The basophil population expands in susceptible AKR/J mice uponT. muris infection.
To confirm whether basophil population expansion was driving the increase in basophil-associated gene expression in the intestine duringT. muris infection in AKR/J mice, we next quantified the accumulation of basophils (gated as CD45+Lineage IgE+FcεR1α+ CD49b+cKit-) in the cecum, spleen, and draining mesenteric lymph nodes (MLNs) by flow cytometry after T. muris infection. In the cecum, we observed a significant infection-induced increase in basophil frequency as a proportion of Lineage-negative cells and total CD45+ immune cells at d7 p.i., which returned to naïve levels on d14, increased again on d19, and then decreased on d35 (Fig. 2A-C). Expansion of the splenic basophil population occurred later, at d19 p.i., and remained elevated at d35 p.i (Fig. 2D-F). These data largely mirror the kinetics of infection-induced changes in basophil abundance in the cecum and spleen of resistant C57BL/6 mice (7). We also observed an infection-induced increase in mast cell (CD45+ LineageIgE+ FcεR1α+CD49b+/- cKit+) (Fig. S1B) frequencies out of Lineage-negative cells in the cecum but not the spleen starting on d14 p.i. (Fig. S1C-D), suggesting that mast cells are also mobilized during infection in AKR/J mice, but not as broadly across tissues as basophils. Consistent with our previous findings in C57BL/6 mice (7) we could not detect a substantial basophil population in the draining MLN (Fig. S1E), and there were no notable differences in basophil population frequencies throughout the time-course in the MLN (Fig. S1F). These data show that the basophil population expands in the spleen and cecum at various timepoints in T. muris -infected AKR/J mice.