Pain killers interfere with antidepressants:

http://www.healthcentral.com/depression/treatment-579181-5.html

In two studies, scientists found that taking antidepressants raises levels of cytokines in a person’s body. These cytokines then boost the levels of a protein called p11. This protein makes more serotonin receptors on the surface of cells. Having more of these receptors makes it easier for them to interact with serotonin. Serotonin is the primary brain chemical that SSRIs are designed to affect. Increasing serotonin usually reduces depression.

painkillers interfered with the production of these cytokines. This reduced the levels of p11 protein, which then reduced serotonin receptors on cells.  Thus, there were fewer serotonin receptors for the brain chemical to work on, and this kept the SSRI antidepressants from working at full strength.

scientists found evidence that non-steroidal anti-inflammatory drugs (NSAIDs) significantly reduce the effectiveness of selective serotonin reuptake inhibitor antidepressants (SSRIs) In fact, NSAIDs were associated with a 10 percent drop in depression remission rates, from 55 percent to 45 percent.What this means is that if you take NSAIDs and SSRI antidepressants together, there’s a 10 percent greater chance you’ll still suffer from depression, even if you’re taking a medication to treat it.

People who suffer from chronic pain could be prescribed other kinds of antidepressants such as tricyclic antidepressants or buproprion (Wellbutrin), which work on neurotransmitters in the brain, but not in the same way.  Or, people with depression could be given other types of medications to treat their pain.

http://www.pnas.org/content/early/2011/04/20/1104836108.abstract

In contrast to the levels detected in serum, we found that frontal cortical levels of certain cytokines (e.g., TNFα and IFNγ) were increased by serotonergic antidepressants and that these effects were inhibited by antiinflammatory agents. The antagonistic effect of antiinflammatory agents on antidepressant-induced behaviors was confirmed by analysis of a dataset from a large-scale real-world human study, “sequenced treatment alternatives to relieve depression” (STAR*D), underscoring the clinical significance of our findings. Our data indicate that clinicians should carefully balance the therapeutic benefits of antiinflammatory agents versus the potentially negative consequences of antagonizing the therapeutic efficacy of antidepressant agents in patients suffering from depression.