Abstract
Intestinal helminth infection promotes a Type 2 inflammatory response in
resistant C57BL/6 mice that is essential for worm clearance. The study
of inbred mouse strains has revealed factors that are critical for
parasite resistance and delineated the role of Type 1 versus Type 2
immune responses in worm clearance. In C57BL/6 mice, basophils are key
innate immune cells that promote Type 2 inflammation and are programmed
via the Notch signaling pathway during infection with the helminthTrichuris muris . However, how the host genetic background
influences basophil responses and basophil expression of Notch receptors
remains unclear. Here we use genetically susceptible inbred AKR/J mice
that have a Type 1-skewed immune response during T. murisinfection to investigate basophil responses in a susceptible host.
Basophil population expansion occurred in AKR/J mice even in the absence
of fulminant Type 2 inflammation during T. muris infection.
However, basophils in AKR/J mice did not robustly upregulate expression
of the Notch2 receptor in response to infection as in C57BL/6 mice.
Blockade of the Type 1 cytokine IFN-γ in infected AKR/J mice was not
sufficient to elicit infection-induced basophil expression of the Notch2
receptor. These data suggest that the host genetic background, outside
of the Type 1 skew, is important in regulating basophil responses duringT. muris infection in susceptible AKR/J mice.
Keywords: Basophils,Trichuris muris , Type 2 inflammation, Notch signaling, AKR-inbred
strain