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Changes in Immunohistochemical Levels and Subcellular Localization After Therapy and Correlation and Colocalization With CD68 Suggest a Pathogenetic Role of Hsp60 in Ulcerative Colitis

Tomasello, Giovanni MD, PhD*; Rodolico, Vito MD; Zerilli, Monica PhD; Martorana, Anna MD; Bucchieri, Fabio MD‡,§; Pitruzzella, Alessandro MSc‡,§; Gammazza, Antonella Marino PhD‡,§; David, Sabrina MSc; Rappa, Francesca MD‡,§; Zummo, Giovanni MD; Damiani, Provvidenza MD; Accomando, Salvatore MD§,¶; Rizzo, Manfredi MD; de Macario, Everly Conway PhD**; Macario, Alberto J.L. MD§,**; Cappello, Francesco MD‡,§

Applied Immunohistochemistry & Molecular Morphology: December 2011 - Volume 19 - Issue 6 - p 552–561
doi: 10.1097/PAI.0b013e3182118e5f
Research Articles
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In an earlier work, the role of heat shock protein (Hsp60) in the pathogenesis of ulcerative colitis (UC) was suggested by its significant increase in the pathological mucosa parallel with an increase in inflammatory cells. More data in this direction are reported in this work. We analyzed by immunohistochemistry biopsies of colon tissue from 2 groups of patients with UC and treated with either 5-aminosalicylic acid (5-ASA) alone or in combination with a probiotic. We looked for inflammatory markers and Hsp60. Both the treatments were effective in reducing symptoms but the group treated with both 5-ASA and probiotics showed better clinical results. Amelioration of symptoms was associated with reduction of both inflammation and Hsp60, a reduction that was most marked in the group treated with 5-ASA and probiotics. The levels of Hsp60 positively correlated with those of CD68-positive cells, and double immunofluorescence showed a high index of colocalization of the chaperonin and CD68 in lamina propria. Immunoelectron microscopy showed that Hsp60—classically a mitochondrial protein—was abundantly also present in cytosol in biopsies taken at the time of diagnosis, but not after the treatment. Our data suggest that Hsp60 is an active player in pathogenesis of UC and it can be hypothesized that the chaperonin is responsible, at least in part, for initiation and maintenance of disease.

*Dipartimento di Chirurgia Generale, d’Urgenza e Trapianti d’Organo

Dipartimento di Patologia Umana

Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche

Dipartimento di Medicina Interna, Malattie Cardiovascolari e Nefrourologiche

Dipartimento Materno-Infantile

Dipartimento di Medicina Interna e delle Malattie Emergenti, Università degli Studi di Palermo

§Istituto Euro-Mediterraneo di Scienza e Tecnologia (IEMEST), Palermo, Italy

**Department of Microbiology and Immunology, School of Medicine, and IMET, University of Maryland, Baltimore, MD

Supported by funds from MIUR ex-60% (V.R., G.Z., F.B., and F.C.) and from Istituto Euro-Mediterraneo di Scienza e Tecnologia (A.J.L.M., and F.C.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Giovanni Tomasello and Vito Rodolico have contributed equally to the present work.

The authors declare no conflict of interest.

Reprints: Francesco Cappello, MD, Dipartimento di Biomedicina Sperimentale e Neuroscienze Cliniche, Sezione di Anatomia Umana, via del Vespro 129, 90127, Palermo, Italy (e-mail: francapp@hotmail.com).

Received October 12, 2010

Accepted January 20, 2011

© 2011 Lippincott Williams & Wilkins, Inc.