کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3395014 1592833 2014 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Host recognition of Clostridium difficile and the innate immune response
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
Host recognition of Clostridium difficile and the innate immune response
چکیده انگلیسی


• Clostridium difficile infection (CDI) is primarily mediated by Toxins A and B.
• Toxins A and B induce pro-inflammatory signaling within the host.
• Multiple Pattern Recognition Receptors (PRRs) also contribute to inflammation.
• Intoxication models show inflammatory signaling can be pathogenic.
• Infection models show that some level of inflammation is required for disease resolution.

Clostridium difficile is a Gram-positive, spore forming bacillus and the most common cause of antibiotic-associated diarrhea in the United States. Clinical outcomes of C. difficile infection (CDI) range from asymptomatic colonization to pseudomembranous colitis, sepsis and death. Disease is primarily mediated by the action of the Rho-glucosylating toxins A and B, which induce potent pro-inflammatory signaling within the host. The role of this inflammatory response during infection is just beginning to be appreciated, with recent data suggesting inflammatory markers correlate closely with disease severity. In addition to the toxins, multiple innate immune signaling pathways have been implicated in establishing an inflammatory response during infection. In intoxication-based models of disease, inflammation typically enhances pathogenesis, while protection from infection seems to require some level of inflammatory response. Thus, the host immune response plays a key role in shaping the course of infection and a balanced inflammatory response which eradicates infection without damaging host tissues is likely required for successful resolution of disease.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Anaerobe - Volume 30, December 2014, Pages 205–209
نویسندگان
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