The role of 2'-5'-oligoadenylate synthase-like protein (OASL1) in biliary and hepatotoxin-induced liver injury in mice.

Following an injury, the liver embarks on a process that drives the accumulation and reformation of the extracellular matrix, leading to hepatic fibrosis. Type I interferons (IFNs), including IFN-α and IFN-ß, play a crucial role in averting chronic liver injury through the activation of IFN-stimulated genes (ISGs), which are instrumental in sculpting adaptive immunity. The role of 2'-5'-oligoadenylate synthase-like protein 1 (OASL1), an antiviral ISG, in the context of liver fibrosis remains to be elucidated. To elicit liver fibrosis, a diet containing 0.1% diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl4) were employed to induce cholestatic- and hepatotoxin-mediated liver fibrosis, respectively. Histological analyses of both models revealed that OASL1-/- mice exhibited reduced liver damage and, consequently, expressed lower levels of fibrotic mediators, notably α-smooth muscle actin. OASL1-/- mice demonstrated significantly elevated IFN-α and IFN-ß mRNA levels, regulated by the IFN regulatory factor 7 (IRF7). Additionally, OASL1-/- ameliorated chronic liver fibrosis through the modulation of nuclear factor-κB (NF-κB) signaling. The effect of OASL1 on type I IFN production in acute liver damage was further explored and OASL1-/- mice consistently showed lower alanine transaminase levels and pro-inflammatory cytokines, but IFN-α and IFN-ß mRNA levels were upregulated, leading to amelioration of acute liver injury. Additionally, the study discovered that F4/80-positive cells were observed more frequently in OASL1-/- CCl4 acutely treated mice. This implies that there is a significant synergy in the function of macrophages and OASL1 deficiency. These results demonstrate that in instances of liver injury, OASL1 inhibits the production of type I IFN by modulating the NF-κB signaling pathway, thereby worsening disease.

The presence of anthracosis is associated with the environmental air quality of zoo, wildlife, and companion animals in Jeollabuk-do Province, South Korea.

OBJECTIVE: To determine pulmonary anthracosis in zoo, wildlife, and companion animals of Jeollabuk-do Province, South Korea. ANIMALS: A total of 350 animals of 61 different species, belonging to 3 classes (mammals: n = 38; avian: 21; and reptiles: 2) from different habitats in Jeollabuk-do Province, were examined. PROCEDURES: Gross lung examination and tissue sampling were done at postmortem, and histopathological analysis was microscopically done on hematoxylin and eosin-stained slides. RESULTS: Macroscopic analysis of anthracotic lung tissue revealed minute (pinpoint size) spots and black pigmentation in a scattered and/or coalescing fashion. The presence of carbon particles was noted in 154 (44%, 154/350) cases. Based on habitation, zoo animals had the highest frequency of anthracosis in the lung (55.2%, 69/125), followed by companion animals (45.2%, 56/124) and wildlife animals (28.7%, 29/101). There was an association between habitation and the presence of anthracosis (P < .05). CLINICAL RELEVANCE: This study revealed evidence that the presence of anthracosis is associated with the environmental air quality of zoo, wildlife, and companion animals in Jeollabuk-do Province, South Korea. Air pollution may affect the respiratory health of the endangered species at the Jeonju Zoo as well as the human population. Continuous monitoring of particulate matter and establishing policies that control industrialization around the province would enable quick action to curb any potential respiratory health risks to animals kept in the urban cities of the province.