Bacillus amyloliquefaciens SQR9 induces dendritic cell maturation and enhances the immune response against inactivated avian influenza virus

Huang, Lulu; Qin, Tao; Yin, Yinyan; Gao, Xue; Lin, Jian; Yang, Qian; Yu, Qinghua

doi:10.1038/srep21363

Cited by 12 publications

(12 citation statements)

References 30 publications

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“…For the first randomized trial, WT mice were randomly divided into 6 groups (each group included 3 replicates, with 4 mice per replicate): 4 groups were challenged intranasally with a nonlethal dose of H1N1 virus (1000 TCID 50 ) ( 23 ) prior to treatment with AFB 1 on d 1, d 7, and d 14 as described previously ( 24 , 25 ), and the other two groups were given equivalent amounts of PBS intranasally. Among the 4 infected groups, three groups were given 10, 20, and 40 μg/kg b.w.…”

Section: Methodsmentioning

confidence: 99%

Aflatoxin B1 Promotes Influenza Replication and Increases Virus Related Lung Damage via Activation of TLR4 Signaling

Sun

Liu

et al. 2018

Front. Immunol.

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Aflatoxin B1 (AFB1), which alters immune responses to mammals, is one of the most common mycotoxins in feeds and food. Swine influenza virus (SIV) is a major pathogen of both animals and humans. However, there have been few studies about the relationship between AFB1 exposure and SIV replication. Here, for the first time, we investigated the involvement of AFB1 in SIV replication in vitro and in vivo and explored the underlying mechanism using multiple cell lines and mouse models. In vitro studies demonstrated that low concentrations of AFB1 (0.01–0.25 μg/ml) markedly promoted SIV replication as revealed by increased viral titers and matrix protein (M) mRNA and nucleoprotein (NP) levels in MDCK cells, A549 cells and PAMs. In vivo studies showed that 10–40 μg/kg of AFB1 exacerbated SIV infection in mice as illustrated by significantly higher lung virus titers, viral M mRNA levels, NP levels, lung indexes and more severe lung damage. Further study showed that AFB1 upregulated TLR4, but not other TLRs, in SIV-infected PAMs. Moreover, AFB1 activated TLR4 signaling as demonstrated by the increases of phosphorylated NFκB p65 and TNF-α release in PAMs and mice. In contrast, TLR4 knockdown or the use of BAY 11-7082, a specific inhibitor of NFκB, blocked the AFB1-promoted SIV replication and inflammatory responses in PAMs. Furthermore, a TLR4-specific antagonist, TAK242, and TLR4 knockout both attenuated the AFB1-promoted SIV replication, inflammation and lung damage in mice. We therefore conclude that AFB1 exposure aggravates SIV replication, inflammation and lung damage by activating TLR4-NFκB signaling.

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Section: Methodsmentioning

confidence: 99%

Aflatoxin B1 Promotes Influenza Replication and Increases Virus Related Lung Damage via Activation of TLR4 Signaling

Sun

Liu

et al. 2018

Front. Immunol.

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“…Indeed, activated B cells can move to the subepithelial dome of PPs, where they interact with DCs, which enhances IgA production by integrin αvβ8-mediated activation of TGF-β (54). The uptake of Bacillus amyloliquefaciens SQR9 by DCs induces the maturation and expression of CD80, CD86, CD40, MHCII, and cytokines in DCs, and secretion of SIgA (55). Also, lung CD103 + DCs and CD24 + CD11b + DCs have been shown to activate B cells through T cell-dependent or -independent pathways (56).…”

Section: Glutamine and Generation Of Intestinal Sigamentioning

confidence: 99%

Glutamine-Induced Secretion of Intestinal Secretory Immunoglobulin A: A Mechanistic Perspective

et al. 2016

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Secretory immunoglobulin A (SIgA) is one important line of defense in the intestinal mucosal surface to protect the intestinal epithelium from enteric toxins and pathogenic microorganisms. Multiple factors, such as intestinal microbiota, intestinal cytokines, and nutrients are highly involved in production of SIgA in the intestine. Recently, glutamine has been shown to affect intestinal SIgA production; however, the underlying mechanism by which glutamine stimulates secretion of intestinal SIgA is unknown. Here, we review current knowledge regarding glutamine in intestinal immunity and show that glutamine-enhanced secretion of SIgA in the intestine may involve intestinal microbiota, intestinal antigen sampling and presentation, induction pathways for SIgA production by plasma cells (both T-dependent and T-independent pathway), and even transport of SIgA. Altogether, the glutamine-intestinal SIgA axis has broad therapeutic implications for intestinal SIgA-associated diseases, such as celiac disease, allergies, and inflammatory bowel disease.

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“…Currently, there is increasing interest in the development of lactic acid bacteria (LAB)-based oral vaccines against enteric viruses; this approach is crucial for the effective induction of a mucosal immune response. Lactobacillus strains have many characteristics that make them promising candidates as delivery systems for presenting compounds with antigens of interest to the mucosa, in particular vaccines [ 5 ]; for example, Lactobacilli can survive in (and colonize) the upper gastrointestinal tract and exert an intrinsic adjuvant activity [ 6 , 7 ]. Moreover, recent reports have shown that Lactobacillus species can effectively elicit production of secretory immunoglobulin A (SIgA), induce anti-inflammatory responses, activate innate cells, and regulate the balance between T cell subset responses [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Oral Delivery of Probiotics Expressing Dendritic Cell-Targeting Peptide Fused with Porcine Epidemic Diarrhea Virus COE Antigen: A Promising Vaccine Strategy against PEDV

Wang

Huang

et al. 2017

Viruses

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Porcine epidemic diarrhea virus (PEDV), an enteric coronavirus, is the causative agent of porcine epidemic diarrhea (PED) that damages intestinal epithelial cells and results in severe diarrhea and dehydration in neonatal suckling pigs with up to 100% mortality. The oral vaccine route is reported as a promising approach for inducing protective immunity against PEDV invasion. Furthermore, dendritic cells (DCs), professional antigen-presenting cells, link humoral and cellular immune responses for homeostasis of the intestinal immune environment. In this study, in order to explore an efficient oral vaccine against PEDV infection, a mucosal DC-targeting oral vaccine was developed using Lactobacillus casei to deliver the DC-targeting peptide (DCpep) fused with the PEDV core neutralizing epitope (COE) antigen. This probiotic vaccine could efficiently elicit secretory immunoglobulin A (SIgA)-based mucosal and immunoglobulin G (IgG)-based humoral immune responses via oral vaccination in vivo. Significant differences (p < 0.05) in the immune response levels were observed between probiotics expressing the COE-DCpep fusion protein and COE antigen alone, suggesting better immune efficiency of the probiotics vaccine expressing the DC-targeting peptide fused with PEDV COE antigen. This mucosal DC-targeting oral vaccine delivery effectively enhances vaccine antigen delivery efficiency, providing a useful strategy to induce efficient immune responses against PEDV infection.

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Bacillus amyloliquefaciens SQR9 induces dendritic cell maturation and enhances the immune response against inactivated avian influenza virus

Cited by 12 publications

References 30 publications

Aflatoxin B1 Promotes Influenza Replication and Increases Virus Related Lung Damage via Activation of TLR4 Signaling

Aflatoxin B1 Promotes Influenza Replication and Increases Virus Related Lung Damage via Activation of TLR4 Signaling

Glutamine-Induced Secretion of Intestinal Secretory Immunoglobulin A: A Mechanistic Perspective

Oral Delivery of Probiotics Expressing Dendritic Cell-Targeting Peptide Fused with Porcine Epidemic Diarrhea Virus COE Antigen: A Promising Vaccine Strategy against PEDV

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