Role of gamma interferon in Helicobacter pylori induction of inflammatory mediators during murine infection.

نویسندگان

  • Marygorret Obonyo
  • Donald G Guiney
  • Julia Harwood
  • Joshua Fierer
  • Sheri P Cole
چکیده

Gamma interferon (IFN-gamma) has been proposed to play an important role in Helicobacter-related gastritis. Using the IFN-gamma gene knockout (IFN-gamma(-/-)) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated that Helicobacter pylori maximally induced macrophage inflammatory protein-2 (MIP-2) and inducible nitric oxide synthase (iNOS) mRNA only in wild-type mice. MIP-2 and iNOS mRNA were also induced by H. pylori in GSM06 cells. Induction of cyclooxygenase 2 mRNA through IFN-gamma was demonstrated in GSM06 cells. These data indicate that IFN-gamma mediates the induction of MIP-2 and iNOS mRNA expression by H. pylori in mice.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Interactions between inducible nitric oxide and other inflammatory mediators during Helicobacter pylori infection.

BACKGROUND Recent studies in both humans and animal models strongly suggest the contribution of the host immune response to Helicobacter pylori-related disease. Inducible nitric oxide synthase has been shown to be up-regulated in the gastric epithelium during H. pylori gastritis, suggesting a role in inflammation. MATERIALS AND METHODS C57BL/6 wild-type and inducible nitric oxide synthase gen...

متن کامل

Role of gamma interferon in Helicobacter pylori-induced gastric inflammatory responses in a mouse model.

The immune responses to Helicobacter pylori infection play important roles in gastroduodenal diseases. The contribution of gamma interferon (IFN-gamma) to the immune responses, especially to the induction of gastric inflammation and to protection from H. pylori infection, was investigated with IFN-gamma gene knockout (IFN-gamma-/-) mice. We first examined the colonizing abilities of eight H. py...

متن کامل

Evaluation of Serum Interleukin-18 levels in Helicobacter Pylori-infected Peptic Ulcer Patients and its Association with Bacterial CagA Virulence Factor

Background: Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide. Predominant T-helper 1 (Th1) responses with increased gamma interferon (IFN- γ) levels have been proposed to play an important role in H. pylori-induced peptic ulcer. However, bacterial factors contributing to the initiation of Th1 polarization of H. pylori-specific immune responses have n...

متن کامل

Serum levels of iron parameters and IL-17 in children with Helicobacter pylori infection compared to healthy group

Helicobacter pylori is related to iron deficiency anemia (IDA) and inflammatory responses causing gastric and duodenal ulcer and carcinoma. Moreover, it leads to deficiency of factors associated with iron adsorption and transfer. In the present study, we recruited 100 children (50 infected with H. pylori and 50 controls) aged 3-14 years old (40% male and 60% female) to evaluate the effect of H....

متن کامل

The Effect of Class II Major Histocompatibility Complex Expression on Adherence of Helicobacter pylori and Induction of Apoptosis in Gastric Epithelial Cells: A Mechanism for T Helper Cell Type 1–mediated Damage

Helicobacter pylori infection is associated with gastric epithelial damage, including apoptosis, ulceration, and cancer. Although bacterial factors and the host response are believed to contribute to gastric disease, no receptor has been identified that explains how the bacteria attach and signal the host cell to undergo apoptosis. Using H. pylori as "bait" to capture receptor proteins in solub...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Infection and immunity

دوره 70 6  شماره 

صفحات  -

تاریخ انتشار 2002