Fibrosclerotic organ diseases, a major cause of morbidity and mortality in the Western world, involve tissues as diverse as the liver, kidney, heart, lung, skin, and intestine. The causes of these diseases are manifold, and specific noxae are implicated in different settings. Nevertheless, most (if not all) of these conditions share common pathogenetic grounds, such as being characterised by derangement of the tissue “wound healing” response. The ability of tissues to respond to injury has evolved to neutralise infectious agents and to limit parenchymal cell damage. The wound healing response comprises recruitment of inflammatory cells, deposition and remodelling of extracellular matrix, and regeneration (or an attempt thereof) of parenchymal cells. The ultimate outcome of this process is dependent on the duration of damage, and on the ability of parenchymal cells of specific tissues to reconstitute the original architecture. Thus chronic damage is often characterised by simultaneous and uncoordinated activation of all components of the wound healing response, resulting in chronic inflammation, destruction of the parenchyma, and progressive scarring. Chronic pancreatitis is a typical example of the transferability of these concepts to the clinical field. In response to several causes, most frequently alcohol abuse, metabolic abnormalities, or autoimmunity, damage to acinar cells leads to chronic inflammation, eventually resulting in substitution of pancreatic parenchyma with bundles of scar tissue and loss of function.¹

The contribution of inflammation to the development of fibrosis varies in different conditions, and understanding the interaction between these processes is relevant to devise therapeutic strategies for chronic diseases such as pancreatitis. Identification of the chemokine system has elucidated the molecular mechanisms regulating leucocyte trafficking in a given tissue. Chemokines are a family of small cytokines …