Cachexia caused by arthritis, cancer and AIDS have all been correlated with elevated TNFα levels [ 46].
This exaggerated response in RAG1 knockout mice was associated with decreased exudate IL-10 and elevated TNFα levels.
Under the assumption that the elevated TNFα levels found in patients with various chronic inflammatory diseases are deleterious, several anti-TNFα therapies are now available to block the action of TNFα.
miR-155-deficiency was found to be associated with decreased TNFα production, a cytokine required for GC formation (Endres et al, 1999), whereas forced expression of miR-155 leads to elevated TNFα levels (Tili et al, 2007).
In these patients, the elevated TNFα levels may be involved in diverse pathological mechanisms and, therefore, a clinical benefit is to be expected under a treatment that diminishes TNFα production.
Thus, it is plausible that elevated TNFα levels may account for the variations in OC ontogeny between HC and PsA shown in Figure 4(b).
Finally, a murine model of ALD confirmed increased miR-155 and TNFα levels in Kupffer cells isolated from ethanol-treated animals compared with control animals, suggesting that miR-155 is an important regulator of TNFα in vivo and likely contributes to the elevated TNFα levels often observed in chronic alcoholics (Bala and Marcos 2011).
This finding is supported by elevated TNFα expression in skeletal muscle of AATD AUG subjects that is not seen in AATD + AUG subjects.
One study demonstrated that elevated TNFα plasma levels do not correlate with SLE disease activity, and another study showed that TNFα levels were actually higher in patients with inactive disease, suggesting a protective role for TNFα in SLE [ 42, 43].
Although elevated plasma TNFα levels are associated with increased blood brain barrier permeability and neuronal apoptosis [ 34], we could not demonstrate any association between plasma TNFα levels and delirium in our cohort.
