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Опухолеассоциированная тканевая эозинофилия определяется как эозинофильная инфильтрация стромы опухоли. Эта реакция, как полагают, играет важную роль в канцерогенезе. Считается, что эозинофилы обладают противоопухолевой активностью за счет высвобождения цитотоксических белков. Цель исследования - изучение молекулярно-генетических механизмов формирования опухолеассоциированной тканевой эозинофилии у больных раком желудка и толстой кишки. Методика. Материалом исследования служили образцы опухолевой ткани пациентов с диагнозом рак желудка или толстой кишки . Подсчитывали количество эозинофилов, инфильтрирующих опухолевую ткань, а также оценивали экспрессию эотаксина-1 (ключевого фактора хемотаксиса эозинофилов) и его рецептора CCR3 в опухолевой ткани методом иммуногистохимии. Было изучено распределение полиморфных вариантов генов CCL11 (А384G) , CCR3 (T51С) , IL5 (С703Т) и IL5R (G80А) . Геномную ДНК выделяли из образцов опухолевой ткани. Генотипирование образцов ДНК по полиморфизмам генов осуществляли путем ПДРФ-анализа продуктов ПЦР-амплификации специфических участков генома с последующей визуализацией в ультрафиолетовом свете. Результаты. Показана более высокая экспрессия эотаксина-1 и CCR3 в ткани опухоли при раке желудка и толстой кишки, ассоциированном с эозинофилией. Установлена ассоциация эозинофильной инфильтрации опухолевой ткани с носительством генотипа СС и аллеля С полиморфизма T51С гена CCR3 и генотипа СС и аллеля С полиморфизма С703Т гена IL5 . Заключение. Формирование опухолеассоциированной тканевой эозинофилии при раке желудка и толстой кишки опосредованно действием эотаксина-1 и его рецептора. Результаты молекулярно-генетического исследования указывают на генетически детерминированный характер эозинофилии при раке желудка и толстой кишки., Tumor-associated tissue eosinophilia is defined as eosinophilic stromal infiltration of a tumor. Tumor-associated tissue eosinophilia is believed to play a significant role in carcinogenesis. It is believed that eosinophils have antitumor activity due to the release of cytotoxic proteins. The aim of this study was to investigate the molecular-genetic mechanisms of formation of tumor-associated tissue eosinophilia in patients with gastric cancer and colon cancer. Methods. Tumor tissue samples from patients with gastric cancer and colon cancer were reviewed. We counted the number of infiltrating eosinophils in neoplastic lesion tissue and we evaluated the expression of eotaxin-1 (a key factor of chemotaxis of eosinophils) and its receptor CCR3 in tumor tissue by immunohistochemical staining. The distribution of polymorphic variants of genes CCL11 (А384G), CCR3 (Т51С), IL5 (С703Т) and of the IL5R (G80А) was studied. DNA was isolated from tumor tissue samples. Genotyping of polymorphisms was carried out by polymerase chain reaction (PCR), followed by digestion with the appropriate restriction enzyme (PCR-RFLP) and agarose-gel electrophoresis. Results. It is shown that higher expression eotaxin-1 and CCR3 is determined in the tumor tissue of gastric cancer and colon cancer associated with eosinophilia. It is established that eosinophilic infiltration of the tumor tissue is associated with the carriers of CC genotype and C allele of the gene CCR3 (Т51С) and CC genotype and C allele of gene IL5 (С703Т) . Conclusion. The formation of tumor-associated tissue eosinophilia in gastric cancer and colon cancer is mediated through the action eotaxin-1 and its receptor. The results of molecular-genetic studies indicate a genetically determined character of eosinophilia in gastric cancer and colon cancer., №4 (2017)

Some issues in etiology and pathogenesis of psoriasis are poorly studied. Therefore, a search for new potential markers is actual for diagnostics of psoriasis in less clear cases. In this study, an attempt was undertaken to evaluate contribution of some chemokines and appropriate receptors into pathogenesis of psoriasis. The main group consisted of the patients with psoriatic arthritis (n = 20) and psoriasis vulgaris (n = 9). A group of comparison consisted of patients with sclerodermia (n = 4), and a control group was represented by healthy persons (n = 9). The specimens were taken from visually normal and affected skin areas from psoriatic patients obtained by punch biopsy. Expression of the following chemokines was performed: CCL3/MIP-1α, CCL4/MIP-1β, CCL5/RANTES, CCL11/eotaxin, CCL24/eotaxin-2, CXCL8/IL-8 and their receptors (CCR1, CCR3, CCR5, CXCR1, CXCR2). In cases with PASI values < 10, an increased expression of the following genes was revealed for CCL11/eotaxin (p = 0.03), CXCR1 (р = 0.008), CXCR2 (р = 0.0006) in virtually intact skin and affected skin areas, as well as increased gene expression of CCL24/eotaxin 2 (p = 0.009), CCL5/RANTES (p = 0.05) in visually normal skin.With PASI values of 10 to 20, an increased gene expression was found for CCL11/eotaxin (p = 0.005), CCL24/eotaxin 2 (p = 0.02), CCL5/RANTES (p = 0.01), CXCR1 (р = 0.0009), CXCR2 (р = 0.002) in skin biopsies from visually healthy and affected skin, as well as increased expression CXCL8 (IL-8) (p = 0.005) in visually normal skin. In cases with PASI > 20, an increased expression of CCL11/eotaxin (p = 0.001), CCL24/eotaxin 2 (p = 0.001), CCL3/MIP-1α (р = 0.02), CXCR1 (p = 0.0001), CXCR2 (p = 0.001) was detected in visually healthy skin samples and affected skin of the patients, as well as higher expression of CCL4/MIP-1β (р = 0.03) in affected skin areas. A reverse correlation was revealed between expression of chemokines, i.e., CCL24/eotaxin 2 (r = –0,94, p = 0.005), CCL3/MIP-1α (r = –0,94, p = 0.005), CCL4/MIP-1β (r = –0,85, p = 0.03) and their receptors: ССR5 (r = –0,79, p = 0.005) and CXCR2 (r = –0,94, p = 0.005) in visually normal skin of the patients with psoriasis and PASI values < 10.A direct correlation was found between expression of mRNAs for CCL11/eotaxin (r = 0.69, p = 0.04) in visually healthy skin from psoriatic patients, and CCR5 (r = 0.82, p = 0.006) in affected skin of the patients with psoriasis and PASI values of 10 to 20. In the group of patients with PASI values over 20, no correlations were detectable. These data allow us of concluding aboutan important contribution of chemokine system to pathogenesis of psoriasis. (Med. Immunol., vol. 10, N 4-5, pp 337-346).