The host immune response to Clostridium difficile

Kelly, Ciarán P.; Kyne, Lorraine

doi:10.1099/jmm.0.030015-0

Cited by 167 publications

(151 citation statements)

References 94 publications

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“…Current vaccine approaches have focused on humoral immunity and neutralization of toxins A and B, which are considered the primary virulence factors (8,9). Thus, vaccines currently in clinical evaluation use parenteral administration of toxoids (A and B) or defined segments of them (10).…”

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confidence: 99%

Mucosal Antibodies to the C Terminus of Toxin A Prevent Colonization of Clostridium difficile

et al. 2017

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Mucosal immunity is considered important for protection against Clostridium difficile infection (CDI). We show that in hamsters immunized with Bacillus subtilis spores expressing a carboxy-terminal segment (TcdA 26 -39 ) of C. difficile toxin A, no colonization occurs in protected animals when challenged with C. difficile strain 630. In contrast, animals immunized with toxoids showed no protection and remained fully colonized. Along with neutralizing toxins, antibodies to TcdA 26 -39 (but not to toxoids), whether raised to the recombinant protein or to TcdA 26 -39 expressed on the B. subtilis spore surface, cross-react with a number of seemingly unrelated proteins expressed on the vegetative cell surface or spore coat of C. difficile. These include two dehydrogenases, AdhE1 and LdhA, as well as the CdeC protein that is present on the spore. Anti-TcdA 26 -39 mucosal antibodies obtained following immunization with recombinant B. subtilis spores were able to reduce the adhesion of C. difficile to mucus-producing intestinal cells. This cross-reaction is intriguing yet important since it illustrates the importance of mucosal immunity for complete protection against CDI.

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confidence: 99%

Mucosal Antibodies to the C Terminus of Toxin A Prevent Colonization of Clostridium difficile

et al. 2017

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“…La letteratura è univoca nel considerare le CDI sequele del trattamento antibiotico [2,4,10,38,39,[42][43][44][45][46][52][53][54] e antisecretivo gastrico [47][48][49][50][52][53][54], singoli o associati, e dello status nutrizionale-immunologico del paziente [55,56].…”

Section: Discussioneunclassified

“…La storia naturale dell'infezione intestinale da C. difficile è ben conosciuta [52][53][54]. C. difficile sotto forma di spore è saprofita umano, diventa virulento in condizioni particolari (riduzione delle difese immunitarie, patologie attive, traumi) con la trasformazione delle spore in forme batteriche attive che producono tossine capaci di determinare il quadro clinico, determinato da: y status immunitario del paziente [55,56]; y microbiota intestinale del paziente [2,4,14,57]. I pazienti portatori anche di forma attiva del C. difficile con assetto immunitario competente e normale microbiota intestinale non sviluppano la malattia, ma rimangono nello stato di colonizzati [31,38,39].…”

Section: Introduzioneunclassified

Fidaxomicin in the treatment of colitis due to Clostridium difficile: preliminary results

Cortese

Meledandri

Ballardini

et al. 2014

CMI

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5y sostenute, anche nello stesso ambito ospedaliero, da ceppi batterici differenti anche con diversa virulenza [21][22][23][24][25]; y complicanze di percorsi clinici intensivi, chirurgici, internistici spesso combinati tra loro [26][27][28][29][30][31][32]; y caratterizzate dalla necessità di intraprendere misure ospedaliere logistiche articolate come l'isolamento dei pazienti [33,34]; y causa di incremento dei costi di ricovero [35,36]. La CDI non è quasi mai un'infezione de novo, ma colpisce soggetti con patologie attive o nel decorso di procedure diagnosticooperative spesso articolate. Sono stati indi- INTRODUZIONEClostridium difficile è un bacillo Gram-positivo, anaerobio e sporigeno. La sua azione patogena si esplica nel 99% dei casi nella colite [1], che configura la Clostridium difficile Infection (CDI) [2][3][4]. Questa condizione rappresenta una vera e propria sindrome in costante e importante incremento in tutto il mondo occidentale [5][6][7][8][9]. Le CDI sono: y nella stragrande maggioranza dei casi infezioni nosocomiali di pazienti complessi nei quali aumentano morbilità e mortalità [10][11][12][13][14][15]; y causa di sindromi differenti con coefficienti di gravità diversi [16][17][18][19][20];

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“…Interestingly, individuals infected with the same C. difficile strain can respond very differently. While the mechanism has not been elucidated, it has been linked to development of antibodies against TcdA and/or TcdB [61,62] . However, this theory has come into question due to the increasing recurrence rates, with recent literature demonstrating that asymptomatic carriers and diseased patients having similar antibody loads towards the toxins [63] .…”

Section: Epidemiology and Risk Factors For CDImentioning

confidence: 99%

Gastrointestinal dysbiosis and the use of fecal microbial transplantation inClostridium difficileinfection

Schenck

Beck

MacDonald

2015

WJGP

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The impact of antibiotics on the human gut microbiota is a significant concern. Antibiotic-associated diarrhea has been on the rise for the past few decades with the increasing usage of antibiotics. Clostridium difficile infections (CDI) have become one of the most prominent types of infectious diarrheal disease, with dramatically increased incidence in both the hospital and community setting worldwide. Studies show that variability in the innate host response may in part impact upon CDI severity in patients. That being said, CDI is a disease that shows the most prominent links to alterations to the gut microbiota, in both cause and treatment. With recurrence rates still relatively high, it is important to explore alternative therapies to CDI. Fecal microbiota transplantation (FMT) and other types of bacteriotherapy have become exciting avenues of treatment for CDI. Recent clinical trials have generated excitement for the use of FMT as a therapeutic option for CDI; however, the exact components of the human gut microbiota needed for protection against CDI have remained elusive. Additional investigations on the effects of antibiotics on the human gut microbiota and subsequent CDI will help reduce the socioeconomic burden of CDI and potentially lead to new therapeutic modalities.

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The host immune response to Clostridium difficile

Cited by 167 publications

References 94 publications

Mucosal Antibodies to the C Terminus of Toxin A Prevent Colonization of Clostridium difficile

Mucosal Antibodies to the C Terminus of Toxin A Prevent Colonization of Clostridium difficile

Fidaxomicin in the treatment of colitis due to Clostridium difficile: preliminary results

Gastrointestinal dysbiosis and the use of fecal microbial transplantation inClostridium difficileinfection

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