Infectious bronchitis (IB) causes significant economic losses to commercial chicken farms due to the failures of vaccine immunization or incomplete protection. In this study, we evaluated the combination effect of Shegandilong (SGDL) granule (a traditional Chinese veterinary medicine) and doxycycline on the prevention of IBV infection and injury in the respiratory tract in broilers. A total of 126, 7-day-old broilers were randomly divided into four groups after vaccination. Group I served as a control. Broilers in Group II were given doxycycline, and Group III was given SGDL granule through drinking water. Broilers in Group IV were given SGDL granule and doxycycline by drinking water. Broilers in all groups were challenged with IBV through intraocular and intranasal routes at day 28. Results showed that the anti-IBV antibody level was higher in group IV compared with the level in other groups. Immunohistochemistry and ELISA results showed that an increase of immunoglobulin A (IgA) was observed in the trachea with the maximum level observed at day 14. In addition, SGDL granule + doxycycline effectively inhibited IBV replication and stopped IBV propagation from the trachea to the lung; modulated the mRNA expressions of IL-1β, IL-6, TNF-α, and IFN-γ; and extenuated the histopathology lesions in trachea and lung. These data imply that a combination of SGDL granule and doxycycline is effective in preventing IBV infection and respiratory tract injury in broilers.
Salmonella typhimurium (S.T) induces damage to the central nervous system; however, the role of Asiatic acid (AA) in this is still unknown. Microglia play a role as macrophages to recognize the invaded pathogenic microbes in the brain. The aim of this study was to investigate the protective effect and mechanism of AA on the central nervous system through an in vitro model of S.T infection in microglia. We pre-treated microglia with AA before S.T infection and explored the anti-infection mechanism of AA by sequencing, quantitative reverse transcription PCR (RT-qPCR), and Western blotting. Long non-coding RNA (lncRNA) sequencing demonstrated that inflammation is a major factor in S.T infection of microglia. RT-qPCR data demonstrated that AA inhibited S.T-induced increases in the mRNA levels of the pro-inflammatory factors interleukin (IL)-1β, IL-6, and IL-18. Western blotting demonstrated that AA inhibited S.T-induced activation of the nuclear factor (NF)-κB pathway and activation of the NLR family, pyrin domain-containing 3 (NLRP3) inflammasome. Expression of the lncRNA TVX1 in microglia was decreased by S.T infection and increased by pretreatment with AA. Inhibition of TVX1 expression reversed the anti-inflammatory effect of AA, and overexpression of TVX1 in microglia suppressed S.T-induced inflammation. In conclusion, AA attenuated S.T-induced microglial inflammation by upregulating the expression of the lncRNA TVX1.
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