Commenced in January 2007
Frequency: Monthly
Edition: International
Paper Count: 30124
Analysis of Formyl Peptide Receptor 1 Protein Value as an Indicator of Neutrophil Chemotaxis Dysfunction in Aggressive Periodontitis

Authors: Prajna Metta, Yanti Rusyanti, Nunung Rusminah, Bremmy Laksono


The decrease of neutrophil chemotaxis function may cause increased susceptibility to aggressive periodontitis (AP). Neutrophil chemotaxis is affected by formyl peptide receptor 1 (FPR1), which when activated will respond to bacterial chemotactic peptide formyl methionyl leusyl phenylalanine (FMLP). FPR1 protein value is decreased in response to a wide number of inflammatory stimuli in AP patients. This study was aimed to assess the alteration of FPR1 protein value in AP patients and if FPR1 protein value could be used as an indicator of neutrophil chemotaxis dysfunction in AP. This is a case control study with 20 AP patients and 20 control subjects. Three milliliters of peripheral blood were drawn and analyzed for FPR1 protein value with ELISA. The data were statistically analyzed with Mann-Whitney test (p>0,05). Results showed that the mean value of FPR1 protein value in AP group is 0,353 pg/mL (0,11 to 1,18 pg/mL) and the mean value of FPR1 protein value in control group is 0,296 pg/mL (0,05 to 0,88 pg/mL). P value 0,787 > 0,05 suggested that there is no significant difference of FPR1 protein value in both groups. The present study suggests that FPR1 protein value has no significance alteration in AP patients and could not be used as an indicator of neutrophil chemotaxis dysfunction.

Keywords: Aggressive periodontitis, chemotaxis dysfunction, FPR1 protein value, neutrophil.

Digital Object Identifier (DOI):

Procedia APA BibTeX Chicago EndNote Harvard JSON MLA RIS XML ISO 690 PDF Downloads 420


[1] Cho C-M, You H-K, Jeong S-N. The clinical assessment of aggressive periodontitis patients. J Periodontal Implant Sci. 2011;41(3):143–8.
[2] Albandar JM, Muranga MB, Rams TE. Prevalence of aggressive periodontitis in school attendees in Uganda. J Clin Periodontol (Internet). 2002;29(9):823–31. Available from:
[3] Timmerman MF, Van der Weijden G a, Armand S, Abbas F, Winkel EG, Van Winkelhoff a J, et al. Untreated periodontal disease in Indonesian adolescents. Clinical and microbiological baseline data. J Clin Periodontol. 1998;25(3):215–24.
[4] Rusyanti Y. "Gambaran Periodontitis Agresif di Klinik Kerja Mahasiswa FKG Universitas Padjadjaran," Unpublished.
[5] Newman M, Takei H, Klokkevold P, Carranza F. Carranza’s Clinical Periodontology. 10th ed. St. Louis: Elsevier Saunders; 2006, pp. 409-414.
[6] Dorward D a, Lucas CD, Chapman GB, Haslett C, Dhaliwal K, Rossi AG. The Role of Formylated Peptides and Formyl Peptide Receptor 1 in Governing Neutrophil Function during Acute Inflammation. Am J Pathol (Internet). 2015;185(5):1172–84. Available from:
[7] Ben-Baruch a., Michiel DF, Oppenheim JJ. Signals and receptors involved in recruitment of inflammatory cells. J Biol Chem. 1995;270(20):11703–6.
[8] Mandal P, Novotny M, Hamilton T a. Lipopolysaccharide induces formyl peptide receptor 1 gene expression in macrophages and neutrophils via transcriptional and posttranscriptional mechanisms. J Immunol. 2005;175(9):6085–91.
[9] Andersson T, Dahlgren C, Lew PD, Stendahl O. Cell surface expression of fMet-Leu-Phe receptors on human neutrophils. Correlation to changes in the cytosolic free Ca2+ level and action of phorbol myristate acetate. J Clin Invest (Internet). 1987;79(4):1226–33. Available from:
[10] Tennenberg SD, Zemlan FP, Solomkin JS. Characterization of N-formyl-methionyl-leucyl-phenylalanine receptors on human neutrophils. Effects of isolation and temperature on receptor expression and functional activity. J Immunol. 1988;141(11):3937–44.
[11] Sengeløv H, Boulay F, Kjeldsen L, Borregaard N. Subcellular localization and translocation of the receptor for N-formylmethionyl-leucyl-phenylalanine in human neutrophils. Biochem J (Internet). 1994;299 (Pt 2:473–9. Available from:
[12] Daniel M a, McDonald G, Offenbacher S, Van Dyke TE. Defective chemotaxis and calcium response in localized juvenile periodontitis neutrophils. J Periodontol (Internet). 1993;64(7):617–21. Available from:
[13] Herrmann JM, Kantarci A, Long H, Bernardo J, Hasturk H, Wray L V, et al. Simultaneous measurements of cytoplasmic Ca2+ responses and intracellular pH in neutrophils of localized aggressive periodontitis (LAP) patients. J Leukoc Biol. 2005;78(3):612–9.
[14] Perez HD, Kelly E, Elfman F, Armitage G, Winkler J. Defective polymorphonuclear leukocyte formyl peptide receptor(s) in Juvenile periodontitis. J Clin Invest. 1991;87(3):971–6.
[15] Perez HD, Vilander L, Andrews WH, Holmes R. Human Formyl Peptide Receptor Ligand Binding Domain(s). J Biol Chem. 1994;269(36):22485–7.
[16] Van Dyke TE, Warbington M, Gardner M, Offenbacher S. Neutrophil surface protein markers as indicators of defective chemotaxis in LJP. J Periodontol (Internet). 1990;61(3):180–4. Available from:
[17] Albandar JM, Brown LJ, Loe H. Clinical features of early-onset periodontitis. J Am Dent Assoc. 1997;128(10):1393–9.
[18] Kowashi Y. Prevalence of Juvenile Periodontitis Among Students at Nagasaki University (kowashi). Adv Dent Res. 1988;2(2):395–6.
[19] Joshipura V, Yadalam U, Brahmavar B. Aggressive periodontitis: A review. J Int Clin Dent Res Organ (Internet). 2015;7(1):11. Available from:
[20] Noack B, Hoffmann T. Aggressive periodontitis. Perio 2004 (Internet). 2004;1(4):335–44. Available from:
[21] Nassar MM, Afifi O, Deprez RD. The prevalence of localized juvenile periodontitis in Saudi subjects. J Periodontol (Internet). 1994;65(7):698–701. Available from:
[22] Melvin WL, Sandifer JB, Gray JL. The prevalence and sex ratio of juvenile periodontitis in a young racially mixed population. J Periodontol. 1991;62(5):330–4.
[23] DeNardin E, DeLuca C, Levine MJ, Genco RJ. Antibodies directed to the chemotactic factor receptor detect differences between chemotactically normal and defective neutrophils from LJP patients. J Periodontol (Internet). 1990;61(10):609–17. Available from:
[24] Genco R, Hamada S, Lehner T, McGhee J, Mergenhagen S. Molecular Pathogenesis of Periodontal Disease. Washington DC: ASM Press; 1994.
[25] Van Dyke T, Levine M, Tabak L, Genco R. Reduced chemotactic peptide binding in juvenile periodontitis. Biochem Biophys Res Commun. 1981;100(3):1278–84.
[26] Van Dyke T, Levine M, Tabak L, Genco R. Juvenile periodontitis as a model for neutrophil function: reduced binding of the complement chemotactic fragment, C5a. PubMed Commons Juvenile periodontitis as a model for neutrophil function: reduced binding of the complement chemotactic fragment. J Dent Rest. 1983;62(8):870–2.
[27] Van Dyke T, Offenbacher S, Kalmar J, Arnold R. Neutrophil defects and host-parasite interactions in the pathogenesis of localized juvenile periodontitis. Adv Dent Res. 1988;2(2):354–8.
[28] Van Dyke TE. Role of the neutrophil in oral disease: Receptor deficiency in leukocytes from patients with juvenile periodontitis. Rev Infect Dis. 1985;7(3):419–25.
[29] Sigusch B, Eick S, Pfister S, Klinger G, Glockmann E. Altered chemotactic behavior of crevicular PMNs in different forms of periodontitis. J Clin Periodontol. 2001; 28:162–7.
[30] Jones BE, Miettinen HM, Jesaitis a J, Mills JS. Mutations of F110 and C126 of the formyl peptide receptor interfere with G-protein coupling and chemotaxis. J Periodontol (Internet). 2003;74(4):475–84. Available from:
[31] Gwinn M, Sharma A, De Nardin E. Single nucleotide polymorphism of the N-formyl peptide receptor in localized juvenile periodontitis. J Periodontol. 1999; 70:1194–201.
[32] Ryder M. Commparison of neutrophil functions in aggressive and chronic periodontitis. Periodontol 2000. 2010; 53:124–37.
[33] De Nardin E. Neutrophil Receptors: N-Formyl-l-Methionyl-l-Leucyl-l-Phenylalanine and Interleukin-8. In: Genco R, Hamada S, Lehner T, McGhee J, Mergenhagen S, editors. Molecular Pathogenesis of Periodontal Disease. Washington DC: ASM Press; 1994. p. 351–61.
[34] Sahagun-Ruiz A, Colla JS, Juhn J, Gao JL, Murphy PM, McDermott DH. Contrasting evolution of the human leukocyte N-formylpeptide receptor subtypes FPR and FPRL1R. Genes Immun. 2001;335–42.
[35] Zhang Y, Syed R, Uygar C, Pallos D, Gorry MC, Firatli E, et al. Evaluation of human leukocyte N-formylpeptide receptor (FPR1) SNPs in aggressive periodontitis patients. Genes Immun (Internet). 2003;4(1):22–9. Available from:
[36] Gunji T, Onouchi Y, Nagasawa T. Functional polymorphisms of the FPR1 gene and aggressive periodontitis in Japanese. Biochem Biophys Res Commun. 2007;364(7-13).
[37] Richard DY, Wang J, Dahlgern C, Gerard C, Parmentier M, Serhan C, et al. International Union of Basic and Clinical Pharmacology LXXIII. Nomenclature for the Formyl Peptide Receptor (FPR) Family. Pharmacol Rev. 2009;61(2):119–61.
[38] Maney P, Walters JD. Formylpeptide Receptor Single Nucleotide Polymorphism 348T>C and Its Relationship to Polymorphonuclear Leukocyte Chemotaxis in Aggressive Periodontitis. J Periodontol. 2009;80(9):1498–505.
[39] Maney P, Emecen P, Mills J, Walters J. Neutrophil formylpeptide receptor single nucleotide polymorphism 348T>C in aggressive periodontitis. 2009;80(3):492–8.
[40] Kalmar J. Antimicrobial Dysfunction in Localized Juvenile Periodontitis Neutrophils. In: Genco R, Hamada S, Lehner T, McGhee J, Mergenhagen S, editors. Molecular Pathogenesis of Periodontal Disease. Washington DC: ASM Press; 1994. p. 337–49.
[41] Van Dyke T, Horoszewicz H, Cianciola L, Genco R. Neutrophil Chemotaxis dysfunction Periodontitis. Infect Immun. 1980; 27:124–32.
[42] Vieira AR, Albandar JM. Role of genetic factors in the pathogenesis of aggressive periodontitis. Periodontol 2000. 2014;65(1):92–106.
[43] Kantarci A, Oyaizu K, Van Dyke TE. Neutrophil-mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis. J Periodontol. 2003;74(1):66–75.