Critical Role of Macrophages and Their Activation via MyD88-NFκB Signaling in Lung Innate Immunity to Mycoplasma pneumoniae
Figure 7
MyD88-NFκB signaling is essential for macrophages to eliminate Mp.
(A), (B) and (C), WT and MyD88−/− BMM were infected with EYFP-Mp or mock infected. (A) One hour after infection with EYFP-Mp (green), BMM were stained with anti-NFκB (p65) (red) to determine the subcellular location of this transcription factor. (B) BMM were stained with anti-α-tubulin (red) to highlight cell morphology. The survival of EYFP-Mp (green) was estimated by microscopy, and (C) the survival of EYFP-Mp was analyzed quantitatively by real-time PCR. (D) and (E), WT BMM were pretreated with the inhibitor of NFκB activation or with the diluent control (DMSO) for 1 h prior Mp infection. Eight hours after infection, BMM were stained with anti-α–tubulin (red) to show cell morphology and surviving EYFP-Mp (green) (D). The survival of EYFP-Mp in the cultures shown in (D) was determined by real-time PCR (E). Data shown are representative of two replicate experiments and are means ± SEM (n = 3).