Advertisement

Serum Levels of High-Sensitivity C-Reactive Protein (hs-CRP) in Helicobacter pylori-Infected Peptic Ulcer Patients and Its Association with Bacterial CagA Virulence Factor

  • A. Jafarzadeh
  • G. H. Hassanshahi
  • M. Nemati
Original Article

Abstract

Objective CRP is a marker of inflammation and infection of the gastric mucosa with Helicobacter pylori, which causes an inflammatory reaction. It has been reported that CagA + H. pylori strains induce more severe gastric inflammation and are also associated with higher risks of peptic ulcer and gastric cancer. The purpose of this study was to compare serum concentrations of hs-CRP in H. pylori-infected peptic ulcer (PU) patients, H. pylori-infected asymptomatic (AS) carriers, and a healthy control group, and their association with bacterial virulence factor CagA. Material and Methods A total of 60 H. pylori-infected PU patients (30 patients were positive for anti-CagA antibody and 30 were negative for anti-CagA antibody), 53 H. pylori-infected AS carriers (25 subjects were positive for anti-CagA antibody and 28 were negative for anti-CagA antibody), and 22 healthy H. pylori-negative subjects (as a control group) were enrolled in the study. Serum concentrations of hs-CRP were measured by use of an ELISA method. Results The mean serum level of hs-CRP in all PU patients (124.9 ± 32.4 μg/dl) was significantly higher than that in all AS subjects (18.6 ± 2.6 μg/dl; P < 0.001) and the healthy uninfected control group (10.7 ± 2.9 μg/dl; P < 0.0001). Moreover, the mean serum level of hs-CRP in the AS group was significantly higher than that observed in the uninfected control group (P < 0.04). No significant difference was observed between mean serum levels of hs-CRP of PU patients with positive test for anti-CagA antibody (132.6 ± 49.4 μg/dl) and PU patients with negative test for anti-CagA antibody (117.1 ± 42.9 μg/dl). Moreover, mean serum levels of hs-CRP were similar in AS subjects with positive test for anti-CagA (18.4 ± 3.1 μg/dl) and in those who were negative for anti-CagA antibody (18.9 ± 4.1 μg/dl). Conclusion The results of this study showed that mean serum concentrations of hs-CRP in PU patients and in H. pylori-infected AS carriers were higher than in a healthy control group. Although H. pylori infection is associated with higher serum levels of hs-CRP, serum concentrations of this inflammatory marker were not affected by expression of bacterial CagA virulence factor.

Keywords

Helicobacter pylori Peptic ulcer Hs-CRP Anti-CagA 

Notes

Acknowledgments

The authors are grateful to Mohammad Ahmad-Beaygi and Mohammad Taghi Rezayati and authorities of the endoscopy unit of Rafsanjan Ali-ebn-Abitaleb Hospital for invaluable help.

References

  1. 1.
    Siavoshi F, Malekzadeh R, Daneshmand M, Ashktorab H. Helicobacter pylori endemic and gastric disease. Dig Dis Sci. 2005;50:2075–2080. doi: 10.1007/s10620-005-3010-1.CrossRefPubMedGoogle Scholar
  2. 2.
    International Agency for Research on Cancer Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, liver flukes and Helicobacter pylori: infection with Helicobacter pylori. IARC Monogr Eval Carcinog Risks Hum. 1994;61:177–240.Google Scholar
  3. 3.
    Jafarzadeh A, Rezayati MT, Nemati M. Specific serum immunoglobulin G to H. pylori and CagA in healthy children and adults (south-east of Iran). World J Gastroenterol. 2007;13(22):3117–3121.PubMedGoogle Scholar
  4. 4.
    Figueiredo C, Marchado JC, Yamaoka Y. Pathogenesis of Helicobacter pylori Infection. Helicobacter. 2005;10(1):14–20. doi: 10.1111/j.1523-5378.2005.00339.x.CrossRefPubMedGoogle Scholar
  5. 5.
    Lu H, Yamaoka Y, Graham DY. Helicobacter pylori virulence factors: facts and fantasies. Curr Opin Gastroenterol. 2005;21:653–659. doi: 10.1097/01.mog.0000181711.04529.d5.CrossRefPubMedGoogle Scholar
  6. 6.
    Kaklikkaya N, Cubukcu K, Aydin F, et al. Significance of CagA status and vacA subtypes of Helicobacter pylori in determining gastric histopathology: virulence markers of H. pylori and histopathology. J Gastroenterol Hepatol. 2006;21(6):1042–1047. doi: 10.1111/j.1440-1746.2006.04199.x.CrossRefPubMedGoogle Scholar
  7. 7.
    Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev. 2006;19(3):449–490. doi: 10.1128/CMR.00054-05.CrossRefPubMedGoogle Scholar
  8. 8.
    Jimenze F, Demaria JL, Ahumada C, et al. Seroprevalence of Helicobacter pylori anti-CagA antibodies and its relationship with epidemiologic factors in Santa Fe. Acta Gastroenterol Latinoam. 2004;34:16–20.Google Scholar
  9. 9.
    Singh SK, Suresh MV, Voleti B, Agrawal A. The connection between C-reactive protein and atherosclerosis. Ann Med. 2008;40(2):110–120. doi: 10.1080/07853890701749225.CrossRefPubMedGoogle Scholar
  10. 10.
    Wilson AM, Ryan MC, Boyle AJ. The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen. Int J Cardiol. 2006;106:291–297. doi: 10.1016/j.ijcard.2005.01.068.CrossRefPubMedGoogle Scholar
  11. 11.
    Jafarzadeh A, Esmaeeli-Nadimi A, Shariati M. High sensitivity C-reactive protein and immunoglobulin G against Chlamydia pneumoniae and chlamydial heat shock protein-60 in ischemic heart disease. Iran J Immunol. 2008;5(1):51–56.PubMedGoogle Scholar
  12. 12.
    Kanbay M, Gür G, Yücel M, Yilmaz U, Boyacioğlu S. Does eradication of Helicobacter pylori infection help normalize serum lipid and CRP levels? Dig Dis Sci. 2005;50(7):1228–1231. doi: 10.1007/s10620-005-2764-9.CrossRefPubMedGoogle Scholar
  13. 13.
    Vermeire S, Van Assche G, Rutgeerts P. C-reactive protein as a marker for inflammatory bowel disease. Inflamm Bowel Dis. 2004;10(5):661–665. doi: 10.1097/00054725-200409000-00026.CrossRefPubMedGoogle Scholar
  14. 14.
    Mehmet N, Refik M, Harputluoglu M, Ersoy Y, Aydin NE, Yildirim B. Serum and gastric fluid levels of cytokines and nitrates in gastric diseases infected with Helicobacter pylori. New Microbiol. 2004;27(2):139–148.PubMedGoogle Scholar
  15. 15.
    Ishida Y, Suzuki K, Taki K, Niwa T, Kurotsuchi S, Ando H, Iwase A, Nishio K, Wakai K, Ito Y, Hamajima N. Significant association between Helicobacter pylori infection and serum C-reactive protein. Int J Med Sci. 2008;5(4):224–229.Google Scholar
  16. 16.
    Lenzi C, Palazzuoli A, Giordano N, et al. H. pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease. World J Gastroenterol. 2006;12:7815–7820.PubMedGoogle Scholar
  17. 17.
    Nomura ANY, Pérez-Pérez GI, Lee J, Stemmermann G, Blaser MJ. Relation between Helicobacter pylori CagA Status and Risk of Peptic Ulcer Disease. Am J Epidemiol. 2002;155(11):1054–1059. doi: 10.1093/aje/155.11.1054.CrossRefPubMedGoogle Scholar
  18. 18.
    Nilsson C, Sillén A, Eriksson L, Strand ML, Enroth H. Correlation between Cag pathogenicity Island composition and Helicobacter pylori-associated gastroduodenal disease. Infect Immun. 2003;71:6573–6581. doi: 10.1128/IAI.71.11.6573-6581.2003.CrossRefPubMedGoogle Scholar
  19. 19.
    Jafarzadeh A, Salari M. Seroprevalence of anti-Helicobacter pylori and anti-CagA antibodies in peptic ulcer and healthy subjects in the city of Rafsanjan. J Res Med Sci. 2006;11:285–291.Google Scholar
  20. 20.
    Jafarzadeh A, Sajadi M. Evaluation of the serum Interleukin-18 levels in Helicobacter pylori-infected peptic ulcer patients and its association with bacterial CagA virulence factor. Iran J Immunol. 2006;3:15–22.Google Scholar
  21. 21.
    Wen S, Velin D, Felley CP, Du L, Michetti P, Pan-Hammarström Q. Expression of Helicobacter pylori virulence factors and associated expression profiles of inflammatory genes in the human gastric mucosa. Infect Immun. 2007;75(11):5118–5126. doi: 10.1128/IAI.00334-07.CrossRefPubMedGoogle Scholar
  22. 22.
    Kim JM, Kim JS, Jung HC, Song IS, Kim CY. Virulence factors of Helicobacter pylori in Korean isolates do not influence proinflammatory cytokine gene expression and apoptosis in human gastric epithelial cells, nor do these factors influence the clinical outcome. J Gastroenterol. 2000;35(12):898–906. doi: 10.1007/s005350070003.CrossRefPubMedGoogle Scholar
  23. 23.
    Audibert C, Janvier B, Grignon B, et al. Correlation between IL-8 induction, CagA status and vacA genotypes in 153 French Helicobacter pylori isolates. Res Microbiol. 2000;151(3):191–200. doi: 10.1016/S0923-2508(00)00139-X.CrossRefPubMedGoogle Scholar
  24. 24.
    Kranzer K, Söllner L, Aigner M, et al. Impact of Helicobacter pylori virulence factors and compounds on activation and maturation of human dendritic cells. Infect Immun. 2005;73(7):4180–4189. doi: 10.1128/IAI.73.7.4180-4189.2005.CrossRefPubMedGoogle Scholar
  25. 25.
    Basso D, Plebani M. H. pylori infection: bacterial virulence factors and cytokine gene polymorphisms as determinants of infection outcome. Crit Rev Clin Lab Sci. 2004;41:313–337. doi: 10.1080/10408360490472804.CrossRefPubMedGoogle Scholar
  26. 26.
    Azuma T. Helicobacter pylori CagA protein variation associated with gastric cancer in Asia. J Gastroenterol. 2004;39(2):97–103. doi: 10.1007/s00535-003-1279-4.CrossRefPubMedGoogle Scholar
  27. 27.
    Miehlke S, Kibler K, Kim JG, et al. Allelic variation in the CagA gene of Helicobacter pylori obtained from Korea compared to the United States. Am J Gastroenterol. 1996;91(7):1322–1325.PubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.Department of Immunology, Medical SchoolRafsanjan University of Medical Sciences and Health ServicesRafsanjanIran

Personalised recommendations