Management of cell death in parasitic infections

TY - JOUR

T1 - Management of cell death in parasitic infections

AU - Bosurgi, Lidia

AU - Rothlin, Carla V

N1 - © 2021. The Author(s).

PY - 2021/8

Y1 - 2021/8

N2 - For a long time, host cell death during parasitic infection has been considered a reflection of tissue damage, and often associated with disease pathogenesis. However, during their evolution, protozoan and helminth parasites have developed strategies to interfere with cell death so as to spread and survive in the infected host, thereby ascribing a more intriguing role to infection-associated cell death. In this review, we examine the mechanisms used by intracellular and extracellular parasites to respectively inhibit or trigger programmed cell death. We further dissect the role of the prototypical "eat-me signal" phosphatidylserine (PtdSer) which, by being exposed on the cell surface of damaged host cells as well as on some viable parasites via a process of apoptotic mimicry, leads to their recognition and up-take by the neighboring phagocytes. Although barely dissected so far, the engagement of different PtdSer receptors on macrophages, by shaping the host immune response, affects the overall infection outcome in models of both protozoan and helminth infections. In this scenario, further understanding of the molecular and cellular regulation of the PtdSer exposing cell-macrophage interaction might allow the identification of new therapeutic targets for the management of parasitic infection.

AB - For a long time, host cell death during parasitic infection has been considered a reflection of tissue damage, and often associated with disease pathogenesis. However, during their evolution, protozoan and helminth parasites have developed strategies to interfere with cell death so as to spread and survive in the infected host, thereby ascribing a more intriguing role to infection-associated cell death. In this review, we examine the mechanisms used by intracellular and extracellular parasites to respectively inhibit or trigger programmed cell death. We further dissect the role of the prototypical "eat-me signal" phosphatidylserine (PtdSer) which, by being exposed on the cell surface of damaged host cells as well as on some viable parasites via a process of apoptotic mimicry, leads to their recognition and up-take by the neighboring phagocytes. Although barely dissected so far, the engagement of different PtdSer receptors on macrophages, by shaping the host immune response, affects the overall infection outcome in models of both protozoan and helminth infections. In this scenario, further understanding of the molecular and cellular regulation of the PtdSer exposing cell-macrophage interaction might allow the identification of new therapeutic targets for the management of parasitic infection.

KW - Animals

KW - Apoptosis

KW - Humans

KW - Macrophages

KW - Parasites

KW - Parasitic Diseases

KW - Phosphatidylserines

U2 - 10.1007/s00281-021-00875-8

DO - 10.1007/s00281-021-00875-8

M3 - SCORING: Review article

C2 - 34279684

VL - 43

SP - 481

EP - 492

JO - SEMIN IMMUNOPATHOL

JF - SEMIN IMMUNOPATHOL

SN - 1863-2297

IS - 4

ER -