Antidepressants induce autophagy dependent-NLRP3-inflammasome inhibition in Major depressive disorder

Pharmacological Research

Volumn 121, Issue , 2017, Pages 114-121

  Alcocer Gómez, Elísabet ^a   Casas Barquero, Nieves ^b   Williams, Matthew R ^c   Romero Guillena, Samuel L ^b   Cañadas Lozano, Diego ^a   Bullón, Pedro ^a   Sánchez Alcazar, José Antonio ^d   Navarro Pando, José M ^e   Cordero, Mario D ^a  

^a UNIVERSITY OF SEVILLE   (Spain)

^b HOSPITAL UNIVERSITARIO VIRGEN MACARENA   (Spain)

^c HAMMERSMITH HOSPITAL   (United Kingdom)

^d INSTITUTO DE SALUD CARLOS III   (Spain)

^e Cátedra de Reproducción y Genética Humana del Instituto para el Estudio de la Biología de la Reproducción Humana INEBIR   (Spain)

Author keywords

Antidepressants; Autophagy; Major depressive disorder; NLRP3 inflammasome

Indexed keywords

AGOMELATINE; AMITRIPTYLINE; ANTIDEPRESSANT AGENT; CRYOPYRIN; DESVENLAFAXINE; FLUOXETINE; IMIPRAMINE; INFLAMMASOME; INTERLEUKIN 18; INTERLEUKIN 1BETA; INTERLEUKIN 6; MESSENGER RNA; MIANSERIN; MIRTAZAPINE; PAROXETINE; TUMOR NECROSIS FACTOR; VENLAFAXINE; NLRP3 PROTEIN, HUMAN;

ADULT; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; AUTOPHAGY; CLINICAL ARTICLE; CONTROLLED STUDY; CYTOKINE RELEASE; DRUG EFFICACY; FEMALE; GENE; GENE EXPRESSION; HUMAN; HUMAN CELL; IN VITRO STUDY; IN VIVO STUDY; MAJOR DEPRESSION; MALE; MIDDLE AGED; MOUSE; NLRP3 GENE; NONHUMAN; OUTCOME ASSESSMENT; PROTEIN BLOOD LEVEL; PROTEIN EXPRESSION; PROTEIN FUNCTION; ANIMAL; ANTAGONISTS AND INHIBITORS; BLOOD; C57BL MOUSE; CELL LINE; DRUG EFFECTS; IMMUNOLOGY;

ADULT; ANIMALS; ANTIDEPRESSIVE AGENTS; AUTOPHAGY; CELL LINE; DEPRESSIVE DISORDER, MAJOR; FEMALE; HUMANS; INFLAMMASOMES; INTERLEUKIN-1BETA; MALE; MICE, INBRED C57BL; MIDDLE AGED; NLR FAMILY, PYRIN DOMAIN-CONTAINING 3 PROTEIN;

EID: 85018736108     PISSN: 10436618     EISSN: 10961186     Source Type: Journal    
DOI: 10.1016/j.phrs.2017.04.028     Document Type: Article

References (31)

1. [1] Murray, C.J., Lopez, A.D., Alternative projections of mortality and disability by cause 1990–2020: global burden of disease study. Lancet 349 (1997), 1498–1504.
2. [2] Greden, J.F., The burden of disease for treatment-resistant depression. J. Clin. Psychiatry 62:Suppl. 16 (2001), 26–31.
3. [3] Kessler, R.C., The costs of depression. Psychiatr. Clin. North Am. 35 (2012), 1–14.
4. [4] Thase, M.E., Preventing relapse and recurrence of depression: a brief review of therapeutic options. CNS Spectr. 11 (2006), 12–21.
5. [5] Cattaneo, A., Gennarelli, M., Uher, R., Breen, G., Farmer, A., Aitchison, K.J., Craig, I.W., Anacker, C., Zunsztain, P.A., McGuffin, P., Pariante, C.M., Candidate genes expression profile associated with antidepressants response in the GENDEP study: differentiating between baseline ‘predictors' and longitudinal ‘targets'. Neuropsychopharmacology 38 (2013), 377–385.
6. [6] Wang, Y., Cui, X.L., Liu, Y.F., Gao, F., Wei, D., Li, X.W., Wang, H.N., Tan, Q.R., Jiang, W., LPS inhibits the effects of fluoxetine on depression-like behavior and hippocampal neurogenesis in rats. Prog. Neuropsychopharmacol. Biol. Psychiatry 35 (2011), 1831–1835.
7. [7] Pineda, E.A., Hensler, J.G., Sankar, R., Shin, D., Burke, T.F., Mazarati, A.M., Interleukin-1β causes fluoxetine resistance in an animal model of epilepsy-associated depression. Neurotherapeutics 9 (2012), 477–785.
8. [8] Leemans, J.C., Cassel, S.L., Sutterwala, F.S., Sensing damage by the NLRP3 inflammasome. Immunol. Rev. 243 (2011), 152–162.
9. [9] Alcocer-Gómez, E., de Miguel, M., Casas-Barquero, N., Núñez-Vasco, J., Sánchez-Alcazar, J.A., Fernández-Rodríguez, A., Cordero, M.D., NLRP3 inflammasome is activated in mononuclear blood cells from patients with major depressive disorder. Brain Behav. Immun. 36 (2013), 111–117.
10. [10] Zhang, Y., Liu, L., Peng, Y.L., Liu, Y.Z., Wu, T.Y., Shen, X.L., Zhou, J.R., Sun, D.Y., Huang, A.J., Wang, X., Wang, Y.X., Jiang, C.L., Involvement of inflammasome activation in lipopolysaccharide-induced mice depressive-like behaviors. CNS Neurosci. Ther. 20 (2013), 119–124.
11. [11] Bowers, S.L., Bilbo, S.D., Dhabhar, F.S., Nelson, R.J., Stressor-specific alterations in corticosterone and immune responses in mice. Brain Behav. Immun. 22:1 (2008 Jan), 105–113.
12. [12] Lu, M., Yang, J.Z., Geng, F., Ding, J.H., Hu, G., Iptakalim confers an antidepressant effect in a chronic mild stress model of depression through regulating neuro-inflammation and neurogenesis. Int. J. Neuropsychopharmacol. 17:9 (2014 Sep), 1501–1510.
13. [13] Gassen, N.C., Hartmann, J., Zschocke, J., Stepan, J., Hafner, K., Zellner, A., Kirmeier, T., Kollmannsberger, L., Wagner, K.V., Dedic, N., Balsevich, G., Deussing, J.M., Kloiber, S., Lucae, S., Holsboer, F., Eder, M., Uhr, M., Ising, M., Schmidt, M.V., Rein, T., Association of FKBP51 with priming of autophagy pathways and mediation of antidepressant treatment response: evidence in cells, mice, and humans. PLoS Me, 11, 2014, e1001755.
14. [14] Zschocke, J., Zimmermann, N., Berning, B., Ganal, V., Holsboer, F., Rein, T., Antidepressant drugs diversely affect autophagy pathways in astrocytes and neurons–dissociation from cholesterol homeostasis. Neuropsychopharmacology 36 (2011), 1754–1768.
15. [15] Menu, P., Vince, J.E., The NLRP3 inflammasome in health and disease: the good, the bad and the ugly. Clin. Exp. Immunol. 166 (2011), 1–15.
16. [16] Iwata, M., Ota, K.T., Duman, R.S., The inflammasome: pathways linking psychological stress, depression, and systemic illnesses. Brain Behav. Immun. 31 (2013), 105–114.
17. [17] Maes, M., Bosmans, E., Meltzer, H.Y., Scharpe, S., Suy, E., Interleukin-1 beta: a putative mediator of HPA axis hyperactivity in major depression?. Am. J. Psychiatry 150 (1993), 1189–1193.
18. [18] Dowlati, Y., Herrmann, N., Swardfager, W., Liu, H., Sham, L., Reim, E.K., Lanctôt, K.L., A metaanalysis of cytokines in major depression. Biol. Psychiatry 67 (2010), 446–457.
19. [19] Rawdin, B.S., Mellon, S.H., Dhabhar, F.S., Epel, E.S., Puterman, E., Su, Y., Burke, H.M., Reus, V.I., Rosser, R., Hamilton, S.P., Nelson, J.C., Wolkowitz, O.M., Dysregulated relationship of inflammation and oxidative stress in major depression. Brain Behav. Immun., 2012 S0889-1591, 00497-7.
20. [20] Hannestad, J., DellaGioia, N., Bloch, M., The effect of antidepressant medication treatment on serum levels of inflammatory cytokines: a metaanalysis. Neuropsychopharmacology 36 (2011), 2452–2459.
21. [21] Schmidt, H.D., Shelton, R.C., Duman, R.S., Functional biomarkers of depression: diagnosis, treatment, and pathophysiology. Neuropsychopharmacology 36 (2011), 2375–2394.
22. [22] Ransohoff, R.M., Brown, M.A., Innate immunity in the central nervous system. J. Clin. Invest. 122 (2012), 1164–1171.
23. [23] Mason, J.L., Suzuki, K., Chaplin, D.D., Matsushima, G.K., Interleukin-1beta promotes repair of the CNS. J. Neurosci. 21 (2001), 7046–7052.
24. [24] Pan, Y., Chen, X.Y., Zhang, Q.Y., Kong, L.D., Microglial NLRP3 inflammasome activation mediates IL-1β-related inflammation in prefrontal cortex of depressive rats. Brain Behav. Immun. 41 (2014), 90–100.
25. [25] Dubovický, M., Császár, E., Melicherčíková, K., Kuniaková, M., Račková, L., Modulation of microglial function by the antidepressant drug venlafaxine. Interdiscip. Toxicol. 7 (2014), 201–207.
26. [26] Lee, J.Y., Kang, S.R., Yune, T.Y., Fluoxetine prevents oligodendrocyte cell death by inhibiting microglia activation after spinal cord injury. J. Neurotrauma 32 (2015), 633–644.
27. [27] Ramirez, K., Shea, D.T., McKim, D.B., Reader, B.F., Sheridan, J.F., Imipramine attenuates neuroinflammatory signaling and reverses stress-induced social avoidance. Brain Behav. Immun. 46 (2015), 212–220.
28. [28] Du, R.H., Tan, J., Sun, X.Y., Lu, M., Ding, J.H., Hu, G., Fluoxetine inhibits NLRP3 inflammasome activation: implication in depression. Int. J. Neuropsychopharmacol., 2016 pii: pyw037.
29. [29] Abdelaziz, D.H., Khalil, H., Cormet-Boyaka, E., Amer, A.O., The cooperation between the autophagy machinery and the inflammasome to implement an appropriate innate immune response: do they regulate each other?. Immunol. Rev. 265:May (1) (2015), 194–204.
30. [30] Horowitz, M.A., Wertz, J., Zhu, D., Cattaneo, A., Musaelyan, K., Nikkheslat, N., Thuret, S., Pariante, C.M., Zunszain, P.A., Antidepressant compounds can be both pro- and anti-inflammatory in human hippocampal cells. Int. J. Neuropsychopharmacol., 18(3), 2014 31.
31. [31] Schulz, M., Iwersen-Bergmann, S., Andresen, H., Schmoldt, A., Therapeutic and toxic blood concentrations of nearly 1,000 drugs and other xenobiotics. Crit. Care, 16, 2012, R136.