lithium-chloride and Swine-Diseases

Porcine contagious pleuropneumonia (PCP) is a very serious respiratory disease which is difficult to prevent and treat. In this study, the therapeutic effects of lithium chloride (LiCl) on PCP were examined using a mouse model. A mouse model of PCP was established by intranasal infections with Actinobacillus pleuropneumoniae (App). Histopathological analysis was performed by routine paraffin sections and an H-E staining method. The inflammatory factors, TLR4 and CCL2 were analyzed by qPCR. The expression levels of p-p65 and pGSK-3ß were detected using the Western Blot Method. The death rates, clinical symptoms, lung injuries, and levels of TLR-4, IL-1ß, IL-6, TNF-α, and CCL2 were observed to decrease in the App-infected mice treated with LiCl. It was determined that the LiCl treatments had significantly reduced the mortality of the App-infected cells, as well as the expressions of p-p65 and pGSK-3ß. The results of this study indicated that LiCl could improve the pulmonary injuries of mice caused by App via the inhibition of the GSK-3β-NF-κB-dependent pathways, and may potentially become an effective drug for improving pulmonary injuries caused by PCP.

Topics: Actinobacillus pleuropneumoniae; Animals; Glycogen Synthase Kinase 3 beta; Lithium Chloride; Lung Injury; NF-kappa B; Swine; Swine Diseases

Pseudorabies virus (PRV) is a swine herpesvirus with a broad host range that causes significant economic losses worldwide. The Wnt/β-catenin signaling pathway is reportedly involved in multiple viruses' proliferation. In this study, we demonstrated that PRV infection significantly activated the Wnt/β-catenin signaling and promoted the nuclear translocation of β-catenin. Applying specific chemical inhibitors (FH535 and iCRT14) caused a remarkable decrease in PRV titers in various cell lines. Knockdown of β-catenin by siRNA also reduced the proliferation of PRV. On the contrary, treatment with lithium chloride (LiCl), an inhibitor of GSK3β, stimulated the Wnt/β-catenin signaling pathway and enhanced the PRV proliferation. Similarly, overexpression of β-catenin promoted PRV proliferation and reversed the antiviral effect of FH535. Moreover, LiCl promoted PRV-induced autophagy, whereas FH535 and iCRT14 showed converse effects. These findings suggest that PRV infection stimulates the canonical Wnt/β-catenin signaling pathway, facilitating PRV proliferation and regulating virus-induced autophagy. These data also provide potential targets for developing antiviral agents against PRV.

Topics: Animals; Autophagy; beta Catenin; Cell Proliferation; Herpesvirus 1, Suid; Lithium Chloride; Pseudorabies; Swine; Swine Diseases; Wnt Signaling Pathway

Porcine epidemic diarrhea virus (PEDV), a member of the Coronaviridae family, causes acute diarrhea, vomiting, dehydration, and high mortality rates in neonatal piglets. Severe outbreaks of PEDV variants have re-emerged in Asia and North America since 2010, causing tremendous economic losses to the swine industry. The lack of effective therapeutic treatment promotes the research for new antivirals. Lithium chloride (LiCl) has been reported as a potential antiviral drug for certain viruses. In this study, the antiviral effect of LiCl on PEDV in Vero cells was evaluated. Real-time quantitative PCR and indirect immunofluorescence assay indicated that LiCl effectively inhibited the entry and replication of PEDV in Vero cells. The expression of viral RNA and protein of PEDV in Vero cells was suppressed in a dose-dependent manner by LiCl. Moreover, addition of LiCl inhibited both early and late cell apoptosis induced by PEDV. Our data implied that LiCl could be a potential antiviral drug against PEDV infection. Further studies are required to explore the antiviral effect of lithium chloride on PEDV infection in vivo.

Topics: Animals; Antiviral Agents; Chlorocebus aethiops; Coronavirus Infections; In Vitro Techniques; Lithium Chloride; Porcine epidemic diarrhea virus; Swine; Swine Diseases; Vero Cells

Porcine parvovirus (PPV) causes reproductive failure in pigs, which leads to economic losses to the industry. As reported previously, LiCl efficiently impairs the replication of a variety of viruses, including the coronavirus infectious bronchitis virus (IBV), transmissible gastroenteritis virus (TGEV), and pseudorabies herpesvirus. We demonstrate for the first time that inhibition of PPV replication in swine testis (ST) cells by LiCl is dose-dependent, and that the antiviral effect of LiCl occurred in the early phase of PPV replication. These results indicate that LiCl might be an effective anti-PPV drug to control PPV disease. Further studies are required to explore the mechanism of the antiviral effect of LiCl on PPV infection in vivo.

Topics: Animals; Antiviral Agents; Cell Line; Lithium Chloride; Parvoviridae Infections; Parvovirus, Porcine; Swine; Swine Diseases; Virus Attachment; Virus Replication

CaCl2 and LiCl cell extracts and a crude hemolysin preparation were isolated from Actinobacillus pleuropneumoniae serotype 1 strain 4074 and tested for protection against A. pleuropneumoniae serotype 1 and 5 in mice. The LiCl cell extract adsorbed on AlPO4 and the crude hemolysin preparation adsorbed on Al(OH)3 showed a highly significant protection (P < 0.01) against both serotypes. Different vaccine preparations were used to immunize pigs by intra-muscular injection at days 0 and 14; the pigs were then challenged at day 21 by intra-tracheal inoculation of 1 x 10(8) colony forming units (CFU) of a serotype 1 strain 4074. A vaccine which combined the LiCl extract and the crude hemolysin preparation adsorbed on Al(OH)3 gave the best protection with no mortality and no sign of morbidity in the vaccinated pigs. In the other experimental groups which included a group immunized with a commercial bacterin, mortality, respiratory disease and extensive pulmonary lesions were noted. This mixture shows good potential as a vaccine against pleuropneumonia in pigs.

Topics: Actinobacillus Infections; Actinobacillus pleuropneumoniae; Animals; Bacterial Proteins; Bacterial Vaccines; Calcium Chloride; Disease Models, Animal; Hemolysin Proteins; Lithium Chloride; Male; Mice; Swine; Swine Diseases; Vaccination; Virulence