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. Author manuscript; available in PMC: 2019 Oct 15.
Published in final edited form as: J Neuroimmunol. 2018 Jul 3;323:152–166. doi: 10.1016/j.jneuroim.2018.06.019

Figure 11.

Figure 11

CCL2 immunoreactivity in BM-macrophages at resting conditions, after exposure to a traumatic noise at 120 dB SPL for 1 hour, and after exposure to LLN for 15 days. A–C. CCL2 immunoreactivity in basal BM-macrophages of a naive control ear. Panel A shows CD45 immunoreactivity, panel B shows CCL2 immunoreactivity and panel C shows the merged view of panels A and B. Note that CCL2 immunoreactivity is very weak in steady-state macrophages (B). D–F. CCL2 immunoreactivity after a 120-dB noise exposure for 1 hour. A large number of smaller round to teardrop shaped cells are present and these cells display very strong CCL2 immunoreactivity, suggesting that exposure to traumatic noise increases the expression of CCL2. G–I. CCL2 immunoreactivity in basal BM-macrophages of a cochlea that sustained LLN for 15 days. Panel G shows CD45 immunoreactivity, panel H shows CCL2 immunoreactivity and panel I shows the merged view of panels G and H. Following LLN stress, basal BM-macrophages exhibit amoeboid morphologies and a weak CCL2 immunoreactivity. J. Comparison of the CCL2 fluorescence levels in BM-macrophages among the naive group, the 120-dB noise group and the LLN group. The 120-dB noise group displays a marked increase in CCL2 immunoreactivity as compared to the naive control group. The LLN group also displays an increase, but the level of the increase is significantly less that that seen in the 120-dB noise group (*** P < 0.001; * P < 0.05).