4 (n = 10), and lipopolysaccharide (LPS) (n = 10). To standardize follicular activity, all mice were initially administered 5 IU equine chorionic gonadotropin (eCG) intraperitoneally (IP). Twenty-four hours following this administration, TLR2/TLR1 and TLR4 activation in the experimental groups was achieved by intraperitoneal administration of 100 µg Pam3CSK4 and 100 µg LPS, respectively, while the control group received an equal volume (100 µL) of phosphate-buffered saline (PBS). Twenty-four hours after the applications, ovarian tissues were collected under general anaesthesia for immunohistochemical evaluation; simultaneously obtained serum samples were analysed for AMH concentrations (ng/mL) using the enzyme immunoassay (EIA) method. Evaluation of the results revealed a marked difference in responses among pathogen-associated molecular patterns (PAMPs). Following administration of the TLR4 activator LPS (6.11 ± 1.3 ng/mL), serum AMH levels were found to be significantly decreased compared to the control group (8.83 ± 1.04 ng/mL) (P 0.05). Immunohistochemical analyses qualitatively demonstrated that neither PAMP treatment affected the follicular distribution or cellular localization of AMH in the ovary. In conclusion, LPS altered serum AMH levels, whereas neither PAMP changed the qualitative ovarian localization of AMH within the 24-hour observation period.

Özet

Bu çalışma, foliküler fazda lipopolisakkarit (LPS) ve Pam3CSK4 (TLR2/1 agonisti) tarafından indüklenen akut inflamasyonun farelerdeki ovaryum ve serum anti-Müllerian hormon (AMH) yanıtları üzerindeki etkilerini araştırmayı amaçlamıştır. Toplam 30 dişi BALB/c fare (6-8 haftalık) üç gruba ayrıldı: kontrol (n = 10), Pam3CSK4 (n = 10) ve lipopolisakkarit (LPS) (n = 10). Foliküler aktiviteyi standardize etmek için, tüm farelere başlangıçta intraperitoneal (IP) olarak 5 IU at koryonik gonadotropini (eCG) uygulandı. Bu uygulamadan yirmi dört saat sonra, deney gruplarında TLR2/TLR1 ve TLR4 aktivasyonu, sırasıyla 100 µg Pam3CSK4 ve 100 µg LPS'nin intraperitoneal olarak uygulanmasıyla sağlandı; kontrol grubuna ise eşit hacimde (100 µL) fosfat tamponlu salin (PBS) verildi. Uygulamalardan yirmi dört saat sonra, genel anestezi altında ovaryum dokuları immünohistokimyasal değerlendirme için toplandı; eş zamanlı olarak elde edilen serum örnekleri, enzim immün testi (EIA) yöntemi kullanılarak AMH konsantrasyonları (ng/mL) açısından analiz edildi. Sonuçların değerlendirilmesi, patojenle ilişkili moleküler paternler (PAMP'ler) arasında yanıtlarda belirgin bir farklılık olduğunu ortaya koydu. TLR4 aktivatörü LPS'nin (6,11 ± 1,3 ng/mL) uygulanmasının ardından, serum AMH düzeylerinin kontrol grubuna (8,83 ± 1,04 ng/mL) kıyasla anlamlı derecede azaldığı bulundu (P 0,05). İmmünohistokimyasal analizler, PAMP tedavilerinin hiçbirinin ovaryumda AMH'nin foliküler dağılımını veya hücresel lokalizasyonunu etkilemediğini niteliksel olarak gösterdi. Sonuç olarak, LPS serum AMH seviyelerini değiştirirken, PAMP'lerin hiçbiri 24 saatlik gözlem süresi içinde AMH'nin yumurtalıktaki niteliksel lokalizasyonunu değiştirmemiştir.

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Cite This Article

Gram, D. Y., Uyanık, G., Abay, M. (2026). Effects of Acute Inflammation Induced by Lipopolysaccharide (LPS) and Pam3csk4 (TLR2/1 Agonist) on Anti-Müllerian Hormone (AMH) Expression and Serum Levels in the Mouse Ovary. Dicle Üniversitesi Veteriner Fakültesi Dergisi, Cilt: 19 Sayı: 1, 70–77. https://doi.org/10.47027/duvetfd.1880361

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References (35)

  1. Wira CR, Fahey JV, Sentman CL, et al. (2005). Innate and adaptive immunity in female genital tract: cellular responses and interactions. Immunol Rev., 206(1):306-335.
  2. Li H, Zang Y, Wang C, et al. (2020). The interaction between microorganisms, metabolites, and immune system in the female genital tract microenvironment. Front Cell Infect Microbiol., 10:609488.
  3. Sheldon IM, Cronin J, Goetze L, et al. (2009). Defining postpartum uterine disease and the mechanisms of infection and immunity in the female reproductive tract in cattle. Biol Reprod., 81(6):1025-1032.
  4. Dahiya S, Kumari S, Rani P, et al. (2018). Postpartum uterine infection & ovarian dysfunction. Indian J Med Res., 148(Suppl 1):S64-S70.
  5. Bazzazan A, Costa M, Segura M, et al. (2025). Prepartum vaginal microbiota and postpartum uterine microbiota in cows. Clin Theriogenology, 17.
  6. Turner ML, Healey GD, Sheldon IM. (2012). Immunity and inflammation in the uterus. Reprod Domest Anim., 47:402-409.
  7. Bromfield JJ, Sheldon IM. (2013). Lipopolysaccharide reduces the primordial follicle pool in the bovine ovarian cortex ex vivo and in the murine ovary in vivo. Biol Reprod., 88(4):98.
  8. Mansouri A, Akthar I, Miyamoto A. (2025). TLR2 and TLR4 bridge physiological and pathological inflammation in the reproductive system. Commun Biol., 8(1):1008.
  9. Liu Z, Shimada M, Richards JS. (2008). The involvement of the Toll-like receptor family in ovulation. J Assist Reprod Genet., 25(6):223-228.
  10. Magata F, Horiuchi M, Miyamoto A, Shimizu T. (2014). Lipopolysaccharide inhibits steroid production in theca cells of bovine follicles in vitro: distinct effect of LPS on theca cell function in pre- and post-selection follicles. J Reprod Dev., 60(4):280-287.
  11. Patel MV, Shen Z, Wira CR. (2018). Poly (I:C) and LPS induce distinct immune responses by ovarian stromal fibroblasts. J Reprod Immunol., 127:36-42.
  12. Price JC, Sheldon IM. (2013). Granulosa cells from emerged antral follicles of the bovine ovary initiate inflammation in response to pathogen-associated molecular patterns via Toll-like receptor pathways. Biol Reprod., 89(5):119.
  13. Duffy DM, Ko C, Jo M, et al. (2019). Ovulation: parallels with inflammatory processes. Endocr Rev., 40(2):369-416.
  14. Taghavi SA, Ashrafi M, Mehdizadeh M, et al. (2014). Toll-like receptors expression in follicular cells of patients with poor ovarian response. Int J Fertil Steril., 8(2):183-190.
  15. Benjelloun F, Quillay H, Cannou C, et al. (2020). Activation of toll-like receptors differentially modulates inflammation in the human reproductive tract: preliminary findings. Front Immunol., 11:1655.
  16. Yamamoto N, Takeuchi H, Yamaoka M, et al. (2023). Lipopolysaccharide suppresses follicle development marker expression and enhances cytokine expressions, which results in failure of granulosa cell proliferation in developing follicle in cows. Reprod Biol., 23(1):100710.
  17. Gökçek İ, Uyanık G. (2025). Protective effects of thymol with hormonal, antiinflammatory and antioxidant pathways in lipopolysaccharide-induced ovarian damage in rats. Vet Sci Pract., 20(1):1-7.
  18. Wang X, Li C, Wang Y, et al. (2020). UFL1 alleviates LPS-induced apoptosis by regulating the NF-κB signaling pathway in bovine ovarian granulosa cells. Biomolecules, 10(2):260.
  19. Takeuchi O, Sato S, Horiuchi T, et al. (2002). Cutting edge: role of Toll-like receptor 1 in mediating immune response to microbial lipoproteins. J Immunol., 169(1):10-14.
  20. Takeuchi O, Akira S. (2010). Pattern recognition receptors and inflammation. Cell, 140(6):805-820.
  21. Gram DY, Abay M, Liman N, et al. (2024). The effects of the activation of TLR2/TLR1 on in vitro angiogenesis in an immortalized ovine luteal endothelial cell line. Reproduction, 168(4).
  22. Oliveira-Nascimento L, Massari P, Wetzler LM. (2012). The role of TLR2 in infection and immunity. Front Immunol., 3:79.
  23. Cedars MI. (2022). Evaluation of female fertility-AMH and ovarian reserve testing. J Clin Endocrinol Metab., 107(6):1510-1519.
  24. Gökçek İ, Uyanık G, Tutar T, et al. (2025). Effects of carvacrol on hormonal, inflammatory, antioxidant changes, and ovarian reserve in polycystic ovary syndrome in Wistar rats. Naunyn Schmiedebergs Arch Pharmacol., 398(4):4607-4616.
  25. Almeida FR, Costermans NG, Soede NM, et al. (2018). Presence of anti-Müllerian hormone (AMH) during follicular development in the porcine ovary. PLoS One, 13(7):e0197894.
  26. Visser JA, Themmen AP. (2005). Anti-Müllerian hormone and folliculogenesis. Mol Cell Endocrinol, 234(1–2):81–86.
  27. Iwase A, Hasegawa Y, Tsukui Y, et al. (2023). Anti-Müllerian hormone beyond an ovarian reserve marker. Front Endocrinol, 14:1273966.
  28. Griesinger G, Dafopoulos K, Buendgen N, et al. (2012). Elimination half-life of anti-Müllerian hormone. J Clin Endocrinol Metab, 97(6):2160–2163.
  29. Visser JA, Themmen AP. (2014). Role of anti-Müllerian hormone and bone morphogenetic proteins in the regulation of FSH sensitivity. Mol Cell Endocrinol, 382(1):460–465.
  30. Price JC, Bromfield JJ, Sheldon IM. (2013). Pathogen-associated molecular patterns initiate inflammation and perturb the endocrine function of bovine granulosa cells via TLR2 and TLR4. Endocrinology, 154(9):3377–3386.
  31. Cui L, Sheng Y, Sun M, et al. (2016). Chronic pelvic inflammation diminished ovarian reserve as indicated by serum anti-Müllerian hormone. PLoS One, 11(6):e0156130.
  32. Ak M, Taş M, Aksoy H, et al. (2023). Effects of chronic urticaria on ovarian reserve. J Health Sci Med, 6(4):772–774.
  33. Qin X, Du J, He R, et al. (2024). Potential mechanisms and therapeutic strategies for LPS-associated female fertility decline. J Assist Reprod Genet, 41(10):2739–2758.
  34. Haziak K, Herman AP, Wojtulewicz K, et al. (2018). Effect of CD14/TLR4 antagonist on GnRH/LH secretion in ewe during central inflammation induced by LPS. J Anim Sci Biotechnol, 9:52.
  35. Ibrahim LA, Kramer JM, Williams RS, Bromfield JJ. (2016). Human granulosa–luteal cells initiate an innate immune response to pathogen-associated molecules. Reproduction, 152(4):261–270.