Anti-inflammatories are often used during infection to prevent tissue damage from an inflammatory cascade.
The only way to explain the deep transmural tissue inflammation in crohn's is that there is direct contact between tissue macrophages in the lamina propria and pathogens. Only macrophages that release TNF-a and dendritic cells that present antigen can cause the adaptive immune system to mount such a deep tissue response.
Inflammation compromises the intestinal wall, resulting in AIEC and other bacteria gaining easy entry into deeper tissue. There they will encounter lamina propria macrophages. These macrophages are everywhere in the intestine, there are more in the intestine than anywhere else in the body. These macrophages are unable to kill AIEC, end up releasing TNF-a, antigen presenting cells set off the adaptive response and you get a chronic loop of bacteria setting off inflammation and exploiting the tissue damaged caused by the inflammation.
The only way a bacteria can become a chronic infection is if it is able to thrive in an inflammatory environment. And yes, there is some irony there that the immune system which does its best to curtail pathogens entering tissue, can also damage that same tissue which allows that bacteria to enter tissue.
The immune system in crohn's disease patients can kill and control AIEC and pathogenic E Coli to a large degree, but these bacteria are able to evade much of the mechanics the immune system uses, especially those of the innate immune system (Xenophagy to name one), which means they become chronic infections, resulting in a chronic disease involving inflammation.
Crohn's is really an immunodeficiency of macrophages, combined with a chronic infection, likely involving E Coli in many patients, and possibly other pathogens in others.