Background: Pyrimethamine and sulfadiazine, while being effective against toxoplasmosis, are limited by significant adverse effects. On the other hand, 2-isopropyl-5-methyl-1,4-benzoquinone has been identified as a key bioactive compound. Moreover, studies on thymoquinone (TQ) have demonstrated its cytotoxic activity, inhibiting the growth of various cancer cell lines, including those of the ovary, prostate, colon, pancreas, osteosarcoma, and breast, as well as leukemia cells. This study sought to determine how TQ affected the tachyzoite type of Toxoplasma gondii. Materials and Methods: Different TQ concentrations (6.25–400 µM) were prepared in microtiter plates for this experiment. The tachyzoite test was used to assess parasite mortality. Flow cytometry was performed to determine whether T. gondii tachyzoites underwent apoptosis. Specifically, 2×10^5 tachyzoites were exposed to TQ at concentrations of 50 µM, 100 µM, and 200 µM, following the kit’s instructions. Results: Light microscopy revealed that TQ had lethal and damaging effects on T. gondii. Based on 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assays, 400 µM of TQ exhibited the most toxic effects on macrophages. Furthermore, the MTT assay determined a half-maximal inhibitory concentration (CC50 ) for macrophages. Flow cytometric analysis indicated that the percentages of total apoptosis in parasites exposed to 50 µM, 100 µM, and 200 µM TQ were 51.3%, 64.9%, and 70.8%, respectively. Conclusion: The results demonstrated that TQ is toxic to T. gondii and induces apoptosis in this parasite. This work provides supporting evidence for the use of TQ in antiparasitic assays.
Campylobacter, a foodborne pathogen, is one of the most important bacterial agents causing human gastroenteritis. Although Guillain-Barré and other neuropathy syndromes have been observed after infection with microorganisms, most cases of these syndromes have occurred post-infection with Campylobacter bacteria. Campylobacter has several virulence factors, but those factors in the bacterial cell wall have the highest effect on causing neurological syndromes. Campylobacter mimics peripheral nerve gangliosides using virulence factors in its cell wall. For this reason, the immune system attacks bacteria and gangliosides as foreign agents and causes neurological diseases. Genetic and phenotype mechanisms are identified as the culprits behind these disorders, including lipooligosaccharide, capsular polysaccharides, phase variation, and protein glycosylation. Using these mechanisms, Campylobacter transforms into different phenotypes and genotypes, producing various virulence factors leading to neurological diseases.
Cryptosporidium spp. and Microsporidia spp., intracellular protozoan parasites, represent significant etiologic agents of opportunistic infections in immunocompromised pediatric cancer patients. These pathogens cause severe gastrointestinal symptoms including persistent diarrhea, abdominal pain, and weight loss which may be fatal in advanced stages. In developing countries with suboptimal sanitation, co-infections exacerbate morbidity among children with cancer. With the global incidence of childhood cancer increasing, immunosuppressive chemotherapy markedly heightens susceptibility to these infections. This review evaluates their epidemiology, clinical manifestations, diagnostic methodologies, and the pivotal role of early detection. The severity of infections hinges on immune competence, nutritional status, and parasite species. Although self-limiting in immunocompetent hosts, these infections persist in immunocompromised children, precipitating dehydration, malnutrition, and delays in cancer therapy. Early diagnosis is imperative to mitigate complications and enhance outcomes through prompt supportive care and infection control measures. Diagnostic techniques, such as modified acid-fast staining for Cryptosporidium spp., modified trichrome staining for Microsporidia spp., and polymerase chain reaction (PCR), exhibit variable sensitivity; however, challenges in consistent detection and therapeutic resistance persist, particularly in resource-constrained settings. In such regions, low-cost diagnostics frequently fail to detect low burden infections, and treatment options beyond rehydration and nutritional support remain limited. Advances in molecular epidemiology have deepened insights into these infections, yet practical obstacles endure in pediatric oncology. Future investigations should prioritize the development of accessible high precision diagnostics such as next generation sequencing and targeted therapeutic strategies to reduce morbidity and improve survival and quality of life in this vulnerable cohort.
Colorectal cancer (CRC) continues to be a significant health concern worldwide, and recent research has highlighted an intriguing association with Fusobacterium nucleatum. The prevalence of F. nucleatum in CRC tissues varies significantly across studies, with estimates ranging from 13% to 80%, complicating efforts to define the bacterium’s precise role in CRC development. Although the involvement of F. nucleatum in the initiation of CRC is still debated, there is a broad consensus regarding its role in cancer progression and metastasis. Elucidating the molecular mechanisms of F. nucleatum-mediated carcinogenesis could provide new avenues for managing CRC. F. nucleatum significantly facilitates the growth of CRC via its FadA adhesion. It attaches to E-cadherin (CDH1) and activates Wnt/β-catenin signaling. Consequently, inflammatory genes, Wnt-related genes, and oncogenes, such as c-Myc and Cyclin D1 (CCND1), are overexpressed. Various preventive and therapeutic strategies against F. nucleatum in CRC have been investigated, including the Fn-AhpC recombinant protein vaccine in mice and the use of metronidazole to reduce intratumoral bacterial load. Additionally, bacteriophages and nanoparticles are emerging as potential therapeutic tools. This review aims to provide a comprehensive overview of the role of F. nucleatum in CRC and to explore its potential as a target for novel therapeutic strategies.
Background: The uncontrolled spread of antibiotic resistance and their low or no efficacy in treating infections caused by multidrug-resistant (MDR) microorganisms has made it urgent to pay more attention to plants, as they are more available and safer natural agents. Curcuma longa, a medical spice, also known as turmeric, has been shown to have high antioxidant, anti-inflammatory, and antimicrobial properties. Objectives: This study aimed to determine the antimicrobial effect of the C. longa extract on six pathogenic bacteria, Pseudomonas aeruginosa, enterohemorrhagic Escherichia coli, Staphylococcus aureus, Salmonella enterica, Streptococcus mutans, and Clostridium difficile, and its positive impact on the growth of two selected probiotic bacteria, Lactobacillus plantarum and Lactobacillus reuteri. Materials and Methods: To evaluate the antibacterial activity of the C. longa extract, the broth dilution method was used, and the minimum inhibitory concentrations of six pathogenic strains underwent evaluation. The prebiotic effect of the extract on two types of lactic acid bacteria (LAB) was also investigated in this study. Results: The results revealed that the C. longa extract had prebiotic properties that could improve the growth of L. plantarum and L. reuteri, and it strongly inhibited the growth of enterohemorrhagic E. coli, P. aeruginosa, S. aureus, C. difficile, and S. mutans. Conclusion: In summary, the C. longa extract has antibacterial properties and prebiotic effects that enhance the growth of beneficial bacteria, making C. longa a suitable candidate for the development of gastrointestinal health.
