Protective antibody responses against<i>Clostridium difficile</i>elicited by a DNA vaccine expressing the enzymatic domain of toxin B

Jin, Ke; Wang, Shixia; Zhang, Chunhua; Xiao, Yanling; Lu, Shan; Huang, Zhibin

doi:10.4161/hv.22434

Cited by 26 publications

(32 citation statements)

References 37 publications

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“…38 The N terminus encompassing the GTD and CPD domains is more conserved between historical and epidemic strains. In our previous study 37 and consistent with others, 35,36 we indicated that the N-terminus of TcdB was able to elicit a protective antibody response. In contrast, the RBD of TcdA has potent adjuvant activity 40 , and has been used as vaccine candidates in several studies.…”

Section: Discussionsupporting

confidence: 61%

“…25,[32][33][34] Recent studies have indicated that the N-terminal GT domain of TcdB can serve as an excellent immunogen. 35,36 This notion was initially supported by our recent construction of a chimeric recombinant vaccine against TcdA and TcdB, i.e., cTxAB, in which the original RBD of a full-length TcdB was replaced with the corresponding portion of TcdA. 37 cTxAB is protective in animal models.…”

Section: Introductionmentioning

confidence: 79%

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A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

Wang

Yan

Kim

et al. 2015

Human Vaccines & Immunotherapeutics

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Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 79%

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

Wang

Yan

Kim

et al. 2015

Human Vaccines & Immunotherapeutics

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“…DNA vaccines comprising either the gene fragments from the glucosyltransferase substrate binding domain from TcdB or the receptor binding domain from TcdA have also been shown to provide a degree of protection in a toxin challenge model in mice [Jin et al 2012], and were able to increase the level of protection when administered in combination with anti-TcdA passive immunotherapy.…”

Section: Parenteral Passive Immunotherapymentioning

confidence: 99%

The host immune response to Clostridium difficile infection

Solomon

2013

Therapeutic Advances in Infection

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Clostridium difficile infection (CDI) is the most common infectious cause of healthcare-acquired diarrhoea. Outcomes of C. difficile colonization are varied, from asymptomatic carriage to fulminant colitis and death, due in part to the interplay between the pathogenic virulence factors of the bacterium and the counteractive immune responses of the host.Secreted toxins A and B are the major virulence factors of C. difficile and induce a profound inflammatory response by intoxicating intestinal epithelial cells causing proinflammatory cytokine release. Host cell necrosis, vascular permeability and neutrophil infiltration lead to an elevated white cell count, profuse diarrhoea and in severe cases, dehydration, hypoalbuminaemia and toxic megacolon. Other bacterial virulence factors, including surface layer proteins and flagella proteins, are detected by host cell surface signal molecules that trigger downstream cell-mediated immune pathways.Human studies have identified a role for serum and faecal immunoglobulin levels in protection from disease, but the recent development of a mouse model of CDI has enabled studies into the precise molecular interactions that trigger the immune response during infection. Key effector molecules have been identified that can drive towards a protective anti-inflammatory response or a damaging proinflammatory response.The limitations of current antimicrobial therapies for CDI have led to the development of both active and passive immunotherapies, none of which have, as yet been formally approved for CDI. However, recent advances in our understanding of the molecular basis of host immune protection against CDI may provide an exciting opportunity for novel therapeutic developments in the future.

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“…Formalin inactivation and genetically engineered inactive toxin variants are an option, as is the delivery of immunogenic non-toxin proteins. DNA vaccines that express Clostridium toxins, but not C. perfringens toxins, have also been tested as vaccine candidates (Saikh et al, 1998;Gardiner et al, 2009;Li et al 2011;Jin et al, 2013).…”

Section: An Overview Of Vaccination Studies Against Necrotic Enteritismentioning

confidence: 99%

Progress and problems in vaccination against necrotic enteritis in broiler chickens

et al. 2014

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Necrotic enteritis in broilers is caused by Clostridium perfringens type A strains that produce the NetB toxin. Necrotic enteritis is one of the gastrointestinal diseases in poultry that has gained worldwide importance during the last decade due to efforts to improve broiler performance. Prevention strategies include avoiding predisposing factors, such as coccidiosis, and in-feed supplementation with a variety of feed additives. However, vaccination with modified toxin or other secreted immunogenic proteins seems a logical preventive tool for protection against a toxin-producing bacterium. Formalin-inactivated crude supernatant has been used initially for vaccination. Several studies have been carried out recently to identify the most important immunogenic and protective proteins that can be used for vaccination. These include the NetB toxin, as well as a number of other proteins. There is evidence that immunization with single proteins is not protective against severe challenge and that combinations of different antigens are needed. Most published studies have used multiple dosage vaccination regimens that are not relevant for practical use in the broiler industry. Single vaccination regimens for 1-day-old chicks appear to be non-protective. This review describes the history of vaccination strategies against necrotic enteritis in broilers and gives an update on future vaccination strategies that are applicable in the field. These may include breeder hen vaccination, in ovo vaccination and live attenuated vectors to be used in feed or in drinking water

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Protective antibody responses againstClostridium difficileelicited by a DNA vaccine expressing the enzymatic domain of toxin B

Cited by 26 publications

References 37 publications

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

A chimeric protein comprising the glucosyltransferase and cysteine proteinase domains of toxin B and the receptor binding domain of toxin A induces protective immunity againstClostridium difficileinfection in mice and hamsters

The host immune response to Clostridium difficile infection

Progress and problems in vaccination against necrotic enteritis in broiler chickens

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