Abstract
Haemophilus parasuis (H. parasuis) is the causative agent of Glässer’s disease, a severe membrane inflammation disorder. Previously we showed that Baicalin (BA) possesses anti-inflammatory effects via the NLRP3 inflammatory pathway in an LPS-challenged piglet model. However, whether BA has anti-inflammatory effects upon H. parasuis infection is still unclear. This study investigated the anti-inflammatory effects and mechanisms of BA on H. parasuis-induced inflammatory responses via the NF-κB and NLRP3 inflammasome pathway in piglet mononuclear phagocytes (PMNP). Our data demonstrate that PMNP, when infected with H. parasuis, induced ROS (reactive oxygen species) production, promoted apoptosis, and initiated transcription expression of IL-6, IL-8, IL-10, PGE2, COX-2 and TNF-α via the NF-κB signaling pathway, and IL-1β and IL-18 via the NLRP3 inflammasome signaling pathway. Moreover, when BA was administrated, we observed a reduction in ROS production, suppression of apoptosis, and inhibition of the activation of NF-κB and NLRP3 inflammasome signaling pathway in PMNP treated with H. parasuis. To our best knowledge, this is the first example that uses piglet primary immune cells for an H. parasuis infection study. Our data strongly suggest that BA can reverse the inflammatory effect initiated by H. parasuis and possesses significant immunosuppression activity, which represents a promising therapeutic agent in the treatment of H. parasuis infection.
Highlights
Haemophilus parasuis (H. parasuis), is the causative agent of Glässer’s disease, whose typical clinical characteristics include polyarthritis, fibrinous polyserositis and meningitis [1]
When the multiplicity of infection (MOI) was 2:1 and 20:1 and the cells were stimulated for 6 h, the concentration of IL-1β, TNF-α and IL-18 in the cell culture supernatant increased compared with the control cells (p < 0.01) (Figure 2)
The results show that the levels of IL-6, IL-8, IL-10, PGE2, COX-2, IL-1β, IL-18, and TNF-α in the cell culture were markedly increased in the cells stimulated with H. parasuis compared with the control (p < 0.05) (Figures 3A–H)
Summary
Haemophilus parasuis (H. parasuis), is the causative agent of Glässer’s disease, whose typical clinical characteristics include polyarthritis, fibrinous polyserositis and meningitis [1]. H. parasuis has become one of the most important pathogens of livestock worldwide and has caused gross economic losses owing to the expensive antibiotic treatment and the high mortality in piglets [2]. Fifteen serovars of H. parasuis have been identified so far [3]. H. parasuis is a normal inhabitant of the upper respiratory tract. A previous study has shown that H. parasuis or its cell wall lipooligosaccharides can initiate innate immune response and induce the production of inflammatory cytokines IL-6 and IL-8 in porcine brain microvascular endothelial cells (PBMEC) and tracheal cells [7, 8]. H. parasuis can activate the inflammatory transcription factor, nuclear factor-kappa B (NF-κB), in a time and dose-dependent manner and cause the release
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