Taken with evidence that both KLK1 and KLK6 are elevated in the serum of MS patients [4], it is tempting to speculate that these proteases may operate in tandem to support inflammation by uniquely enhancing immune cell survival and proliferation.
TRPs not only induce the sensation of pain but also support inflammation via secretion of pro-inflammatory neuropeptides.
It has been shown that the sympathetic nervous system supports inflammation during the asymptomatic phase of CIA, whereas it inhibits inflammation during the chronic symptomatic phase [ 36].
However, sympathetic signaling is increased in adipose tissue surrounding the synovium, which is responsible for generating energy-rich substrates to support inflammation [ 91].
mTOR-dependent infiltration of macrophages and production of proinflammatory cytokines, such as MCP-1, might support inflammation during diabetic nephropathy [ 18, 19, 21– 25].
Exposure to degenerating epithelia, altering extracellular matrix, unbalanced electrolytes, growth factors, interleukins and hormones supports inflammation but does not promote development of implanted cells [ 8- 11].
Transient receptor potential channel (TRP) modulation by cannabinoids might be explicitly important since these receptors not only influence sensation of pain, but also support inflammation [ 19].
These data suggest that a Prevotella-defined microbiome may have the propensity to support inflammation in the context of a genetically susceptible host.
The impact of Th1/Th2 balance on immune responses to antigen perturbation is crucial: Th1 responses supports inflammation and T and macrophage cell activation, while Th2 actives primarily B cells, resulting in antigen specific antibody.
