Acne vulgaris, which is mostly associated with the colonization of Cutibacterium acnes (C. acnes), is a common skin inflammatory disease in teenagers. However, over the past few years, the disease has extended beyond childhood to chronically infect approximately 40% of adults. While antibiotics have been used for several decades to treat acne lesions, antibiotic resistance is a growing crisis; thus, finding a new therapeutic target is urgently needed. Studies have shown that phage therapy may be one alternative for treating multi-drug-resistant bacterial infections. In the present study, we successfully isolated a C. acnes phage named TCUCAP1 from the skin of healthy volunteers. Morphological analysis revealed that TCUCAP1 belongs to the family Siphoviridae with an icosahedral head and a non-contractile tail. Genome analysis found that TCUCAP1 is composed of 29,547 bp with a G+C content of 53.83% and 56 predicted open reading frames (ORFs). The ORFs were associated with phage structure, packing, host lysis, DNA metabolism, and additional functions. Phage treatments applied to mice with multi-drug-resistant (MDR) C.-acnes-induced skin inflammation resulted in a significant decrease in inflammatory lesions. In addition, our attempt to formulate the phage into hydroxyethyl cellulose (HEC) cream may provide new antibacterial preparations for human infections. Our results demonstrate that TCUCAP1 displays several features that make it an ideal candidate for the control of C. acnes infections.

Background: Increasing evidence shows that Fusobacterium nucleatum (F. nucleatum) largely affects colorectal cancer (CRC) growth and progression; therefore, the inhibition of intratumoral F. nucleatum may be one realistic approach to combat CRC. Although antibiotics are helpful in eliminating bacteria, the major problem remains the rise of potential antibiotic-resistant strains and antibiotic-associated adverse effects. Currently, bacteriophage therapy has gained interest because of its high selectivity to bacterial hosts and may become a realistic approach in treating bacteria-associated cancers. Methods: In this study, a new F. nucleatum bacteriophage, ØTCUFN3, was isolated and its biological characteristics were identified. In vitro and in vivo studies were performed to investigate the effect of ØTCUFN3 in combating F. nucleatum-induced CRC growth. Results: By applying ØTCUFN3 to F. nucleatum-induced CRC cell lines, p53^+/+, and p53^−/− isogenic HCT116 cells, our results revealed an inhibition of CRC proliferation and the expression of epithelial-to-mesenchymal transition (EMT) markers. ØTCUFN3 injection also reduced the growth of F. nucleatum-induced mouse xenografts. Conclusions: Our results demonstrated the use of F. nucleatum bacteriophage against CRC, laying the foundation for the future usage of bacteriophage in cancer treatment.

Schistosomiasis is an inflammatory disease that occurs when schistosome species eggs are deposited in the liver, resulting in fibrosis and portal hypertension. Schistosomes can interact with host inflammasomes to elicit host immune responses, leading to mitochondrial damage, generation of high levels of reactive oxygen species (ROS) and activation of apoptosis during inflammation. This study aims to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation inSchistosoma mansoni-infected mouse livers. We examine the relationship between inflammasome activation, mitochondrial damage and ROS production in mouse livers infected withS. mansoni. We demonstrate a significant release of ROS and superoxides and increased NF-κB (p65) inS. mansoni-infected mouse livers. Moreover, activation of the NLRP3 and AIM2 inflammasomes was triggered byS. mansoniinfection. Stimulation of HuH-7 hepatocellular carcinoma cells with soluble egg antigen induced activation of the AIM2 inflammasome pathway. In this study, we demonstrate thatS. mansoniinfection promotes both NLRP3 and AIM2 inflammasome activation.

Schistosomiasis is second only to malaria as the most devastating parasitic disease in the world. It is caused by the helminthsSchistosoma mansoni(S.mansoni),S.haematobium, orS.japonicum. Typically, patients with schistosomiasis suffer from symptoms of liver fibrosis and hepatosplenomegaly. Currently, patients were treated with praziquantel. Although praziquantel effectively kills the worm, it cannot prevent re-infection or resolve liver fibrosis. Also, current treatment options are not ample to completely cure liver fibrosis and splenic damages. Moreover, resistance of praziquantel has been reported in vivo and in vitro studies. Therefore, finding new effective treatment agents is urgently needed. Schisandrin B (Sch B) ofSchisandra chinensishas been shown to protect against different liver injuries including fatty liver disease, hepatotoxicity, fibrosis, and hepatoma. We herein investigate the potential of using Sch B to treatS.mansoni-induced liver fibrosis. Results from the present study demonstrate that Sch B is beneficial in treatingS.mansoni-induced liver fibrosis and splenic damages, through inhibition of inflammasome activation and apoptosis; and aside from that regulates host immune responses. Besides, Sch B treatment damages male adult worm in the mice, consequently helps to reduce egg production and lessen the parasite burden.

Giardia duodenalis is a zoonotic protozoan parasite causing diarrhea through waterborne or fecal-oral infection. The cysts can live in the drinking water and cause pandemic diseases. In Taiwan, very little information is available regarding the epidemiology of G. duodenalis in domestic animals. Fecal samples were collected from cattle (n = 156) and pigs (n = 141) in Hualien country, eastern Taiwan. Detection and genotyping were done by microscopy examination of fecal samples and amplification of the β-giardin gene using nested PCR. The prevalence of G. duodenalis infection was 19.87% for cattle (31/156) and 4.26% for pigs (6/141). Using nested PCR, 30 infected samples found in cattle belonged to Assemblage E, and one sample belonged to Assemblage D. For pigs, four samples belonged to Assemblage E, one belonged to Assemblage D, and another one belonged to Assemblage A. In addition, these results showed that G. duodenalis Assemblage A was detected in pigs and may cause zoonotic transmission. This is the first epidemiological investigation of G. duodenalis infection in animals in Hualien, Taiwan. These results could provide epidemiological information for disease control and public health protection.

Schistosomiasis is one of the most devastating tropical diseases in the world. Currently, praziquantel (PZQ) represents the best pharmacological option for the treatment of schistosomiasis as it effectively kills the worm. However, the inability to reverse established liver damages often makes treatment futile. In the current study, we investigate whether combining the use of wogonin, a compound that was found to be liver-protective, with PZQ can attribute to the greatest beneficial effect in Schistosoma mansoni-infected mice. To determine the protective effect of PZQ-wogonin treatment on S. manosni-infected mice, histopathological analysis was done to evaluate the granuloma size and fibrotic areas in the liver. Western blotting was performed to analyze several injuries-related markers including fibrotic markers, inflammasomes, and apoptotic markers. Scanning electron microscopy was done to evaluate the effect of wogonin on the worms, and the worm and egg burden was calculated. Our results showed that PZQ-wogonin treatment significantly improved liver histopathology of S. mansoni-infected mice. Further analysis showed that PZQ-wogonin combinations are more effective in reducing fibrosis, inflammation, and apoptosis in the liver than that of individual drug use. Furthermore, our results revealed that wogonin is anthelmintic; and it works better with PZQ in reducing hepatic egg burden, further lessen the disease progression. In general, this combinatorial strategy may represent a new and effective approach to schistosomiasis treatment.