Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

The cytolethal distending… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

The cytolethal distending toxin of Haemophilus ducreyi aggravates dermal lesions in a rabbit model of chancroid

Artikel i vetenskaplig tidskrift
Författare Catharina Wising
Lena Mölne
Ing-Marie Jonsson
Karin Ahlman
Teresa Lagergård
Publicerad i Microbes Infect
Volym 7
Nummer/häfte 5-6
Sidor 867-74
Publiceringsår 2005
Publicerad vid Institutionen för särskilda specialiteter, Avdelningen för dermatologi och venereologi
Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Institutionen för medicinsk mikrobiologi och immunologi
Sidor 867-74
Språk en
Länkar dx.doi.org/10.1016/j.micinf.2005.02...
Ämnesord Animals, Bacterial Toxins/*toxicity, Chancroid/*pathology, Comparative Study, Haemophilus Infections/pathology, Haemophilus ducreyi/*pathogenicity, Haemophilus influenzae, Rabbits, Research Support, Non-U.S. Gov't, Skin/pathology
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

Haemophilus ducreyi, the etiologic agent of the sexually transmitted disease chancroid, produces a cytolethal distending toxin (HdCDT) that inhibits cultured cell proliferation, leading to cell death. A rabbit model of dermal infection was used to investigate the roles of H. ducreyi bacteria and HdCDT in the development, clinical appearance, and persistence of infection. A non-toxin producing H. ducreyi strain, and for comparison purposes a non-capsulated Haemophilus influenzae strain, were inoculated intradermally, with and without co-administration of purified HdCDT. Co-administration of HdCDT resulted in significant aggravation of H. ducreyi-induced inflammatory lesions, and development of ulcers in rabbit skin. Less pronounced inflammatory lesions and lack of epithelial eruption were observed after inoculation with H. influenzae. Histopathological sections of the H. ducreyi-induced lesions, in both the presence and absence of HdCDT, showed dense infiltrates of the same type inflammatory cells, with the exception of a prominent endothelial cell proliferation noted in sections from lesions caused by H. ducreyi and toxin. Signs of chronic inflammation with involvement of T cells, macrophages, eosinophils, and granuloma formation were observed after H. ducreyi inoculation both with and without toxin. In conclusion, H. ducreyi causes a pronounced, chronic inflammation with involvement of T cells and macrophages, and in combination with HdCDT production of ulcers in the rabbit model. These pathogenic mechanisms may promote the development and persistence of chancroid ulcers.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?