Background: The main targets of the host’s immune system inTrichinella spiralisinfection are the adult worms (AW), at the gut level, and the migrant or newborn larvae (NBL), at systemic and pulmonary levels. Most of the studies carried out in the gut mucosa have been performed on the Payer’s patches and/or the mesenteric lymph nodes but not on the lamina propria, therefore, knowledge on the gut immune response againstT. spiralisremains incomplete.Methods: This study aimed at characterizing the early mucosal immune response againstT. spiralis, particularly, the events taking place between 1 and 13 dpi. For this purpose, Wistar rats were orally infected with muscle larvae ofT. spiralisand the humoral and cellular parameters of the gut immunity were analysed, including the evaluation of the ADCC mechanism exerted by lamina propria cells.Results: A marked inflammation and structural alteration of the mucosa was found. The changes involved an increase in goblet cells, eosinophils and mast cells, and B and T lymphocytes, initially displaying a Th1 profile, characterised by the secretion of IFN-γ and IL-12, followed by a polarization towards a Th2 profile, with a marked increase in IgE, IgG1, IL-4, IL-5 and IL-13 levels, which occurred once the infection was established. In addition, the helminthotoxic activity of lamina propria cells demonstrated the role of the intestine as a place of migrant larvae destruction, indicating that not all the NBLs released in the gut will be able to reach the muscles.Conclusions: The characterization of the immune response triggered in the gut mucosa duringT. spiralisinfection showed that not only an effector mechanism is directed toward the AW but also towards the NBL as a cytotoxic activity was observed against NBL exerted by lamina propria cells.

New antiviral treatments are needed to deal with the unpredictable emergence of viruses. Furthermore, vaccines and antivirals are only available for just a few viral infections, and antiviral drug resistance is an increasing concern. Cyanidin (a natural product also called A18), a key flavonoid that is present in red berries and other fruits, attenuates the development of several diseases, through its anti-inflammatory effects. Regarding its mechanism of action, A18 was identified as an IL-17A inhibitor, resulting in the attenuation of IL-17A signaling and associated diseases in mice. Importantly, A18 also inhibits the NF-κB signaling pathway in different cell types and conditions in vitro and in vivo. In this study, we report that A18 restricts RSV, HSV-1, canine coronavirus, and SARS-CoV-2 multiplication, indicating a broad-spectrum antiviral activity. We also found that A18 can control cytokine and NF-κB induction in RSV-infected cells independently of its antiviral activity. Furthermore, in mice infected with RSV, A18 not only significantly reduces viral titers in the lungs, but also diminishes lung injury. Thus, these results provide evidence that A18 could be used as a broad-spectrum antiviral and may contribute to the development of novel therapeutic targets to control these viral infections and pathogenesis.

After intestinal or multivisceral transplant, closing the abdominal wall can be challenging, as negative pressure dressing or synthetic meshes pose risks like infections and fistulas. Clinical practice has evolved from vascularized abdominal wall transplants to non-vascularized Abdominal Rectus Fascia (TxARF). Although it was successful, many immunological aspects remain unknown, highlighting the need for further research. The technique was developed by reproducing the technical aspects of the procedure described for humans in rats (Wistar and Sprague Dawley). Twenty-six Isogenic and Allogeneic TxARF procedures were performed and followed until 30 and 120 post-transplant days (PTD). The non-implanted fascias served as a control group. Rats were then re-assessed for engraftment on 7, 11, 30 and 120 PTD. Fascia samples were taken to assess neovascularization by quantifying cell composition and blood vessels using H&E and Orcein staining. All animals (N=26) survived at 30 and 120 PTD, with 4 (15.4 %) developed subcutaneous serum collection. Upon reoperation, grafts showed neovascularization. No adhesions were observed between the intestines and the grafts. The principal cell compound of the fascia was represented by Fibroblasts (18.35 cells/field) and Myocytes (6.57 cells/field). A significant increment of the number of blood vessels were observed during the period studied (p=0.046). Our report on TxARF in rats, proves the feasibility of this experimental and translational model, showing similar results to those published in the clinical field. Further studies are required to evaluate the immunogenicity as well as the changes in ARF overtime.