Supervision of The Complement System by Toxoplasma During Neural Infections (Areview)

Abstract

Chronic infections with Toxoplasma gondii occur in the brain of mammalian hosts. The understanding of the relationship between Toxoplasma gondii, CNS, and the immune system assists in comprehending how Toxoplasma affects the complement system and how it exerts a defense mechanism against Toxoplasma. This review focuses on the supervision of the complement system by Toxoplasma gondii during neural infections. There are three possible mechanisms by which the protozoan can invade the brain. Tachyzoites in bloodstreams multiply, invade, and bind to endothelial cells before migrating into parenchymas via transcellular crossing mechanisms. Secondly, the immune cells become like the Trojan horse, which carries intracellular parasites across the blood–brain barrier (BBB). In the third mechanical process, the BBB can directly be crossed through the brain at the tight junction (TJ) by the tachyzoites. It is concluded that C3 manipulation of the integrity of the BBB can be used to increase T.gondii invasion into the CNS..

A retrospective study of Crimean-Congo hemorrhagic fever in Iraq

“…In addition, protein recombination techniques 40 can be used in preparing high-efficacy vaccines and diagnostic kits for local strains of CCHF. It is recommended to do more immunological studies to explain how the virus can evade the immune response as it is referred to the role of complement in the pathogen's infections 41 , 42 .…”

The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host’s Complement System

“…Toxoplasma parasite can significatively induce and upregulate the C3 and C1q and disrupt the tight junction of the BBB in the CNS thus facilitating the parasite penetration to the brain tissue via the intercellular space [ 53 ]. Globally, the increase of C4b, C3 and C1q during toxoplasmosis infection induces nerve cell disruption including synaptic loss and other plausible neurodegeneration in addition to their roles for parasite entrance [ 54 ].…”

“…It is known that T. gondii disrupts the TJ of BBB and facilitates parasite to pass into the CNS mediated by the crucial role of complement components such as C3 [ 53 , 54 ]. Since the overexpression or overactivation of different complement components (or parasite-host’s complement interaction) has been reported in Toxoplasma ( Table 1 ) [ 51 , 53 , 63 ], the pharmacological or genetic suppression of such critical complement components may decrease the damage in the host and suggesting a therapeutic opportunity.…”

“…In addition, Toxoplasma infection can increase neural cell death, alteration in neural gene expression and the release of inflammatory mediators in neurospheres [ 132 ]. Thus, this infection could be correlated with psychiatric diseases and human CNS disorders including Alzheimer, dementia, depression and schizophrenia [ 54 , 133 , 134 , 135 , 136 ]. On the other hand, due to the overexpression of complement components in Toxoplasma -infected brain [ 53 , 63 ], and the upregulation of C1q, C3, and C4b in some mental disorders including schizophrenia, alzheimer’s disease, aging and multiple sclerosis [ 54 , 137 , 138 , 139 , 140 ], it could be interesting to focus on therapeutic studies that share more information regarding the possible correlations between parasitic disease including toxoplasmosis and mental disorders and their association with the complement system.…”