Abstract
The present study evaluated the avian macrophage responses against Clostridium perfringens that varied in their ability to cause necrotic enteritis in chickens. Strains CP5 (avirulent-netB+), CP1 (virulent-netB+), and CP26 (highly virulent-netB+tpeL+) were used to evaluate their effect on macrophages (MQ-NCSU cells) and primary splenic and cecal tonsil mononuclear cells. The bacilli (whole cells) or their secretory products from all three strains induced a significant increase in the macrophage transcription of Toll-like receptor (TLR)21, TLR2, interleukin (IL)-1β, inducible nitric oxide synthase (iNOS), and CD80 genes as well as their nitric oxide (NO) production and major histocompatibility complex (MHC)-II surface expression compared to an unstimulated control. The CP1 and CP26-induced expression of interferon (IFN)γ, IL-6, CD40 genes, MHC-II upregulation, and NO production was significantly higher than that of CP5 and control groups. Furthermore, splenocytes and cecal tonsillocytes stimulated with bacilli or secretory products from all the strains showed a significant increase in the frequency of macrophages, their surface expression of MHC-II and NO production, while CP26-induced responses were significantly higher for the rest of the groups. In summary, macrophage interaction with C. perfringens can lead to cellular activation and, the ability of this pathogen to induce macrophage responses may depend on its level of virulence.
Highlights
Innate immune defense forms an integral component of host immunity against infectious agents
The findings showed that the interaction of macrophages with C. perfringens can induce cellular activation, and the ability of this pathogen to activate macrophages depended on the level of virulence with the two necrotic enteritis (NE)-producing strains used in the present study inducing a more robust macrophage activation than the avirulent strain
The present study’s findings showed that bacilli from all three strains induced a significant increase in the transcription of TLR21 and TLR2 receptors, IL-6 and IL-1β cytokines, and CD80 costimulatory genes in macrophages compared to an unstimulated control
Summary
Innate immune defense forms an integral component of host immunity against infectious agents. The importance of macrophages in the defense against several bacterial pathogens [2,3], including those affecting chickens such as avian pathogenic Escherichia coli [4], have been reported. Virulent strains of Clostridium perfringens cause necrotic enteritis (NE) in chickens, an economically important disease affecting poultry worldwide. We have previously shown that antibodies to alphatoxin and certain metabolic enzymes and proteins are important in NE immunity and these proteins may have a role in NE pathogenesis [9,10]. The pathogenesis of NE is complex, and while NetB has been shown to be a critical virulence factor, TpeL toxin has been reported to enhance the virulence of some netB+ C. perfringens strains [11,12]. Recent reports suggest that there are NE-causing unique strains that possess certain signature
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