Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1 (5-Year IF – 2.0)
Journal Citation Indicator (JCI) (2023) – 0.4
Scopus CiteScore – 3.7 (CiteScore Tracker – 4.0)
Index Copernicus  – 171.00; MNiSW – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
Periodicity – monthly

Download original text (EN)

Advances in Clinical and Experimental Medicine

2008, vol. 17, nr 1, January-February, p. 33–40

Publication type: original article

Language: English

Expression of Basic Fibroblast Growth Factor in Nasal Polyps

Ekspresja zasadowego czynnika wzrostu fibroblastów w polipach nosa

Beata Rostkowska−Nadolska1,, Katarzyna Pazdro−Zastawny1,, Piotr Ziółkowski2,, Elżbieta Gamian2,, Marzena Jaworska1,, Marek Bochnia1,, Agnieszka Jabłonka1,

1 Department of Otolaryngology, Silesian Piasts University of Medicine in Wrocław, Poland

2 Department of Pathological Anatomy, Silesian Piasts University of Medicine in Wrocław, Poland

Abstract

Background. The pathogenesis of nasal polyposis remains unclear. The proliferation of fibroblasts contributes to their development and growth. Basic fibroblast growth factor (bFGF) is a member of the heparin−binding growth factor family and may be involved in various pathological processes, including tissue lesion in the upper respiratory tract.
Objectives. The aim of this study was to determine the role of bFGF in the pathogenesis of nasal polyps by comparative analysis of its expression in neutrophilic and eosinophilic polyps, including patients with aspirin triad.
Material and Methods. The study group included 28 patients (20 males and 8 females) with nasal polyposis undergoing polypectomy. The control group consisted of 10 normal nasal mucosa specimens from patients undergoing septoplasty. Twenty of the nasal polyps were histopathologically classified as eosinophilic and eight as neutrophilic. Immunohistochemistry was used to examine the expression of bFGF in the nasal polyp tissues.
Results. bFGF immunostaining was detected both in the neutrophilic and eosinophilic polyp tissues. Particularly intense immunolabeling of bFGF was present in the nasal polyps with a high degree of neutrophil infiltration.
Conclusion. The expression of bFGF was more intense in nasal polyp tissues than in normal mucosa. The examined factor was mainly localized in the vascular endothelium and inflammatory cells. Considering the stimulatory properties of bFGF on epithelial blood vessels and fibroblast proliferation, this growth factor seems to be involved in the pathogenesis of nasal polyposis.

Streszczenie

Wprowadzenie. Patogeneza polipów nosowych nie jest dokładnie poznana. Uznaje się, że proliferacja fibroblastów może przyczyniać się do ich powstawania i wzrostu. Zasadowy czynnik wzrostu fibroblastów (bFGF) należy do rodziny białek wiążących heparynę. bFGF może wpływać na wiele fizjologicznych i patologicznych procesów biologicznych, włączając w to uszkodzenie tkanek w górnych drogach oddechowych.
Cel pracy. Określenie roli zasadowego czynnika wzrostu fibroblastów (bFGF) w patogenezie polipów nosa za pomocą analizy porównawczej jego ekspresji w polipach neutrofilowych i eozynofilowych, a także u osób z triadą aspirynową w porównaniu z prawidłową błoną śluzową.
Materiał i metody. Materiał do badań stanowiło 28 tkanek polipów nosowych pobranych od pacjentów (20 mężczyzn i 8 kobiet) podczas polipektomii. Grupę kontrolną stanowiło 10 wycinków prawidłowej błony śluzowej nosa pobranych podczas zabiegu septoplastyki. Pod względem histopatologicznym 20 polipów było rozpoznawanych jako eozynofilowe, a 8 jako neutrofilowe. Badany bFGF oznaczono metodą immunohistochemiczną.
Wyniki. Zarówno w tkankach polipów neutrofilowych, jak i eozynofilowych uzyskano ekspresję bFGF. Szczególnie intensywny odczyn występował w polipach z przeważającym naciekiem neutrofilów. Poziom ekspresji był wyższy w tkankach polipów niż w prawidłowej błonie śluzowej.
Wnioski. Badany czynnik występował przede wszystkim w komórkach endotelialnych wokół naczyń krwionośnych, a także w komórkach nacieku zapalnego. Ze względu na swoje właściwości stymulujące proliferację komórek zarówno śródbłonka naczyń, jak i fibroblastów wydaje się, że czynnik ten ma znaczenie w patogenezie polipów nosowych.

Key words

nasal polyps, basic fibroblast growth factor, immunohistochemistry, aspirin triad

Słowa kluczowe

polipy nosowe, zasadowy czynnik wzrostu fibroblastów, immunohistochemia, triada aspirynowa

References (34)

  1. Pawankar R: Nasal polyps: an update: editorial review. Curr Opin Allergy Clin Immunol 2003, 3, 1–6.
  2. Bikfalvi A, Klein S, Pintucci G, Rifkin DB: Biological roles of fibroblast growth factor−2. Endocr Rev 1997, 18, 26–45.
  3. Hughes SE, Hall PA: Immunolocalization of fibroblast growth factor receptor 1 and its ligands in human tissues. Lab Invest 1993, 69, 173–182.
  4. Kanazawa S, Tsunoda T, Onuma E, Majima T, Kagiyama M, Kikuchi K: VEGF, basic−FGF, and TGF−beta in Crohn’s disease and ulcerative colitis: a novel mechanism of chronic intestinal inflammation. J Gastroenterol 2001, 96, 822–828.
  5. Gravdal K, Halvorsen OJ, Haukaas SA, Akslen LA: Expression of bFGF/FGFR−1 and vascular proliferation related to clinicopathologic features and tumor progress in localized prostate cancer. Virchows Arch 2005, 12, 1–7
  6. Jawerzat S, Auguste P, Bikfalvi A: The role of fibroblast growth factors in vascular development. Trends Mol Med 2002, 8, 483–489.
  7. Han R, Liu J, Tanswell AK, Post M: Expression of basic fibroblast growth factor and receptor: immunolocalization studies in developing rat fetal lung. Pediatr Res 1992, 31, 435–440.
  8. Norlander T, Westermark A, van Setten G, Valtonen H, Ishizaki H, Pyykko I: Basic fibroblast growth factor in nasal polyps immunohistochemical and quantitative findings. Rhinology 2001, 39, 88–92.
  9. Powers MR, Qu Z, LaGesse PC, Liebler JM, Wall MA, Rosenbaum JT: Expression of basic fibroblast growth factor in nasal polyps. Ann Otol Rhinol Laryngol 1998, 107, 891–897.
  10. Klimaschewski L, Nindl W, Feurle J, Kavakebi P, Kostron H: Basic fibroblast growth factor isoforms promote axonal elongation and branching of adult sensory neurons in vitro. Neuroscience 2004, 126, 347–353.
  11. Hakvoort T, Altun V, van Zuijlen PP, de Boer WI, van Schadewij WA, van der Kwast TH: Transforming growth factor−beta(1), −beta(2), −beta(3), basic fibroblast growth factor and vascular endothelial growth factor expression in keratinocytes of burn scars. Eur Cytokine Netw 2000, 11, 233–239.
  12. Hicks D, Courtois Y: Fibroblast growth factor stimulates photoreceptor differentiation in vitro. J Neurosci 1992, 12, 2022–2033.
  13. Neubauer M, Fischbach C, Bauer−Kreisel P, Lieb E, HackerM, Tessmar J, Schulz MB, Goepferich A, Blunk T: Basic fibroblast growth factor enhances PPARgamma ligand−induced adipogenesis of mesenchymal stem cells. FEBS Lett 2004, 577, 277–283.
  14. Harduf H, Halperin E, Reshef R, Ron D: Sef is synexpressed with FGFs during chick embryogenesis and its expression is differentially regulated by FGFs in the developing limb. Dev Dyn. 2005, 233, 301–312.
  15. Ito A, Shimokava H, Fukumoto Y, Kadokami T, Nakaike R, Takayanagi T, Egashira K, Sueishi K, Takeshita A: The role of fibroblast growth factor−2 in the vascular effects of interleukin–1 beta in porcine coronary arteries in vivo. Cardiovasc Res 1996, 32, 570–579.
  16. Lajeunie E, Ma HW, Bonaventure J, Munnich A, Le Merrer M: FGFR2 mutations in Pfeiffer Syndrome. Nat Gen 1995, 9, 108–112.
  17. Jabs EW, Li X, Scott AF, Meyers G, Chen W, Eccles M, Mao JI, Charnas LR, Jackson CE, Jaze M: Jackson Weiss and Crouzon syndromes are allelic with mutations in fibroblast growth factor receptor 2. Nat Genet 1994, 8, 275–172.
  18. Wilkie AO, Slaney SF, Oldridge M, Poole MD, Ashworth GJ, Hockley AD, Hayward RD, David DJ, Pulleyn IJ, Rutland P: Apert syndrome results from localized mutations of FGFR2 and is allelic with Crouzon syndrome. Nat Genet 1995, 9, 165–172.
  19. Rousseau F, Bonaventure J, Legal Mallet L, Pelet A, Royet JM, Maroteaux P, Le Merrer M, Munich A: Mutation in the gene encoding fibroblast growth factor receptor 3 in achondroplasia. Nature 1994, 371, 252–325.
  20. Rousseau F, Saugier P, Le MerrerM, Delezoide AL, Maroteaux P, Bonaventure J: Stop codon FGFR3 mutations in thanatophoric dwarfism type 1. Nat Genet 1995, 10, 11–12.
  21. Laham RJ, Garcia L, Baim DS, Post M, Simons M: Therapeutic angiogenesis using basic fibroblast growth factor and vascular endothelial growth factor using various delivery strategies. Curr Interv Cardiol Rep 1999, 1, 228–233.
  22. Ma Y, Zhao H, Zhou X: Topical treatment with growth factors for tympanic membrane perforations: progress towards clinical application. Acta Otolaryngol 2002, 122, 586–599.
  23. Mayer E, Cardoso PF, Puskas JD, De Campos K, Oka T, Dardick I, Patterson GA: The effect of basic fibroblast growth factor and omentopexy on revascularization and epithelial regeneration of heterotopic rat tracheal isografts. J Thorac Cardiovasc Surg 1992, 104, 180–188.
  24. Coste A, Rateau J−G, Roudot−Thoraval F, Chapelin C, Gilain L, Poron F, Peynegre R, Bernaudin J−F, Escudier E: Increased epithelial cell proliferation in nasal polyps. Arch Otolaryng Head Neck Surg 1996, 122, 432–436.
  25. Kowalski LM, Pawliczak R, Woźniak J, Siuda K, Poniatowska M, Iwaszkiewicz J, Kornatowski T, Kaliner MA: Differential metabolism of arachidonic acid in nasal polyp epithelial cells cultured from aspirin−sensitive and aspirin−tolerant patients. Am J Respir Crit Care Med 2000, 161, 391–398.
  26. Caye−Thomasen P, Larsen K, Tingsgaard P, Tos M: Basic fibroblast growth factor expression in recurrent versus non−recurrent nasal polyposis. Eur Arch Otorhinolaryngol 2004, 261, 321–325.
  27. Li H, Xu G, Li Y, Xie M, Xu R: Expressions of vascular endothelial growth factor and basic fibroblast growth factor in nasal polyp and its role. Zhonghua Er Bi Yan Hou Ke Za Zhi 2001, 36, 87–89.
  28. Takagi S, Takahashi K, Katsura Y, Matsuoka T, Ohsaka A: Basic fibroblast growth factor modulates the surface expression of effector cell molecules and primes respiratory burst activity in human neutrophils. Acta Heamatol 2000, 103, 78–83.
  29. Totani L, Piccoli A, Pellegrini GG, Di Santo A, Lorenzet R: Polymorphonuclear leukocytes enhance release of growth factors by cultured endothelial cells. Arterioscler Thromb 1994, 14, 125–132.
  30. Zhang H, Issekutz AC: Growth regulation of neutrophil−endothelial cell interactions. J Leukoc Biol 2001, 70, 225–232.
  31. Tokushige E, Itoh K, Ushikai M, Katahisa S, Fukuda K: Localization of IL−1B mRNA and cell adhesion molecules in the maxillary sinus mucosa of patients with chronic sinusitis. Laryngoscope 1994, 104, 1245–1250.
  32. Shimomura A, Ikeda K, Suzuki H, Nakabayashi S, Oshima T, Furukawa M, Takasaka T, Ando N, Ohtani H, Nagura H: The expression of adhesion molecules in nonalllergic chronic sinusitis. Laryngoscope 1997, 107, 1519–1524.
  33. Itoh K, Katahira S, Matsuzaki T, Ohyama M, Fukuda K: Retention fluids of chronic sinusitis induce neutrophil adherence to microvascular endothelial cells. Acta Otolaryngol (Stockh) 1992, 112, 882–889.
  34. Yamamoto Y, Ikeda K, Watanabe M, Shimomura A, Suzuki H, Oshima T, Imamura Y, Ohuchi K, Takasaka T: Expression of adhesion molecules in cultured human nasal mucosal microvascular endothelial cells activated by interleukin−1 beta or tumor necrosis factor−alpha: effects of dexamethasone. Int Arch Allergy Immunol 1998, 117, 68–77.
© Wroclaw Medical University