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Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model

Kaoru Geddes1, Stephen Rubino, Catherine Streutker

  • 1Department of Immunology, University of Toronto, Toronto, Ontario M6G 2T6, Canada.

Infection and Immunity
|October 6, 2010
PubMed

Insights

Nod1 and Nod2 pattern recognition molecules reduce inflammation and bacterial load during Salmonella colitis. Their function in controlling inflammation is dependent on the Salmonella pathogenicity island 2 type III secretion system.

Area of Science:

  • Immunology
  • Microbiology
  • Gastroenterology

Background:

  • Nod1 and Nod2 are crucial for intestinal homeostasis.
  • Their role in bacterial colitis-induced inflammation remains unclear.

Purpose of the Study:

  • To investigate the impact of Nod1 and Nod2 on inflammation during Salmonella colitis.
  • To determine the contribution of hematopoietic and nonhematopoietic cells to Nod-mediated inflammation.

Main Methods:

  • Streptomycin-treated mouse model of Salmonella colitis.
  • Analysis of mice deficient in Nod1, Nod2, and Rip2.
  • Assessment of inflammatory pathology, cytokine levels, and bacterial colonization.
  • Evaluation of the role of Salmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS).

Main Results:

  • Mice lacking Nod1 and Nod2 exhibited reduced inflammation and lower inflammatory cytokine levels.
  • Nod1 and Nod2 deficiency led to increased Salmonella colonization.
  • Both hematopoietic and nonhematopoietic Nod1 and Nod2 contributed to inflammation.
  • Rip2 deficiency recapitulated these phenotypes, but only under SPI-2 TTSS-inducing conditions.

Conclusions:

  • Nod1 and Nod2 modulate inflammation and promote bacterial clearance in Salmonella colitis.
  • The function of Nod1, Nod2, and Rip2 in this context is dependent on SPI-2 TTSS expression.

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