Multiple lines of evidence have implicated increased brain inflammation (neuroinflammation) in mental health disorders. One example is autoimmunity, where inappropriate targeting of brain proteins by the immune system can increase neuroinflammation, negatively affecting brain function.[1] Neuroinflammation isn’t always caused by autoimmunity, however, since increased systemic levels of pro-inflammatory cytokines, such as interleukin-1 beta (IL-β) and tumor necrosis factor-alpha (TNF-α), have been shown to cause social withdrawal, triggering “sickness behavior”[2], a mechanism that may have evolved to encourage social isolation to decrease transmission of communicable diseases. While the mechanisms by which inflammation induces sickness behavior aren’t completely understood, experiments with lipopolysaccharide (LPS, an inflammation-inducing component from the cell wall of certain bacteria) have shown that increased levels of inflammation can have direct effects on the brain in humans. In one study where healthy participants were injected with low doses of LPS, reward signaling in the brain was suppressed, causing anhedonia (the inability to feel pleasure), a common symptom in people with depression.[3]
References
- ^The American College of Rheumatology nomenclature and case definitions for neuropsychiatric lupus syndromes.Arthritis Rheum.(1999 Apr)
- ^Dantzer R, O'Connor JC, Freund GG, Johnson RW, Kelley KWFrom inflammation to sickness and depression: when the immune system subjugates the brain.Nat Rev Neurosci.(2008-Jan)
- ^Eisenberger NI, Berkman ET, Inagaki TK, Rameson LT, Mashal NM, Irwin MRInflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward.Biol Psychiatry.(2010-Oct-15)