Skip to main content
. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Pain. 2011 Jun 17;152(9):2036–2051. doi: 10.1016/j.pain.2011.04.033

Figure 4. SIV infection in rhesus macaques results in an increase of CGRP-IL in epidermal keratinocytes.

Figure 4

A–E) CGRP-IL is increased among palmar glabrous skin keratinocytes from SIV-infected animals compared with control epidermis. A) Control monkey epidermal primary ridge depicting CGRP-IL among fine delicate innervation of the epidermis, and upper dermal compartments (downward and upward arrows, respectively). B–E) Compared with the control monkey, all monkeys infected with SIV had increased CGRP-IR, although the intensity varied between monkeys. B) As seen in an aged monkey with AIDS and severe SIV encephalitis (SIVE), moderate CGRP-IL is detected among the epidermal keratinocytes. C) This young adult monkey had no AIDS defining illness, but did show abundant systemic viral replication and had severe colitis at the time of sacrifice. Dramatic increases in CGRP-IL of keratinocytes can be seen. D) This represents a similarly young adult monkey with SIV infection, with the most subtle increase in epidermal keratinocyte CGRP-IL observed. In this animal, CGRP-IL among keratinocytes was only slightly higher compared with the control or other SIV animals, and CGRP-IL innervation was observed (arrows). E) This represents another young adult SIV infected animal, demonstrating robust CGRP-IL of epidermal keratinocytes, and CGRP-IL among upper dermal nerves (arrow). Magnification bar (A) =50µm for A–E. Anti-CGRP (guinea pig polyclonal, 1:800; Peninsula Labs, San Carlos, CA) was used.