Алкоголь-индуцированная активация системы хемокинов и развитие нейровоспаления

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Хемокины являются иммунорегуляторными белками с плейотропными функциями, участвующими в процессах нейромодуляции, нейрогенезе и нейротрансмиссии. Действие хемокинов на ЦНС играет важную роль в модуляции различных состояний, которые могут иметь негативные последствия для функций ЦНС, включая развитие расстройств, связанных с употреблением алкоголя. В данном обзоре мы проанализировали имеющиеся данные литературы, посвященные проблеме участия хемокинов в патогенезе, формировании клинической картины и ремиссии алкогольной зависимости как на животных моделях, так и при исследовании пациентов с алкоголизмом. Представленные данные подтверждают гипотезу о том, что индуцированная алкоголем выработка хемокинов может модулировать процессы хронического нейровоспаления. Таким образом, обобщенные и представленные в настоящем обзоре данные посвящены актуальному направлению исследований в области психиатрии, которые будут востребованы как учеными, так и специалистами клинического направления.

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Е. В. Михалицкая

Томский национальный исследовательский медицинский центр РАН

Автор, ответственный за переписку.
Email: Uzen63@mail.ru
Россия, 634014, Томск

Н. М. Вялова

Томский национальный исследовательский медицинский центр РАН

Email: Uzen63@mail.ru
Россия, 634014, Томск

Н. А. Бохан

Томский национальный исследовательский медицинский центр РАН

Email: Uzen63@mail.ru
Россия, 634014, Томск

С. А. Иванова

Томский национальный исследовательский медицинский центр РАН

Email: Uzen63@mail.ru
Россия, 634014, Томск

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2. Рис. 1. Вклад хемокинов в развитие нейровоспаления при интоксикации алкоголем. Этанол (EtOH) своим действием на клетки печени и ЦНС приводит к увеличению (↑) экспрессии одних хемокинов и их рецепторов (CCL2, 11, C3AR1, CXCL1, -2, -4, -5, -6, -8, -10) и снижению (↓) экспрессии других (CXCL12, CX3CL1). Хемокины, в свою очередь, взаимодействуя со своими GPCR-рецепторами на поверхности микроглии и нейронов, способствуют активации (!) микроглии, хемотаксису и инфильтрации нейтрофилов и макрофагов в очаг воспаления, активации окислительного стресса и экспрессии ряда провоспалительных факторов. Измененная экспрессия хемокинов в ЦНС также приводит к активации дофаминовой системы и увеличению потребления алкоголя, что, в свою очередь, ведет к еще большему изменению экспрессии хемокинов. Таким образом, развитие нейровоспаления приводит к нарушению нейрогенеза, нейродегенерации и апоптозу нейронов

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