Serum levels of iron parameters and IL-17 in children with Helicobacter pylori infection compared to healthy group

Document Type : Short Communication

Authors

1 Department of Microbiology, Faculty of Basic Sciencs, Ayatollah Amoli Branch, Islamic Azad University, Amol, Iran

2 Department of Microbiology, Faculty of Paramedical Sciences, Jondi Shapour University, Ahvaz, Iran

Abstract

Helicobacter pylori is related to iron deficiency anemia (IDA) and inflammatory responses causing gastric and duodenal ulcer and carcinoma. Moreover, it leads to deficiency of factors associated with iron adsorption and transfer. In the present study, we recruited 100 children (50 infected with H. pylori and 50 controls) aged 3-14 years old (40% male and 60% female) to evaluate the effect of H. pylori on anemia and some of its related factors (i.e., total iron binding capacity [TIBC], ferritin, and transferrin) and also the amount of IL-17 expression. For the assessment of H. pylori, Euroimmune (Germany) kit was used for the ELISA test according to the instructions of manufacturer. Furthermore, for the measurement of IL-17 level, ELISA test (IBL commercial specific kit, Germany) was employed. The mean iron levels in the control and infected groups were 81.5 mg/dl and 43 mg/dl, respectively, which showed a significant difference between the two groups (P=0.007). The mean levels of transferrin in the control and infected children were 291 mg/dl and 249 mg/dl respectively, demonstrating a significant difference (P=0.008). Moreover, the ferritin levels were 64.5 ng/dl and 14 ng/dl in the control and infected groups, respectively (P=0.001). The TIBC levels were 329 mg/dl and 301 mg/dl, respectively (P=0.86). The mean levels of IL-17 in the healthy and infected children were 3.93±0.93 pg/ml and 8.887±1.46 pg/ml, respectively (P=0.002). Our findings revealed that H. pylori can play a role in anemia and induction of inflammatory responses through reducing iron-related parameters and significantly enhancing IL-17 level among the infected children compared to the healthy group.

Keywords

Main Subjects


Article Title [French]

Comparaison des paramètres du bilan martial et du taux d’IL-17 entre les sérums d’enfants infectés et non-infectés par l’Helicobacterpylori

Abstract [French]

L’Helicobacter pyloriest responsable d’anémies ferriprives et de réponses inflammatoires à l’origine d’ulcères gastriques ou duodénales et de carcinomes. De plus, cette infection peut également être associée à des déficiences dans l’absorption et le transfert ferriques. Dans cette étude, 100 enfants (50 infectés et 50 non-infectés par l’ H. pylori) âgés de 3 à 14 ans ont été sélectionnés (40% de garçons pour 60%de filles) afin d’évaluer l’effet de l’H. pylorisur l’anémie et ses facteurs associés (total iron binding capacity [TIBC], ferritine et transferrine) ainsi que sur le taux d’expression de l’IL-17. La présence d’H. pylori a été évaluée par le kit ELISA Euroimmune (Allemagne) selon les instructions du fabricant. Un test ELISA commercial (IBL commercial specific kit, Allemagne) a été employé pour l’évaluation du taux d’IL-17. Le niveau moyen de fer sérique variait de façon significative entre les deux groupes témoin et infecté (P=0,007) et tombait de 81.5 mg/dl à 43 mg/dl. Le niveau moyen de transferrine des groupes témoins et infectés s’élevait respectivement à 291 mg/dl et 249 mg/dl et montrait une différence significative (P=0.008). De plus, le taux de ferritine diminuait également dans le groupe infecté (14 ng/dl) comparé au groupe témoin (64.5 ng/dl). Le taux de TIBC des groupes témoin et infecté était respectivement de 329 mg/dl et 301 mg/dl (P=0.86). Une augmentation significative (P=0.002) du taux moyen d’IL-17 a été observée dans le groupe infecté (8.887±1.46 pg/ml) comparé au groupe témoin (3.93±0.93 pg/ml). Nos résulats ont donc révélé que l’ H. pylori peut être à l’origine d’anémie et de réponses inflammatoires en réduisant paramètres ferriques et en augmentant de façon significative le taux d’expression d’IL-17 chez les enfants infectés.

Keywords [French]

  • Helicobacter pylori
  • Anémie
  • inflammation
  • IL-17
Akcam, M., Aslan, N., 2015. Helicobacter pylori Related Health Problems in Children. Iran J Pub Health 44, 877.
Amedei, A., Munari, F., Della Bella, C., Niccolai, E., Benagiano, M., Bencini, L., 2014. Helicobacter pylori secreted peptidyl prolyl cis, trans-isomerase drives Th17 inflammation in gastric adenocarcinoma. Int Emerg Med 9, 303-309.
Arnason, J.E., Campigotto, F., Neuberg, D., Bussel, J.B., 2012. Abnormalities in IgA and IgM are associated with treatment-resistant ITP. Blood 119, 5016-5020.
Bagheri, N., Rahimian, G., Salimzadeh, L., Azadegan, F., Rafieian-Kopaei, M., Taghikhani, A., et al., 2013. Association of the virulence factors of Helicobacter pylori and gastric mucosal interleukin-17/23 mRNA expression in dyspeptic patients. EXCLI J 12, 5-14.
Baker, R.D., Greer, F.R., 2010. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0–3 years of age). Pediatrics 126, 1040-1050.
Bazmamoun, H., Razavi, Z., Esfahani, H., Arefian, M.S., 2014. Evaluation of Iron deficiency anemia and BMI in children suffering from Helicobacter pylori infection. Iran J Ped Hematol Oncol 4, 167-171.
Beydoun, M.A., Dore, G.A., Canas, J.A., Beydoun, H.A., Zonderman, A.B., 2015. Helicobacter pylori Seropositivity’s Association with Markers of Iron, 1-Carbon Metabolism, and Antioxidant Status among US Adults: A Structural Equations Modeling Approach. PloS one 10, e0121390.
Bhuiyan, T.R., Islam, M.M., Uddin, T., Chowdhury, M.I., Janzon, A., Adamsson, J., et al., 2014. Th1 and Th17 responses to Helicobacter pylori in Bangladeshi infants, children and adults. PLoS One 9, e93943.
Carbo, A., Olivares-Villagómez, D., Hontecillas, R., Bassaganya-Riera, J., Chaturvedi, R., Piazuelo, M.B., et al., 2014. Systems modeling of the role of interleukin-21 in the maintenance of effector CD4+ T cell responses during chronic Helicobacter pylori infection. MBio 5, e01243-01214.
Chan, J.C.W., Liu, H.S.U., Kho, B.C.S., Sim, J.P.U., Lau, T.K.H., Luk, Y.W., 2006. Pernicious anemia in Chinese: a study of 181 patients in a Hong Kong hospital. Medicine 85, 129-138.
Darvishi, M., Ziari, K., Mohebi, H., Alizadeh, K., 2015. Association between Iron Deficiency Anemia and Helicobacter Pylori Infection among Children Under Six Years in Iran. Acta Med Iran 53, 220-224.
El-Omar, E.M., 2013. Iron deficiency and Helicobacter pylori–induced gastric cancer: too little, too bad. J Clin Invest 123, 113.
Gil, J.H., Seo, J.W., Cho, M.-S., Ahn, J.-H., Sung, H.Y., 2014. Role of Treg and TH17 cells of the gastric mucosa in children with Helicobacter pylori gastritis. Journal of pediatric gastroenterology and nutrition 58, 245-251.
Horvath Jr, D.J., Washington, M.K., Cope, V.A., Algood, H.M.S., 2012. IL-23 contributes to control of chronic Helicobacter pylori infection and the development of T helper responses in a mouse model. Front  Immunol 3.
Hu, Q., Akatsuka, S., Yamashita, Y., Ohara, H., Nagai, H., Okazaki, Y., et al., 2010. Homozygous deletion of CDKN2A/2B is a hallmark of iron-induced high-grade rat mesothelioma. Labo Invest 90, 360-373.
Janulczyk, R., Pallon, J., Björck, L., 1999. Identification and characterization of a Streptococcus pyogenes ABC transporter with multiple specificity for metal cations. Molecul Microbiology 34, 596-606.
Lopez, A., Cacoub, P., Macdougall, I.C., Peyrin-Biroulet, L., 2015. Iron deficiency anaemia. The Lancet.
Miernyk, K., Bruden, D., Zanis, C., McMahon, B., Sacco, F., Hennessy, T., et al., 2013. The effect of Helicobacter pylori infection on iron stores and iron deficiency in urban Alaska Native adults. Helicobacter 18, 222-228.
Milman, N., Rosenstock, S., Andersen, L., Jørgensen, T., Bonnevie, O., 1998. Serum ferritin, hemoglobin, and Helicobacter pylori infection: a seroepidemiologic survey comprising 2794 Danish adults. Gastroenterology 115, 268-274.
Monzón, H., Forné, M., Esteve, M., Rosinach, M., Loras, C., Espinós, J.C., et al., 2013. Helicobacter pylori infection as a cause of iron deficiency anaemia of unknown origin. World J Gastroenterol 19, 4166-4171.
Mubarak, N., Gasim, G.I., Khalafalla, K.E., Ali, N.I., Adam, I., 2014. Helicobacter pylori, anemia, iron deficiency and thrombocytopenia among pregnant women at Khartoum, Sudan. Transactions of The Royal Society of Tropical Medicine and Hygiene 108, 380-384.
Noto, J.M., Gaddy, J.A., Lee, J.Y., Piazuelo, M.B., Friedman, D.B., Colvin, D.C., et al., 2013. Iron deficiency accelerates Helicobacter pylori–induced carcinogenesis in rodents and humans. J Clin Invest 123, 479-492.
Pandya, H.B., Patel, J.S., Agravat, H.H., 2014. Non-Invasive Diagnosis of Helicobacter pylori: Evaluation of Two Enzyme Immunoassays, Testing Serum IgG and IgA Response in the Anand District of Central Gujarat, India. J Clin Diagnos Research: JCDR 8, DC12.
Plummer, M., Franceschi, S., Vignat, J., Forman, D., de Martel, C., 2015. Global burden of gastric cancer attributable to Helicobacter pylori. Int J Cancer 136, 487-490.
Queiroz, D., Harris, P.R., Sanderson, I.R., Windle, H.J., Walker, M.M., Rocha, A., et al., 2013. Iron status and Helicobacter pylori infection in symptomatic children: an international multi-centered study. PLoS One 8, e68833.
Rahman, A.S., Sarker, S.A., Ahmed, T., Islam, R., Wahed, M.A., Sack, D.A., 2013. Relationship of intestinal parasites, H. pylori infection with anemia or iron status among school age children in rural Bangladesh. J Gastroenterol Hepatol Res 2.
Sapmaz, F., Başyiğit, S., Kalkan, İ.H., Kısa, Ü., Kavak, E.E., Güliter, S., 2016. The impact of Helicobacter pylori eradication on serum hepcidin-25 level and iron parameters in patients with iron deficiency anemia. Wiener klinische Wochenschrift, 1-6.
Sato, Y., Yoneyama, O., Azumaya, M., Takeuchi, M., Sasaki, S.y., Yokoyama, J., et al., 2015. The Relationship Between Iron Deficiency in Patients with Helicobacter Pylori‐Infected Nodular Gastritis and the Serum Prohepcidin Level. Helicobacter 20, 11-18.
Shi, Y., Liu, X.-F., Zhuang, Y., Zhang, J.-Y., Liu, T., Yin, Z., et al., 2010. Helicobacter pylori-induced Th17 responses modulate Th1 cell responses, benefit bacterial growth, and contribute to pathology in mice. J Immunol 184, 5121-5129.
Turkina, M.V., Olofsson, A., Magnusson, K.-E., Arnqvist, A., Vikström, E., 2015. Helicobacter pylori vesicles
carrying CagA localize in the vicinity of cell–cell contacts and induce histone H1 binding to ATP in epithelial cells. Microbiol Letters 362, fnv076.
Xie, C., Xu, L.-Y., Li, W., Yang, Z., Lu, N.-H., 2014. Helicobacter pylori infection in Mongolian gerbils does not initiate hematological diseases. World J Gstroenterol 20, 12308.
Yamanouchi, J., Azuma, T., Yakushijin, Y., Hato, T., Yasukawa, M., 2014. Dramatic and prompt efficacy of Helicobacter pylori eradication in the treatment of severe refractory iron deficiency anemia in adults.  Annals Hematol 93, 1779.
Zhuang, Y., Shi, Y., Liu, X.-F., Zhang, J.-Y., Liu, T., Fan, X., et al., 2011. Helicobacter pylori-infected macrophages induce Th17 cell differentiation. Immunobiology 216, 200-207.