Sarcocystis is a zoonotic pathogen that threatens public health and the quality of food safety. To determine the Sarcocystis spp. prevalence in ruminants (Ruminantia) in China, we conducted a systematic review and meta-analysis. Data were collected from English databases (PubMed and Web of Science) and Chinese databases (Chinese Web of knowledge (CNKI), Database for Chinese Technical Periodicals (VIP) and Wan Fang databases). A total of 20,301 ruminants from 54 publications were evaluated. The pooled prevalence of Sarcocystis spp. among ruminants in mainland China was 65% (95% CI: 57–72%). Our results indicate that sarcocystosis is prevalent in ruminants, which show significant geographical differences. Therefore, it there is a need for continuous monitoring of infections of Sarcocystis spp. in ruminants to reduce the threat to human health and economic losses to the animal industry.
Background Iron possesses redox abilities and plays a crucial role in in biosynthesis, energy metabolism, and other biological processes. It represents an indispensable nutrient for the survival of Toxoplasma gondii. In response to Toxoplasma-infection, host cells employ a defensive strategy referred to as "nutritional immunity" to restrict the availability of iron, thus impeding T. gondii from obtaining sufficient amounts of this vital element. The present research aims to examine the impact of iron stress on T. gondii, including iron deficiency and iron overload, and to explore the feasibility of disturbing the iron homeostasis as a potential treatment for toxoplasmosis. Methods An iron-deficient environment was induced by supplementing the culture medium with the permeable iron chelator, deferoxamine mesylate (DFO), while ammonium iron(II) sulfate was utilized as an iron supplement to establish an iron overload environment. Experiments were conducted to assess the impact of different iron levels on T. gondii's proliferation ability, invasion ability, escape ability, and plaque formation, Additionally, the redox ability of T. gondii under varying iron stress conditions was examined. Transcriptome analysis was employed to investigate the differential gene expression of T. gondii under iron deficiency and iron overload. Lastly, iron chelation therapy and iron supplementation therapy were administered to mice infected with T. gondii to assess the potential of targeting iron homeostasis disruption for the treatment of toxoplasmosis. Results Iron supplementation and the iron chelating agent significantly influence the growth of T. gondii. Low iron stress inhibits the proliferation of T. gondii and greatly reduces plaque formation, whereas high iron stress increases the invasion ability while significantly reducing proliferation. Altered iron levels perturb the redox capacity of T. gondii, resulting in a substantial increase in oxidation products (GSSG and MDA), reactive oxygen species (ROS), and superoxide anions under high iron stress. Under iron deficiency, specific genes pertaining to bradyzoites are up-regulated, thereby facilitating the conversion of tachyzoites to bradyzoites in the Pru strain. Conversely, under iron overload, a significant up-regulation of surface protein genes in T. gondii occurs, leading to an enhanced adhesion ability. Notably, the administration of iron supplements and iron chelating agents has no discernible effect on the mortality rates of Toxoplasma-infected mice. Nevertheless, mice infected with T. gondii exhibit significant weight loss and aggravated symptoms following iron supplementation therapy. Conclusions This study unequivocally confirms the essentiality of iron as a nutrient for T. gondii survival. Iron stress, including iron deficiency and iron overload, affects the growth of T. gondii.
Toxoplasma gondii (T.gondii) hijacks host immune cells as 'Trojan Horse' and the infected cells accelerated the parasites dissemination. During acute infection, T.gondii specificity crosses the blood-brain-barrier to enter the brain. This selective mode of parasite transmission may be associated with the directed migration of infected immune cells. Immune cells follow various environmental cues for directional migration. However, the effect of T.gondii infection on the recognition of mechanical cues by immune cells remains unknown. Here, we examined the adhesion and migration of T.gondii-infected dendritic cells (DCs) on high and low stiffness substrates. We found that T.gondii infection alters the durotaxis migration of DCs. Infected DC exhibited stronger adhesion and lower migration on low stiffness substrates. In contrast to uninfected DCs, infected DCs migrated towards the low stiffness environment. TgWIP and TgROP17 co-regulate the F-actin structure of DCs and are involved in the formation of abnormal F-actin filaments. Rearrangement of the F-actin structure resulting from T.gondii infection regulates DC's abnormal recognition response to the mechanical cues. Recognition of DCs to the mechanical signals is independent of beta2-integrin expression. Meanwhile, challenging DCs with T.gondii increased the phosphorylation of focal adhesion kinase (FAK). Treatment with a FAK inhibitor (VS-6063) influences the recognition response of infected DCs. FAK inhibition in adoptively transferred infected DCs effectively prevents the dissemination of T.gondii to the brain. The data reveal that T.gondii infection inversely affects the durotaxis of DCs by altering the phosphorylation level of FAK and remodeling of F-actin structure. T.gondii utilizes the change in DC's durotaxis migration to accelerate the parasites crossing the blood-brain-barrier.
Sarcocystis spp., Neospora caninum and Toxoplasma gondii are globally ubiquitous pathogens, and domestic sheep are considered to be one of the intermediate hosts. 83 myocardial samples of sheep were collected from 12 retail stores in Beijing, China. Sarcocystis spp., N. caninum and T. gondii were identified by PCR amplification of the 18S rRNA gene, Nc-5 gene and 529bp DNA fragment with a prevalence of 86.7% (95% CI: 77.5–93.2) and 43.4% (95% CI: 32.5–54.7) for Sarcocystis spp. and N. caninum infections, respectively, and no T. gondii was detected. The co-infection prevalence of Sarcocystis and N. caninum was 38.6% (95% CI: 28.1–49.9). Two Sarcocystis species were subtyped by analyzing 18SrRNA sequences and were identified as Sarcocystis tenella and Sarcocystis arieticanis. The prevalence of S. tenella and S. arieticanis infections was 84.3% (95% CI: 74.7–91.4) and 56.6% (95% CI: 45.3–67.5), respectively. This study shows that sheep have a high risk of infection with Sarcocystis and N. caninum, suggests that effective prevention measures are needed to avoid the spread of these parasites in sheep. Toxoplasmosis in sheep poses a threat to human and animal health and requires monitoring and preventing continuously.
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