Does phytic acid influence Crohn's?

Phytic Acid on Wikipedia
"Phytic acid (known as inositol hexakisphosphate (IP6), or phytate when in salt form) is the principal storage form of phosphorus in many plant tissues, especially bran and seeds.[1] Phytate is not digestible to humans or nonruminant animals, however, so it is not a source of either inositol or phosphate if eaten directly. Morever, it chelates and thus makes unabsorbable certain important minor minerals such as zinc and iron, and to a lesser extent, also macro minerals such as calcium and magnesium. ...
Phytic acid may be considered a phytonutrient, providing an antioxidant effect.[1][21] Phytic acid's mineral binding properties may also prevent colon cancer by reducing oxidative stress in the lumen of the intestinal tract. ...
As a food additive, phytic acid is used as a preservative, as E391."

Phytic Acid: Tips for Consumers from Food Science

"Inhibition of chronic ulcerative colitis associated adenocarcinoma development in mice by inositol compounds" in Carcinogenesis (2006)
" Further mechanistic studies showed that the inhibition of UC-associated carcinogenesis by inositol compounds might relate to their function on the modulation of macrophage mediated inflammation, nitro-oxidative stress and cell proliferation in UC-associated carcinogenesis. This study indicates that inositol compounds may have the potential to serve as preventive agents for chronic inflammation-carcinogenesis." [Emphases mine.]

"Effect of Inositol Hexaphosphate on Lipopolysaccharide-Stimulated Release of TNF-α from Human Mononuclear Cells" [full text]
"This study also showed that at doses significantly exceeding IP6 cellular contents, it acted as an agonist up-regulating TNF-α secretion. Moreover, IP6 appeared to influence differentially the responsiveness of mononuclear cells to secondary stimulus. Up-regulation by IP6 of TNF-α release, referred to as priming, was observed under the influence of S. minnesota LPS [LipoPolySaccharide]. Priming is considered one of the regulatory mechanisms implicated in controlling immune cell responses. This event improves the ability of immune cells to locate and kill invading microorganisms and hence may be critical to effective neutrophil functions. In this connection, IP6 can take part in the defense against invasive bacteria, such as S minnesota species. On the other hand, priming is implicated in neutrophil- and lymphocyte-mediated tissue injury both in vitro and in vivo. In this context, IP6 by down-regulating TNFα release from cells stimulated with D. desulfuricans and E. coli LPSs which showed higher potency compared to S. minnesota LPS in this study, may diminish the tissue damage caused by lymphocytes. Thus, the effects of IP6 released from necrotic cells at an inflammatory focus may be beneficial for a variety of inflammatory diseases, including septic shock.
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In conclusion, the present findings demonstrate an extracellular role for IP6, which in this study has appeared to act as a bi-functional modulator of TNF-á release from mononuclear cells in response to bacterial challenge. The enhancing or diminishing effects of IP6 may control the level of activation states and subsequent responses of mononuclear cells, depending on the particular Gramnegative bacteria’ endotoxins."