Роль интерлейкина 1 в развитии атеросклероза

В настоящее время атеросклероз рассматривается как хроническое воспалительное заболевание сосудов, связанное с «патологической» активацией врожденного и приобретенного иммунитета, характеризующееся отложением липидов, лейкоцитарной инфильтрацией и пролиферацией сосудистых гладкомышечных клеток. Субклиническое (low grade) воспаление играет фундаментальную роль на всех стадиях прогрессирования атеросклеротического процесса и определяет развитие кардиоваскулярных катастроф и летальности. Среди многочисленных медиаторов, участвующих в иммунопатогенезе как атеросклероза, так и РА, важное место занимают такие «провоспалительные» цитокины, как интерлейкин 1 (ИЛ1), ИЛ6, фактор некроза опухоли α (ФНОα), ИЛ17, ИЛ18, ИЛ27, ИЛ33, ИЛ37, тесно взаимодействующие друг с другом в рамках «цитокиновой» сети. Особое внимание привлекает ИЛ1β, играющий важную роль в развитии многих острых и хронических иммуновоспалительных заболеваний. ИЛ1β в развитии атеросклероза определяется многими механизмами, такими как «прокоагулянтная» активность, усиление адгезии моноцитов и лейкоцитов к сосудистому эндотелию, роста сосудистых гладкомышечных клеток и др. В качестве прямого доказательства фундаментальной роли воспаления в развитии атеросклероза особый интерес представляют исследования «антиатеросклеротических» эффектов препарата канакинумаб. Особый интерес представляет рандомизированное плацебоконтролируемое исследование CANTOS (Canakinumab ANti-inflammatory Thrombosis Otcomes Study), посвященное изучению эффективности терапии канакинумабом как нового подхода к вторичной профилактике кардиоваскулярных осложнений в общей популяции больных с тяжелым атеросклеротическим поражением сосудов. Результаты исследования CANTOS в сочетании со знаниями, накопленными в ревматологии в отношении кардиоваскулярных эффектов противовоспалительных препаратов, имеют огромное значение для персонификации подходов к вторичной профилактике связанных с атеросклерозом кардиоваскулярных осложнений и вносит вклад в развитие «воспалительной» теории патогенеза атеросклероза в целом.

атеросклероз, ревматоидный артрит, подагра, цитокины, интерлейкин 1β, канакинумаб, колхицин

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