Open AccessMurine splenocytes produce inflammatory cytokines in a MyD88‐dependent response to Bacillus anthracis spores
Author(s) -
Glomski Ian J.,
Fritz Jörg H.,
Keppler Selina J.,
Balloy Viviane,
Chignard Michel,
Mock Michèle,
Goossens Pierre L.
Publication year - 2007
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2006.00806.x
Subject(s) - biology , nod1 , microbiology and biotechnology , bacillus anthracis , splenocyte , innate immune system , tlr2 , tlr4 , proinflammatory cytokine , immune system , nod2 , immunology , bacteria , inflammation , genetics
Summary Bacillus anthracis is a sporulating Gram‐positive bacterium that causes the disease anthrax. The highly stable spore is the infectious form of the bacterium that first interacts with the prospective host, and thus the interaction between the host and spore is vital to the development of disease. We focused our study on the response of murine splenocytes to the B. anthracis spore by using paraformaldehyde‐inactivated spores (FIS), a treatment that prevents germination and production of products associated with vegetative bacilli. We found that murine splenocytes produce IL‐12 and IFN‐γ in response to FIS. The IL‐12 was secreted by CD11b cells, which functioned to induce the production of IFN‐γ by CD49b (DX5) NK cells. The production of these cytokines by splenocytes was not dependent on TLR2, TLR4, TLR9, Nod1, or Nod2; however, it was dependent on the signalling adapter protein MyD88. Unlike splenocytes, Nod1‐ and Nod2‐transfected HEK cells were activated by FIS. Both IL‐12 and IFN‐γ secretion were inhibited by treatment with B. anthracis lethal toxin. These observations suggest that the innate immune system recognizes spores with a MyD88‐dependent receptor (or receptors) and responds by secreting inflammatory cytokines, which may ultimately aid in resisting infection.