The content of apoptosis mediators in children with anemia of inflammation acquired on the background of acute bacterial diseases of respiratory organs
DOI:
https://doi.org/10.14739/2310-1237.2019.2.177112Keywords:
infants, respiratory tract diseases, caspase-7, caspase-9, anemia of inflammationAbstract
Aim. Determine the activity of apoptosis processes in young children with anemia of inflammation acquired on the background of acute bacterial diseases of respiratory organs.
Material and methods. The content of caspase-7 and caspase-9 was identified in blood serum of 87 kids by the method of immunoenzyme assay. Main group included 57 kids with acute bacterial diseases of the respiratory tract (38 patients had acute bacterial bronchitis, 19 - pneumonia). The main group was divided into two subgroups. The first subgroup included 27 children with developed anemia of inflammation acquired on the background of acute bacterial disease of the respiratory tract. Second subgroup - 30 children with acute bacterial diseases of the respiratory tract without anemia. Experimental group - 10 children with iron deficiency anemia without symptoms of inflammatory diseases of the respiratory system. The control group was represented by 20 conditionally healthy children.
Results. The presence of pneumonia in children was accompanied by the highest numbers of caspase-9 (14.8 ± 1.8 ng/ml), which was almost 3 times higher than the control group (5.82 ± 0.58 ng/ml). The levels of the studied enzyme were 1.6 times lower in patients with bacterial bronchitis (8.34 ± 0.90 ng/ml), which was significantly higher (P < 0.05) than in the control group. The content of caspase-7 in the experimental group and the 2nd subgroup of the main group did not differ from the control group (P > 0.05) (0.38 ± 0.03 ng/ml and 0.32 ± 0.02 ng/ml), and children of the 1st subgroup (0.27 ± 0.02 ng/ml) showed its significant decrease.
Conclusions. Anemia of inflammation in children with acute bacterial diseases of respiratory organs is accompanied by the activation of apoptosis, which, obviously, is inefficient due to the nature of the active necrotic processes acquired on the background of acute inflammation.
References
Blokhin, D. Yu. (2003) Programmirovannaya gibel' kletok: put' ot indukcii do ispolneniya [Programmed cell death: from induction to performance]. Patogenez, 2, 25–33. [in Russian].
van Delft, M. F., Smith, D. P., Lahoud, M. H., Huang, D. C., & Adams, J. M. (2009). Apoptosis and non-inflammatory phagocytosis can be induced by mitochondrial damage without caspases. Cell Death & Differentiation, 17(5), 821–832. doi: 10.1038/cdd.2009.166
Novikov, V. V., Baryshnikov, A. Yu., & Karaulov, A. V. (2007). Rastvorimye formy membrannykh antigenov kletok immunnoj sistemy [Soluble forms of membrane antigens of cells of the immune system]. Immunologiya, 4, 249–253. [in Russian].
Laskay, T., van Zandbergen, G., & Solbach, W. (2008). Neutrophil granulocytes as host cells and transport vehicles for intracellular pathogens: Apoptosis as infection-promoting factor. Immunobiology, 213(3–4), 183–191. doi: 10.1016/j.imbio.2007.11.010
Bulgakova, V. A. (2009) The clinical significance of studying markers of activation and apoptosis of immunocompetent cells in children with atopic bronchial asthma. Pediatriya, 87(2), 12–18.
Pavlyshyn, H. A., Sarapuk, I. M., & Sarapuk, H. S. (2013). Osoblyvosti apoptozu pry riznykh patolohichnykh protsesakh [Peculiarities of apoptosis in various pathological processes]. Neonatolohiia, khirurhiia ta perynatalna medytsyna, 4, 118–122.
Vyaltseva, Yu. V. (2007). Rol apoptozu pry іnfektsіinykh khvorobakh [Role of apoptosis at infectious diseases]. Infektsiini khvoroby, 1, 57–63. [in Ukrainian].
Kondrashova, N. M., Plekhova, N. G., Zavorueva, D. V., Somova, L. M., Geltser, B. I., & Kostyushko, A. V. (2010) Kletochnye faktory mestnoj zashhity pri vnebol'nichnoj pnevmonii [Cellular factors of local protection under community acquired pneumonia]. Cytology, 57(7), 588. [in Russian].
McIlwain, D., Berger, T., & Mak, T. (2013). Caspase Functions in Cell Death and Disease. Cold Spring Harbor Perspectives in Biology, 5(4), a008656. doi: 10.1101/cshperspect.a008656
Guicciardi, M., & Gores, G. (2009). Life and death by death receptors. The FASEB Journal, 23(6), 1625–1637. doi: 10.1096/fj.08-111005
Brentnall, M., Rodriguez-Menocal, L., De Guevara, R., Cepero, E., & Boise, L. (2013). Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis. BMC Cell Biology, 14(1), 32. doi: 10.1186/1471-2121-14-32
Rakba, N., Loyer, P., Gilot, D., Delcros, J. G., Glaise, D., Baret, P., et al. (2000). Antiproliferative and apoptotic effects of O-Trensox, a new synthetic iron chelator, on differentiated human hepatoma cell lines. Carcinogenesis, 21(5), 943–951. doi: 10.1093/carcin/21.5.943
Simonart, T., Heenen, M., Degraef, C., Andrei, G., Mosselmans, R., Hermans, P., et al. (2000). Iron Chelators Inhibit the Growth and Induce the Apoptosis of Kaposi's Sarcoma Cells and of their Putative Endothelial Precursors. Journal of Investigative Dermatology, 115(5), 893–900. doi: 10.1046/j.1523-1747.2000.00119.x
Kovář, J., Kühn, L., Richardson, V., Seiser, C., Kriegerbecková, K., & Musílková, J. (1997). The inability of cells to grow in low iron correlates with increasing activity of their iron regulatory protein (IRP). In Vitro Cellular & Developmental Biology Animal, 33(8), 633–639. doi: 10.1007/s11626-997-0114-2
Koc, M., Nad'ová, Z., & Kovář, J. (2006). Sensitivity of cells to apoptosis induced by iron deprivation can be reversibly changed by iron availability. Cell Proliferation, 39(6), 551–561. doi: 10.1111/j.1365-2184.2006.00411.x
Ryazantseva, N. V., Zhavoronok, T. V., Stepovaya, E. A., Starikov, Y. V., Ageeva, T. S., Mitasov, V. Y., & Sokolovich, E. G. (2010) Okislitel'nyj stress v modulyacii apoptoza nejtrofilov v patogeneze ostrykh vospalitel'nykh zabolevanij [Oxidative stress in neutrophil cell death modulation during pathogenesis of acute inflammatory diseases]. Byulleten' Sibirskogo otdeleniya Rossijskoj akademii medicinskikh nauk,
(5), 58–63. [in Russian].
Oved, K, Cohen, A, Boico, O., Navon, R., Friedman, T., Etshtein, L., et al. (2015) A Novel Host-Proteome Signature for istinguishing between Acute Bacterial and Viral Infections. PLoS One, 10(3), e0120012. doi: 10.1371/journal.pone.0120012
Pavlyshyn, H. A., & Sarapuk, I. M. (2013) Pokaznyky efektyvnostі obektyvіzatsіi otsinky klіnіchnoho perebіhu nehospіtalnoi pnevmonіi u dіtei rannoho vіku [Parameters of effectiveness of objectification of evaluation of clinical course of hospitalized pneumonia in children of early age]. Visnyk naukovykh doslidzhen, 2, 62–66. [in Ukrainian].
Hallett, J. M., Leitch, A. E., Riley, N. A., Duffin, R., Haslett, C., & Rossi, A. G. (2008). Novel pharmacological strategies for driving inflammatory cell apoptosis and enhancing the resolution of inflammation. Trends in Pharmacological Sciences, 29(5), 250–257. doi: 10.1016/j.tips.2008.03.002
Downloads
How to Cite
Issue
Section
License
Authors who publish with this journal agree to the following terms:- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (SeeThe Effect of Open Access).