Helicobacter pylori (H. pylori) can stimulate immune responses and lead to the release of proinflammatory factors and antimicrobial peptides as LL-37, mannose-binding lectin (MBL) and M –ficolin. The aim of this study was to determine the level of changes in serum levels of the three mentioned factors in people with gastritis and their association with the presence or absence of H. Pylori. Subjects were divided into two groups of 35 gastritis individuals with H. pylori and 25 individuals without H. pylori. Biopsy and blood samples were collected from each subject. H. pylori positivity was investigated regarding the serum level by enzyme-linked immunosorbent assay (ELISA) kit and its presence in the tissue was examined by histopathology observations and rapid urease test (RUT). LL-37, MBL and M-ficolin serum levels indicated that 58% of the subjects were infected with H. pylori. Subjects with MBL levels lower than 500 ng/mL in the sera were significantly infected with H. pylori, and subjects with MBL levels higher than 1000 ng/ml often did not have H. pylori infection. The level of LL-37 was increased, while M-ficolin showed no significant change in the presence of H. pylori. Findings indicated that lower levels of MBL and higher levels of LL-37 might be involved in H. pylori infection, while M-ficolin seems to be less effective in the infection.
Munthe-Fog L, Hummelshoj T, Honoré C, Moller ME, Skjoedt MO, Palsgaard I, et al. Variation in FCN1 affects biosynthesis of ficolin-1 and is associated with outcome of systemic inflammation. Genes & Immunity. 2012;13(7):515–22.
2.
Craig PM, Territo MC, Karnes WE, Walsh JH. Helicobacter pylori secretes a chemotactic factor for monocytes and neutrophils. Gut. 1992;33(8):1020–3.
3.
Graham DY, Osato MS, Olson CA, Zhang J, Figura N. Effect of H. pylori Infection and CagA Status on Leukocyte Counts and Liver Function Tests: Extra‐Gastric Manifestations of H. pylori Infection. Helicobacter. 1998;3(3):174–8.
4.
Liu Y, Endo Y, Iwaki D, Nakata M, Matsushita M, Wada I, et al. Human M-Ficolin Is a Secretory Protein That Activates the Lectin Complement Pathway. The Journal of Immunology. 2005;175(5):3150–6.
5.
Miranda KA, Vasconcelos LRS, Coelho LCBB, Lima Filho JL, Cavalcanti MSM, Moura P. High levels of serum mannose-binding lectin are associated with the severity of clinical signs of leptospirosis. Brazilian Journal of Medical and Biological Research. 2009;42(4):353–7.
Strapagiel D, Grebowska A, Rozalska B. Natural mannose-binding lectin (MBL) down-regu-lates phagocytosis of Helicobacter pylori. Polish J Microbiol. 2006;55:95–101.
8.
BP-D MC, Hirmo S, Rudnicka W, Utt M, Wadström T. Helicobacter pylori – interactions with phagocytes. Helicobacter. 1998;
9.
Bak-Romaniszyn L, Swierzko A, Szemraj J. Mannan-binding lectin (MBL) in duodenal ulcer and gastritis. Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskieg. 2009;26:412–5.
10.
Müller S, Schaffer T, Flogerzi B, Seibold-Schmid B, Schnider J, Takahashi K, et al. Mannan-binding lectin deficiency results in unusual antibody production and excessive experimental colitis in response to mannose-expressing mild gut pathogens. Gut. 2010;59(11):1493–500.
11.
Leszczyńska K, Namiot A, Fein DE, Wen Q, Namiot Z, Savage PB, et al. Bactericidal activities of the cationic steroid CSA-13 and the cathelicidin peptide LL-37 against Helicobacter pylori in simulated gastric juice. BMC Microbiology. 2009;9(1).
12.
MISIEWICZ JJ. The Sydney System: A new classification of gastritis. Introduction. Journal of Gastroenterology and Hepatology. 1991;6(3):207–8.
13.
Ammitzbøll CG, Kjær TR, Steffensen R, Stengaard-Pedersen K, Nielsen HJ, Thiel S, et al. Non-Synonymous Polymorphisms in the FCN1 Gene Determine Ligand-Binding Ability and Serum Levels of M-Ficolin. PLoS ONE. 7(11):e50585.
14.
Rugge M, Pennelli G, Pilozzi E, Fassan M, Ingravallo G, Russo VM, et al. Gastritis: The histology report. Digestive and Liver Disease. 2011;43:S373–84.
15.
Endo Y, Matsushita M, Fujita T. The role of ficolins in the lectin pathway of innate immunity. The International Journal of Biochemistry & Cell Biology. 2011;43(5):705–12.
16.
Ricklin D, Lambris JD. Complement in Immune and Inflammatory Disorders: Therapeutic Interventions. The Journal of Immunology. 2013;190(8):3839–47.
17.
Matsushita M. Ficolins: Complement-Activating Lectins Involved in Innate Immunity. Journal of Innate Immunity. 2010;2(1):24–32.
18.
Bucki R, Leszczyńska K, Namiot A, Sokołowski W. Cathelicidin LL-37: A Multitask Antimicrobial Peptide. Archivum Immunologiae et Therapiae Experimentalis. 2010;58(1):15–25.
19.
Reinholz M, Ruzicka T, Schauber J. Cathelicidin LL-37: An Antimicrobial Peptide with a Role in Inflammatory Skin Disease. Annals of Dermatology. 2012;24(2):126.
20.
Kościuczuk EM, Lisowski P, Jarczak J, Strzałkowska N, Jóźwik A, Horbańczuk J, et al. Cathelicidins: family of antimicrobial peptides. A review. Molecular Biology Reports. 2012;39(12):10957–70.
21.
Guarner J, Kalach N, Elitsur Y, Koletzko S. Helicobacter pylori diagnostic tests in children: review of the literature from 1999 to 2009. European Journal of Pediatrics. 2010;169(1):15–25.
22.
Gaddy JA, Radin JN, Loh JT, Zhang F, Washington MK, Peek RM, et al. High Dietary Salt Intake Exacerbates Helicobacter pylori-Induced Gastric Carcinogenesis. Infection and Immunity. 2013;81(6):2258–67.
23.
Schoep TD, Fulurija A, Good F, Lu W, Himbeck RP, Schwan C, et al. Surface Properties of Helicobacter pylori Urease Complex Are Essential for Persistence. PLoS ONE. 5(11):e15042.
24.
Masrour-Roudsari J, Ebrahimpour S. Casual role of infectious agents in cancer: An overview. Caspian J Int Med. 2017;8:153–8.
25.
Nejati S, Karkhah A, Darvish H, Validi M, Ebrahimpour S, Nouri HR. Influence of Helicobacter pylori virulence factors CagA and VacA on pathogenesis of gastrointestinal disorders. Microbial Pathogenesis. 2018;117:43–8.
26.
Salama NR, Hartung ML, Müller A. Life in the human stomach: persistence strategies of the bacterial pathogen Helicobacter pylori. Nature Reviews Microbiology. 2013;11(6):385–99.
The statements, opinions and data contained in the journal are solely those of the individual authors and contributors and not of the publisher and the editor(s). We stay neutral with regard to jurisdictional claims in published maps and institutional affiliations.