Fig. 3

Macrophage recruitment to amyloid transgenic fly brain aggravates neurodegeneration upon intestinal infection. a Immunostaining of plasmatocyte (green, NimC1 signals) recruited to the transgenic brain upon intestinal infection; n = 15 in each group for quantification (right panel). yellow, mushroom body (FasII signals); blue, DAPI signal; left panel. b, c Immunostaining of the recruited hemocytes (upper and middle panels) and brain histology (lower panel) b and life span analysis c in the transgenic flies with or without dom ¹ /l(3)hem ² hemocyte-deficient background. Green, NimC1 signals; blue, DAPI signal; n = 10 in each group for quantification of brain histology; n = 100 in each group for lifespan assay. d Coimmunostaining of NimC1 and Eiger in brains of the Ecc15-infected transgenic flies. (Right panel shows high magnification view from white dotted line labeled region of left panel). The location of Mushroom body is masked with yellow dotted lines; Eiger, red; recruited plasmatocytes, green; transgenic brain, blue. e–g qRT-PCR analysis of eiger expression e and immunostaining f as well as western blot analysis g of JNK phosphorylation in brains of the transgenic flies with or without hemocyte-deficient background. Quantitative data are presented as the mean±SD of three independent experiments. elav>Aβ42 transgenic or control (elav alone) flies with or without Ecc15 intestinal infection were analyzed at 10 dpi for plasmatocyte recruitment, eiger expression, and JNK activation. *P < 0.05, ***P < 0.001; NS, not significant, H&E, haematoxylin and eosin. Scale bars, 50 μm