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Background: One of the main strategies to control neonatal porcine diarrhoea (NPD) is through vaccination of the sows. This study aimed to compare the efficacy of two commercial vaccination schemes under field conditions on a farm where a C. perfringens type A cpb2-positive strain was implicated in NPD. Methods: This study was performed in a farrow-to-wean herd with 5500 sows, already using an E. coli and C. perfringens vaccine but still suffering NPD. Where the presence of a C. perfringens type A cpb2-positive strain was confirmed, Enteroporc Coli AC® (Ceva) was administrated to the sows in group A according to the manufacturer’s instructions. Sows in group B were vaccinated using two other combined commercial vaccines. In each group, piglets from 10 litters were ear-tagged and individually weighed at birth and at 8 and 22 days of age. The incidence of diarrhoea, general piglet body condition, and antimicrobial treatment were recorded within 10 consecutive days after birth. Results: A total of 234 piglets (119 in group A and 115 in group B) were included. The mean weight gain of piglets from birth to 22 days of age was significantly higher in group A (4.99 kg) than in group B (4.66 kg) (p = 0.039). The rest of the recorded parameters such as the presence of diarrhoea, the piglet’s body condition score, and the number of days with antimicrobial treatment did not differ significantly between groups. Conclusions: This study confirmed the efficiency of the Enteroporc Coli AC® vaccine in reducing clinical symptoms of diarrhoea in piglets, which was comparable with the other vaccines used in the study. The positive effect on piglets’ productive performance during the lactation phase was observed.

Microvascular endothelial cells maintain a tight barrier to prevent passage of plasma and circulating immune cells into the extravascular tissue compartment, yet endothelial cells respond rapidly to vasoactive substances, including thrombin, allowing transient paracellular permeability. This response is a cornerstone of acute inflammation, but the mechanisms responsible are still incompletely understood. Here, we demonstrate that thrombin triggers MALT1 to proteolytically cleave cylindromatosis (CYLD). Fragmentation of CYLD results in microtubule disruption and a cascade of events leading to endothelial cell retraction and an acute permeability response. This finding reveals an unexpected role for the MALT1 protease, which previously has been viewed mostly as a driver of pro-inflammatory NF-κB signaling in lymphocytes. Thus, MALT1 not only promotes immune cell activation but also acutely regulates endothelial cell biology, actions that together facilitate tissue inflammation. Pharmacologic inhibition of MALT1 may therefore have synergistic impact by targeting multiple disparate steps in the overall inflammatory response.