Open AccessA role for natural killer cells in intestinal inflammation caused by infection with Salmonella enterica serovar Typhimurium
Author(s) -
Harrington Lynne,
Srikanth Chittur V.,
Antony Reuben,
Shi Hai Ning,
Cherayil Bobby J.
Publication year - 2007
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2007.00313.x
Subject(s) - salmonella , salmonella enterica , biology , microbiology and biotechnology , mesenteric lymph nodes , immunology , inflammation , cytokine , interleukin 12 , salmonella infection , interferon gamma , serotype , immune system , in vitro , bacteria , cytotoxic t cell , biochemistry , genetics
Acute gastroenteritis caused by Salmonella infection is a significant public health problem. Using a mouse model of this condition, the authors demonstrated previously that the cytokine gamma interferon (IFN‐γ) is required for a normal intestinal inflammatory response to the pathogen. In the present study, these experiments are extended to show that natural killer (NK) cells constitute an early source of intestinal IFN‐γ during Salmonella infection, and that these cells have a significant impact on intestinal inflammation. It was found that infection of mice with Salmonella increased both intestinal IFN‐γ production and the numbers of NK cells in the intestine and mesenteric lymph nodes. NK cells, along with other types of lymphocytes, produced IFN‐γ in response to the bacteria in vitro , while antibody‐mediated depletion of NK cells in vivo resulted in a significant reduction in Salmonella ‐induced intestinal IFN‐γ expression. In a mouse strain lacking NK cells and T and B lymphocytes, intestinal production of IFN‐γ and Salmonella ‐induced intestinal inflammation were both significantly decreased compared with a strain deficient only in T and B cells. The authors' observations point to an important function for NK cells and NK‐derived IFN‐γ in regulating the intestinal inflammatory response to Salmonella .