In Crohn's, is IL-6 inflammation a beast worth slaying?

There appears to be a number of nutrients that show promise in attenuating IL-6 inflammation.  These include vitamins like K and choline, antioxidants like astaxanthin, curcumin, and resveratol, and amino acids such as arginine, glutamate, and tyrisone.

Perhaps it is possible to gain some control over IL-6 inflammation by increasing the presence of these nutrients through diet and supplements.  But even then, is IL-6 inflammation a beast worth slaying?  How big a player is it in Crohn's inflammation?  Will a reduction in IL-6 inflammation result in perceptable improvements in Crohn's symptoms?

Interleukin 6 from Wikipedia

"The wolf in sheep's clothing: the role of interleukin-6 in immunity, inflammation and cancer" in Trends in Molecular Medicine, Review (2008) [PDF full article]
"Recent discoveries involving the cytokine interleukin (IL)-6 have originated from diverse disciplines, revealing roles in biological processes that are likewise varied. The most novel findings suggest a connection between inflammation and diseases, such as insulin resistance associated with diabetes mellitus and cancer, which had not or only weakly been appreciated previously. The IL-6 pathway is one of the mechanisms linking inflammation to these disease processes. In addition, new evidence points toward IL-6 as one of the mediators coordinating the interface between adaptive and innate immunity. Here, we review the evidence linking IL-6 to inflammatory diseases and cancer.
...
In acute inflammation, neutrophils form the largest component of leukocytes recruited. As the acute inflammation resolves, the leukocyte population changes from predominately neutrophilic to mostly monocytic. This transition from acute to sustained inflammation is in large part orchestrated by IL-6. ... Thus, IL-6 is a key signal in the transition from the initial innate immune response to infection to a more sustained, adaptive immune response....
More recently, IL-6 has emerged as a key regulatory signal in the development of the newly described effector T-cell subset, so-called Th17 cells, named for their production of the cytokine IL-17.
...
Thus, we find IL-6 at the intersection where T cells can either go on to become suppressors (Treg) or activators (Th17) of the adaptive immune system.  In this way, IL-6 helps to coordinate the innate immune system (from which it comes initially) and the adaptive immune system.
...What about states of chronic inflammation?  It can be said with little hesitation that, in nearly every disease condition involving chronic inflammation, where serum IL-6 levels have been assayed, they are elevated.  Examples include ... IBDs....
...
In idiopathic IBD ... there is pathogenic build-up of CD4*T cells at sites of inflammation, mediated in part by IL-6, which provides ... an anti-apoptotic signa to T cells through the induction of Bcl-2 and Bcl-xL and promotes Th17 lineage differentiation.  IL-17 is upregulated in patients with both types of IBD.  IL-6 levels are elevated markedly in the serum of patients with IBD, decrease with treatment of inflammation and are predictive of IBD relapse.
...
... a chronic inflammatory state is created, in which IL-6 has the part of a proinflammatory effector signal for NF-kB. ... The pathogenic role that IL-6 has in IBD is effected by trans-signaling (on T cells) and induction of STAT3, which decreases T-cell apoptosis in Crohn's disease and colitis models.
...
A pilot trial of a humanized monoclonal antibody to the IL-6 receptor was undertaken in 2004 with Crohn's disease patients and showed clinical improvement ... in the patients receiving the drug.  Despite the clinical improvement, however, there was little improvement seen endoscopically or histologically."