Basophil responses in susceptible AKR mice upon infection with the
intestinal helminth parasite Trichuris muris
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 helminth
Trichuris 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. muris
infection 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 during
T. muris infection in susceptible AKR/J mice.