Background: Eimeria spp. are responsible for chicken coccidiosis which is the most important enteric protozoan disease resulting in tremendous economic losses in the poultry industry. Understanding the interaction between the avian cecal microbiota and coccidia is of interest in the development of alternative treatments that do not rely on chemotherapeutics and do not lead to drug resistance. Methods: We utilized 16S rRNA gene sequencing to detect the dynamics of the cecal microbial community in AA broilers challenged with Eimeria tenella. Histopathological analysis of the cecum was also conducted. Results: We found that microbial shifts occur during the infection. Lactobacillus, Faecalibacterium, Ruminococcaceae UCG-013, Romboutsia and Shuttleworthia decreased in abundance. However, the opportunistic pathogens Enterococcus and Streptococcus increased in abundance over time in response to the infection. Conclusions: Eimeria tenella disrupts the integrity of the cecal microbiota and could promote the establishment and growth of potentially pathogenic bacteria. Defining bacterial populations affected by coccidial infection might help identify bacterial markers for intestinal disease as well as populations or species that could be beneficial in maintaining and restoring gut homeostasis during and after infection with E. tenella.

Trichinellosis is an important foodborne zoonosis, and no effective treatments are yet available. Nod-like receptor (NLR) plays a critical role in the host response against nematodes.

Background: Trichinellosis is an important food-borne zoonosis, and no effective treatments are yet available. Nod-like receptor plays a critical role in the host response against nematodes. Therefore, we aimed to explore the role of the NLRP3 inflammasome (NLRP3) during the adult, migrating, and encysted stages of Trichinella spiralis (T. spiralis) infection. Methods: The mice were treated with the specific NLRP3 inhibitor MCC950 after inoculation with T. spiralis. Then, NLRP3 plays the role in T. spiralis-infected mice were evaluated using ELISA, Western blotting, Flow cytometry, Histopathological evaluation, Bone marrow-derived macrophage (BMDM) stimulation and immunofluorescenceResults: The in vivo results showed that NLRP3 enhanced the Th1 immune response in the adult stage and the migrating stage and weakened the Th2 immune response in the encysted stage. NLRP3 promoted the release of proinflammatory factors (INF-γ) and suppressed the release of anti-inflammatory factors (IL-4). Pathological changes were also improved in the absence of NLRP3 in mice during T. spiralis infection. Importantly, a significant reduction in adult worm burden and muscle larvae burden at 7 and 35 days post infection was observed in mice treated with the specific NLRP3 inhibitor MCC950. In vitro, we first demonstrated that NLRP3 in macrophages can be activated by T. spiralis proteins and promotes IL-1β and IL-18 release. Conclusions: This study revealed that the NLRP3 is involved in the host response to T. spiralis infection and that targeted inhibition of NLRP3 enhanced the Th2 response and accelerated T. spiralis expulsion. These findings may help in the development of protocols for controlling trichinellosis.