IMMUNOLOGICAL STUDY IN CHILDREN WITH RENAL DISEASES LIVING IN REGIONS WITH UNFAVORABLE ENVIRONMENTAL CONDITIONS

Abstract. Seventy-nine children participated in the study including 33 children living in region with developed cement industry (12 with glomerulonephritis, and 21 with obstructive pyelonephritis). A group of comparison consisted of 46 children living in Moscow, including 17 subjects with glomerulon...

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Autores principales: M. V. Kudin, A. V. Skripkin
Formato: article
Lenguaje:RU
Publicado: SPb RAACI 2014
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Acceso en línea:https://doaj.org/article/386f3f33806d46918c4f891ccc133b34
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Sumario:Abstract. Seventy-nine children participated in the study including 33 children living in region with developed cement industry (12 with glomerulonephritis, and 21 with obstructive pyelonephritis). A group of comparison consisted of 46 children living in Moscow, including 17 subjects with glomerulonephritis and 29 children with obstructive pyelonephritis, and control group of 26 healthy children. ELISA method was used to perform immunological studies. The levels of sCD4, IL-2, IL-6, IL-10, sICAM-1, TNFα were evaluated in blood sera. The data obtained show significant increase of TNFα levels and decreased IL-6 levels (p < 0,05) in children with nephropathy living in regions with unfavorable environmental conditions as compared with control group. A seven-fold increase in TNFα levels, along with more than twofold decrease in IL-6 was revealed among children with obstructive pyelonephritis, as compared with control group (p < 0,05). In children with glomerulonephritis and obstructive pyelonephritis, a distinct increase of sCD4 , as well as decreased IL-2 level (p < 0,05) was registered, as compared with control group. Meanwhile, IL-10 contents in this group of patients was 22,4 times less than the in controls (p < 0,05). In the main group, no enhanced sICAM synthesis was found, both in children with glomerulonephritis and pyelonephritis. In children affected by adverse environmental pathogens, we have shown a prevailing immune inflammation due to hyperproduction of TNFα, IL-6, and activation of sCD4 helpers. Adverse environmental effects inhibit cytokine synthesis, thus reducing production of both pro- and anti-inflammatory cytokines.