REVIEW: Inactivation of Inflammasomes by Pathogens Regulates Inflammation

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F. Yu. Garib^1,2,3*, A. P. Rizopulu⁴, A. A. Kuchmiy⁵, and V. F. Garib⁶

¹Lomonosov Moscow State University, Biological Faculty, 119991 Moscow, Russia

²Russian Medical Academy of Postgraduate Education, Department of Immunology, 123995 Moscow, Russia

³Sechenov First Moscow State Medical University, Department of Immunology, 119991 Moscow, Russia; E-mail: fgarib@yandex.ru

⁴Committee on Science and High Technologies, State Duma of Russian Federation, 103265 Moscow, Russia; E-mail: annarizopulu@inbox.ru

⁵Ghent University, Inflammation Research Center, VIB, Zwijnaarde, B-9052, Belgium, Department of Internal Medicine, B-9000 Ghent, Belgium; E-mail: kuchmiyanna@gmail.com

⁶Medical University of Vienna, Department of Pathophysiology and Allergy Research, 1090 Vienna, Austria; E-mail: viktoriya.garib@meduniwien.ac.at

^* To whom correspondence should be addressed.

Received July 8, 2016; Revision received July 28, 2016

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Inflammatory response is initiated and sustained by the action of quintessential pro-inflammatory cytokines of immune system namely IL-1β and IL-18. The maturation process of those cytokines is ensured by caspase-1 enzymatic activity, that is in turn is tightly controlled by multiprotein complexes called inflammasomes. Inflammasomes are activated in cells of innate immune system in response to recognition of conservative parts of microbes (pathogen-associated molecular patterns) or by sensing molecular signs of tissue damage (damage-associated molecular patterns). Inflammasome activation apart of cytokines secretion leads to pro-inflammatory cell death, so-called pyroptosis. That culminates in release of cytoplasmatic content of cells including cytokines and alarmins that boost immune response against pathogens, as well as pyroptosis destroys replicative niches of intracellular pathogens. During co-evolution with the host, bacterial and viral pathogens developed a range of molecular inhibitors targeting each step of inflammasome activation. In current review, we will discuss the latest knowledge of inflammasomes’ signaling pathways and tricks that pathogens use to avoid immune recognition and clearance. Our better understanding of inflammasome inhibition by pathogens can lead to better therapeutic approaches for the treatment of infectious diseases.

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KEY WORDS: inflammasome, IL-1β, IL-18, evasion, bacterial and viral pathogens, pyroptosis

DOI: 10.1134/S0006297916110109

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