Changes in immunohistochemical levels and subcellular localization after therapy and correlation and colocalization with CD68 suggest a pathogenetic role of Hsp60 in ulcerative colitis.

In an earlier work, the role of heat shock protein(Hsp60) in the pathogenesis of ulcerative colitis (UC) wassuggested by its significant increase in the pathological mucosaparallel with an increase in inflammatory cells. More data in thisdirection are reported in this work. We analyzed by immunohistochemistrybiopsies of colon tissue from 2 groups of patients withUC and treated with either 5-aminosalicylic acid (5-ASA) alone orin combination with a probiotic. We looked for inflammatorymarkers and Hsp60. Both the treatments were effective in reducingsymptoms but the group treated with both 5-ASA and probioticsshowed better clinical results. Amelioration of symptoms wasassociated with reduction of both inflammation and Hsp60, areduction that was most marked in the group treated with 5-ASAand probiotics. The levels of Hsp60 positively correlated withthose of CD68-positive cells, and double immunofluorescenceshowed a high index of colocalization of the chaperonin and CD68in lamina propria. Immunoelectron microscopy showed thatHsp60Fclassically a mitochondrial proteinFwas abundantlyalso present in cytosol in biopsies taken at the time of diagnosis,but not after the treatment. Our data suggest that Hsp60 is anactive player in pathogenesis of UC and it can be hypothesizedthat the chaperonin is responsible, at least in part, for initiationand maintenance of disease.