Academic literature on the topic 'Beta-defensine'

Background and Objectives: The morphopathogenesis of adhesions is a complex process, characterized by the accumulation of an extracellular matrix, inflammation and hypoxia. The regulatory role between morphopathogenic factors in adhesions has not yet been defined. The aim was to investigate the appearance of transforming growth factor beta (TGFβ), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF-2), fibroblast growth factor receptor 1 (FGFR1), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP 9.5), chromogranin A (CgA), interleukin-1 alpha (IL-1α), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-8 (IL-8), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), human beta defensine-2 (HBD-2), matrix metaloproteinase-2 (MMP-2) and matrix metaloproteinase-2 tissue inhibitor (TIMP-2) in intraabdominal adhesions. Materials and Methods: The study material was obtained from 49 patients under one year of age with total or partial bowel obstruction. All factors were detected using immunohistochemistry methods and their relative distribution was evaluated by means of the semiquantitative counting method. Results: Intraabdominal adhesions are characterized by increased TGFβ, FGFR1, VEGF and decreased FGF-2, HGF, PGP 9.5, IL-1, IL-4, IL-8, TIMP-2 findings. The most significant changes observed were the remodulation of the extracellular matrix, promotion of neoangiogenesis and the maintenance of a prolonged inflammation. Conclusions: The increase in TGFβ, relative to the decrease of HGF, as well as the disbalance between MMP-2 and TIMP-2 proves an increased fibrosis in intraabdominal adhesions. Less detected FGF-2 and more prominent FGR1 findings points out a compensatory receptor stimulation in response to the lacking same factor. The decrease in PGP 9.5 and the increase in VEGF-positive macrophages indicate hypoxic injury and proves the stimulation of neoangiogenesis. An unpronounced IL-1 and marked IL-10 finding indicate the local tissue protection reaction, the decrease in IL-4 could be the direct cause of giant cells, but the decrease of IL-8 could confirm a delayed chemotaxis of inflammatory cells.

ROLE OF Β-DEFENSINS IN IMMUNE RESPONSE IN TUBERCULOSIS PATIENTS Shevchenko O., Pohorielova O. Expanding of tuberculosis drug-resistance makes host-directed treatment an important part of tuberculosis treatment. Host-directed treatment is aimed at stimulating the production of antimicrobial peptides by the patient's immune cells. The use of β-defensins is very interesting in this field because of their pronounced bactericidal and bacteriostatic effects, as well as the ability to stimulate the chemotaxis of immune cells. The article presents a review on the immunological properties of the defensin family and the possibility of their use in practice. To complete the review 114 articles from “PubMed” resource were analyzed to perform the study. 34 of them were chosen to review immunomodulatory and antimicrobial action of β-defensins. The own research results on Human-beta-defensine-1 use as tuberculosis severity marker are also added to the research. To obtain our own research results, 100 TB patients and 20 healthy persons were included in the study. Human-beta-defensin-1 level in serum was investigated in all the patients at the treatment onset and in healthy persons. Mann-Whitney U test (for comparison of 2 independent groups) and Spearman's rank correlation coefficient were used for statistical data processing. It was found that Human-beta-defensin-1 level was significantly higher in TB patients than in healthy persons. A correlation of medium strength (r=+0.53, p<0.05) between Human-beta-defensin-1 and tuberculosis lesion volume was revealed. The data obtained allows to use human β-defensin-1 as a diagnostic marker of tuberculosis. Key words: tuberculosis, β-defensins, immunity, prognostic marker Резюме. РОЛЬ Β-ДЕФЕНЗИНІВ В ІМУННІЙ ВІДПОВІДІ У ХВОРИХ НА ТУБЕРКУЛЬОЗ Шевченко О.С., Погорєлова О.О. Розширення лікарської стійкості туберкульозу робить лікування, спрямоване на активацію власних резервів організму-хазяїна, важливою частиною терапії. Таке лікування спрямоване на стимулювання продукції антимікробних пептидів імунними клітинами пацієнта. Використання β-дефензинів в даній області є перспективним через їх виражену бактерицидну і бактеріостатичну дію, а також здатність стимулювати хемотаксис імунних клітин. У статті представлений огляд імунологічних властивостей сімейства дефензинів і можливостей їх використання на практиці. Для створення огляду було проаналізовано 114 статей з ресурсу «PubMed». З них 34 були обрані для вивчення імуномодулюючої і антимікробної дії β-дефензинів. Результати власного дослідження можливостей використання β-дефензину-1 також були включені в роботу. Для отримання власних результатів у дослідження було включено 100 хворих на туберкульоз і 20 здорових людей. Рівень β-дефензіну-1 в сироватці крові був досліджений у всіх пацієнтів на початку лікування і у здорових людей. U-критерій Манна-Уїтні (для порівняння 2 незалежних груп) і коефіцієнт кореляції застосовувалися для статистичної обробки даних. Було виявлено, що рівень β-дефензину-1 був значно вищим у хворих на туберкульоз, ніж у здорових людей. Виявлено кореляцію середньої сили (r = + 0,53, р <0,05) між рівнем β-дефензину-1 і об’ємом туберкульозного ураження. Отримані дані дозволяють використовувати β-дефензин-1 в якості діагностичного маркеру перебігу туберкульозу. Ключові слова: туберкульоз, β-дефензини, імунітет, прогностичний маркер Резюме. РОЛЬ Β-ДЕФЕНЗИНОВ В ИММУННОМ ОТВЕТЕ У БОЛЬНЫХ ТУБЕРКУЛЕЗОМ Шевченко О.С., Погорелова О.А. Расширение лекарственной устойчивости туберкулеза делает лечение, направленное на активацию резервов организма-хозяина, важной частью терапии. Такое лечение направлено на стимулирование производства антимикробных пептидов иммунными клетками пациента. Использование β-дефензинов в данной области является перспективным из-за их выраженного бактерицидного и бактериостатического действия, а также способности стимулировать хемотаксис иммунных клеток. В статье представлен обзор иммунологических свойств семейства дефензинов и возможности их использования на практике. Для создания обзора было проанализировано 114 статей из ресурса «PubMed». 34 из них были выбраны для изучения иммуномодулирующего и антимикробного действия β-дефензинов. Собственные результаты исследования возможностей использования β-дефензина-1 в качестве маркера тяжести туберкулеза также были включены в работу. Для получения собственных результатов в исследование были включены 100 больных туберкулезом и 20 здоровых людей. Уровень β-дефензина-1 в сыворотке был исследован у всех пациентов в начале лечения и у здоровых людей. U-критерий Манна-Уитни (для сравнения 2 независимых групп) и коэффициент корреляции Спирмена были использованы для статистической обработки данных. Было обнаружено, что уровень β-дефензина-1 был значительно выше у больных туберкулезом, чем у здоровых людей. Выявлена ​​корреляция средней силы (r = + 0,53, р <0,05) между уровнем β-дефензина-1 и туберкулезного поражения. Полученные данные позволяют использовать β-дефензин-1 в качестве диагностического маркера течения туберкулеза. Ключевые слова: туберкулез, β-дефензины, иммунитет, прогностический маркер

Objective — to investigate the dynamics of life quality in patients with pulmonary tuberculosis against the background of the appointment of an essential amino acids complex. Materials and methods. The study included 100 patients with pulmonary tuberculosis who received treatment and diagnosis in accordance with the WHO recommendations and current state protocols. The patients were divided into 3 groups: group 1 (n = 50) did not receive additional complex of amino acids in pathogenetic therapy; group 2 (n = 25) received a complex of amino acids in tablet form for 30 days; group 3 (n = 25) received injectable amino acids complex for 10 days and then was transferred to tablet form for 20 days. At the beginning of treatment, after 30 days and after 60 days, the patients were interviewed using the SF-36 questionnaire. Also, the patients were measured the level of Human-beta-defensine-1 in the blood plasma by ELISA at the beginning of treatment. Results and discussion. After 30 doses of anti-tuberculosis treatment, better quality of life parameters were observed in groups 2 and 3 than in group 1. Thus, the PF in group 1 was 54.73 ± 2.99, in group 2 — 80.87 ± 2.82, in group 3 — 66. 4.23; RP was in group 1 — 20.27 ± 3.47, in group 2 — 81.52 ± 3.92, in group 3 — 55.00 ± 7.07; GH was 16.68 ± 1.79 in group 1, 45.48 ± 3.09 in group 2, 34.04 ± 3.35 in group 3; VT was in group 1 — 13.38 ± 1.55, in group 2 — 45.87 ± 2.86, in group 3 — 33.60 ± 3.68; SF was 43.45 ± 2.39 in group 1, 69.02 ± 2.06 in group 2, and 60.50 ± 3.53 in group 3; RE was in group 1 — 27.03 ± 4.80, in group 2 — 95.65 ± 3.18, in group 3 — 73.33 ± 7.69; MH was in group 1 — 39.22 ± 1.36, in group 2 — 60.00 ± 2.12, in group 3 — 56.00 ± 2.71, p < 0.05. This ratio between the groups remained at 60 doses of chemotherapy: PF was 62.17 ± 3.47 in group 1, 82.95 ± 2.39 in group 2, and 76.52 ± 3.42 in group 3; RP in group 1 was 28.33 ± 4.90, in group 2 — 90.91 ± 3.09, in group 3 — 66.30 ± 7.14; GH was 22.97 ± 2.13 in group 1, 52.63 ± 3.14 in group 2, 46.78 ± 4.22 in group 3; VT was 19.33 ± 1.91 in group 1, 50.68 ± 2.72 in group 2, and 40.87 ± 3.98 in group 3; SF was 50.67 ± 2.31 in group 1, 75.00 ± 2.18 in group 2, and 68.48 ± 3.84 in group 3; RE was 36.67 ± 6.26 in group 1, 98.49 ± 1.52 in group 2, 82.61 ± 6.91 in group 3; MH was 42.73 ± 1.62 in group 1, 63.82 ± 2.01 in group 2, 59.83 ± 2.75 in group 3, p < 0.05. Conclusions. The appointment of a complex of amino acids as an additional pathogenetic therapy in patients with pulmonary tuberculosis improves the quality of life, and the appointment of an injectable form of amino acids accelerates patients’ adaptation and increases adherence to treatment, which is one of the key factors in the effectiveness of therapy.

2008/2009
I peptidi in difesa dell’ospite (HDPs) esercitano molteplici ruoli nell’immunità, agendo sia come molecole antimicrobiche ad azione diretta sia come agenti immuno-moduatori. Il ruolo all’interfaccia tra immunità innata ed adattativa li rende molecole ideali per la futura applicazione nel trattamento di malattie infettive. Lo scopo di questo lavoro è stato quello di valutare le caratteristiche funzionali e strutturali di Catelicidine e Defensine selezionate al fine di correlare queste proprietà con l’ attività selettiva su cellule eucariotiche e procariotiche. Metodi biofisici e biochimici sono stati applicati alla catelicidina umana LL37 ed alcuni analoghi (ortologhi di primate e peptidi artificiali) con lo scopo di studiare la loro struttura e aggregazione in contatto con membrane biologiche e modello (i). Lo stesso approccio è stato anche applicato alle defensine umane hBD2 e 3 ed a loro analoghi. Inoltre, tecniche di microscopia, quali la microscopia a trasmissione elettronica (TEM), la microspettroscopia infrarossa in trasformata di fourier accoppiata ad una sorgente di sicrotrone (µSR-FTIR) e la citofluorimetria, sono state utilizzate in modo complementare al fine di studiare l’interazione a breve termine di hBD2 con cellule presentanti l’antigene, in particolare le cellule dendritiche immature (ii). (i) Lo studio strutturale e l’interazione di membrana di catelicidine ortologhe ci ha permesso di scoprire come l’evoluzione abbia lavorato sulla sequenza dei peptidi inducendo una diversa capacità di strutturare nei diversi ortologhi. Questo ha portato ad un’interazione differenziata e specifica con le membrane e a diversi meccanismi di lisi di membrana cellulare e probabilmente diversi modi di interagire con le cellule dell’ospite. (ii) Inoltre, abbiamo individuato una rapida interazione di hBD2 con le cellule presentanti l’antigene. hBD2 sembra indurre un riarrangiamento generale dei lipidi cellulari che sembra comportare un aumento nella fluidità di membrana e una ri- organizzazione del sistema endomembranoso. Queste variazioni potrebbero essere responsabili di un cambiamento morfologico delle cellule che promuoverebbe la mobilità cellulare in risposta a stimuli esterni. Questo studio dimostra l’esistenza di un posibile meccanismo alternativo di motilità cellulare rispetto alla chemotassi recettore-mediata, indicando un meccanimo di azione di hBD2 sulle iDC più complesso rispetto quanto riportato fino ad oggi.
XXII Ciclo
1980