Till sidans topp

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

Tipsa en vän
Utskriftsversion

The role of IL-17A and IF… - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

The role of IL-17A and IFN gamma in vaccine-induced protection against Helicobacter pylori infection

Paper i proceeding
Författare Louise Sjökvist Ottsjö
Carl-Fredrik Flach
Staffan Nilsson
R. D. Malefyt
A. Walduck
Sukanya Raghavan
Publicerad i Cytokine
Volym 70
Nummer/häfte 1
Sidor 65-65
ISSN 1043-4666
Publiceringsår 2014
Publicerad vid Institutionen för matematiska vetenskaper, matematisk statistik
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 65-65
Språk en
Länkar dx.doi.org/10.1016/j.cyto.2014.07.1...
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

The aim of the project was to evaluate mechanisms of vaccine-induced protection against Helicobacter pylori infection in mice. In particular, to elucidate the role of cytokines induced by H. pylori infection in promoting the protective or pathogenic immune responses in the stomach. Our group has previously shown that sublingual (SL; under the tongue) vaccination with H. pylori antigens and cholera toxin as an adjuvant was efficient in reducing the bacterial load in the stomach of mice with enhanced IFNγ and IL-17A responses in the stomach compared to unvaccinated mice. Using gene knockout mice and neutralizing antibodies, the impact of cytokines IFNγ and IL-17A on the bacterial load, immune responses and gastric inflammation was addressed. We report that after SL vaccination, IFNγ gene knockout (IFNγ−/−) mice were protected against H. pylori infection and had elevated IL-17A production and lower inflammation scores in the stomach compared to vaccinated wild-type mice. Furthermore, in vivo neutralization of IL-17A in sublingually vaccinated IFNγ−/−mice totally abrogated protection against H. pylori infection. We next examined the mechanisms for induction and maintenance of IL −17A after SL vaccination by studying the role of cytokines IL−1β and IL-23 using gene knockout mice either lacking IL-1 signaling or IL-23 production respectively. Our results show that after SL vaccination with H. pylori antigens and cholera toxin, IL-23p19−/− mice, but not IL-1RI−/− mice were protected against H. pylori infection. Gastric IL-17A responses could not be induced after challenge in the absence of IL-1 signaling, but could be maintained in the absence of IL-23. In summary, we report that IL-17A is important in reducing the bacterial load on the stomach of vaccinated mice which is dependent on intact IL-1 signaling, while IFNγ may promote inflammation. Based on our results, mechanisms of vaccine-induced protection against H. pylori infection and the role of specific cytokines will be discussed.

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?