gondii infection is a positive predictive factor for entrepreneurial activity ( 15). Although it is known that behavioral changes are directly related to cyst burden, Jenniffer et al. gondii even has an effect on suicide attempts and road rage ( 13, 14). Johnson et al. For example, infected rats and mice exhibited a significant decreased aversion to cat urine, and they even showed an unexpectedly attraction ( 12). gondii infection has been linked to several mental diseases, such as schizophrenia, Parkinson’s disease (PD) and bipolar disorders ( 9– 11). There have been numerous studies that have shown that T. gondii infection is associated with specific behavioral modifications in animals and humans. While the combination of sulfadiazine and pyrimethamine is highly effective against the tachyzoites, neither it, nor any of the other currently used drugs is capable of eradicating the cyst form of T. The protozoan parasite will then differentiate into slow-growing bradyzoites that will persist in the host muscle and brain for the entire life ( 8). Acute infection is characterized by rapidly replicating tachyzoites which can infect all nucleated cells and disseminate throughout the body via bloodstream ( 7). Usually, an infected host especially rodents will undergo two phases, including acute infection and chronic infection. Unfortunately, there are no commercial vaccines that can stop or significantly lessen the chances of Toxoplasma infection. Worthy to mention, unborn children might undergo diseases of the nervous system and eyes if their mothers are newly infected with Toxoplasma during or just before pregnancy ( 6). However, Toxoplasma can be reactive in immunocompromised individuals, such as AIDS patients and transplant recipients, leading to retinochoroiditis, encephalitis and even death ( 5). Although it is estimated that approximately 30% of the world’s human population carry this parasite, most people show no obvious clinical symptoms as the immune system can suppress parasite replication ( 4). gondii by eating undercooked contaminated meat or ingestion of oocysts shed by infected cats ( 3). Human infection with the obligate intracellular parasite Toxoplasma gondii has been considered an underestimated threat ( 1, 2). These results demonstrated the usefulness of quantitative peptidomics in determining bioactive peptides and elucidating their functions in the regulation of behavior modification during T. We also identified three novel neuropeptides derived from the precursor protein cholecystokinin.
Quantitative analysis revealed 478 and 344 significantly differentially expressed peptides (DEPs) in the acute and chronic infection stages, respectively. Functional analysis of DEPs by Gene Ontology suggested these DEPs mainly originated from cell part and took part in cellular process. Using a label-free peptidomics approach (LC–MS/MS), we identified a total of 2,735 endogenous peptides from acutely infected, chronically infected and control brain samples following T.
gondii infection has never been investigated. Peptides are important native molecules responsible for a wide range of biological functions within the central nervous system. However, peptidome profiling in host brain during T. Toxoplasma gondii is an obligate intracellular parasite capable of establishing persistent infection within the host brain and inducing severe neuropathology.
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