Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells

Abstract

Toxoplasma gondii (T. gondii) is an obligate intracellular parasite. During the parasitic invasion, T. gondii creates a parasitophorous vacuole, which enables the modulation of cell functions, allowing its replication and host infection. It has effective strategies to escape the immune response and reach privileged immune sites and remain inactive in a controlled environment in tissue cysts. This current review presents the factors that affect host cells and the parasite, as well as changes in the immune system during host cell infection. The secretory organelles of T. gondii (dense granules, micronemes, and rhoptries) are responsible for these processes. They are involved with proteins secreted by micronemes and rhoptries (MIC, AMA, and RONs) that mediate the recognition and entry into host cells. Effector proteins (ROP and GRA) that modify the STAT signal or GTPases in immune cells determine their toxicity. Interference byhost autonomous cells during parasitic infection, gene expression, and production of microbicidal molecules such as reactive oxygen species (ROS) and nitric oxide (NO), result in the regulation of cell death. The high level of complexity in host cell mechanisms prevents cell death in its various pathways. Many of these abilities play an important role in escaping host immune responses, particularly by manipulating the expression of genes involved in apoptosis, necrosis, autophagy, and inflammation. Here we present recent works that define the mechanisms by which T. gondii interacts with these processes in infected host cells.

Toxoplasma gondii eIF-5A Modulates the Immune Response of Murine Macrophages In Vitro

“…Apoptosis is a form of programmed cell death that has an important role in the resistance to intracellular parasite infections [ 36 ]. To ensure that the parasite can complete its complex life cycle and transmit in different hosts, T. gondii has evolved a wide array of mechanisms to arrest apoptosis and maintain the viability of host cells [ 37 ]. On the other hand, the molecular mechanisms of T. gondii to arrest the host cell apoptosis are not clear yet.…”

Contrasting Disease Progression, Microglia Reactivity, Tolerance, and Resistance to <em>Toxoplasma gondii</em> Infection in Two Mouse Strains

“…The innate immune system, in particular, plays a pivotal role in both resistance and disease tolerance by recognizing pathogen-associated molecular patterns (PAMPs) and then coordinating the inflammatory response [8]. Experimental studies employing murine models have shed light on the T. gondii evasion strategies against the host immune system and have emphasized the interplay between parasite virulence factors and host immune pathways [9][10][11]. While acute infections are typically controlled, chronic infections may persist, leading to cyst formation, particularly within the brain [12][13].…”

A potential cure for tumor‐associated immunosuppression by Toxoplasma gondii

“…Individuals react differently to T. gondii ‐based therapy influenced by genetic, immunological, and environmental factors. 137 To enhance therapeutic results, it is imperative to design individualized treatment plans tailored to the unique characteristics of each patient. Treatment regimens consist of determining biomarkers and other predictive indicators for guiding treatment choices.…”

“…Personalized medicineIndividuals react differently to T. gondii-based therapy influenced by genetic, immunological, and environmental factors 137. To enhance therapeutic results, it is imperative to design individualized treatment plans tailored to the unique characteristics of each patient.Treatment regimens consist of determining biomarkers and other predictive indicators for guiding treatment choices.10.5 | Long-term monitoring and follow-upTo better understand how T. gondii-based treatment impacts patients' general health and immune systems over time, prolonged monitoring and follow-up studies are needed.…”