Trichinella britovi belongs to the encapsulated clade of the Trichinella genus. It is a widely distributed parasitic nematode, transmitted through ingestion of raw or poorly cooked meat containing muscle larvae, mainly distributed in most of Europe (excluding some islands and the very north), north and west Africa, and Southwest Asia [1]. The parasite causes a clinical picture usually mild in humans because of low fertility of female worms [2].

Most of the knowledge about the immune response to the parasitic nematode Trichinella spp. derives from studies in experimental infection in rodents where an initial Th1 activation is followed by a stable Th2 polarization [3]. The immune response, particularly at cellular level, in human infections is poorly investigated, being based on few studies which highlight the Th2 polarization of the immune response [4] or a mixed Th1-Th2 response [5]. Furthermore, the mechanisms of the inflammatory response at either intestinal or skeletal muscle level are not known in human infection.

The key molecules for inflammation are chemokines codified by genes upregulated and increasingly produced in neutrophils properly activated. As a consequence, the pattern of chemokines released by neutrophils depends markedly on the type of the stimulus [6].

Neutrophil-derived chemokine levels are increased in pathological conditions and participate in the inflammatory response by recruiting immune cells to the site of inflammation; they are important mediators of inflammatory and immune responses, underlying the induction of interferon (IFN)-γ and IFN-γ dependent CXC chemokines [7], [8], [9], [10]. Examples are represented by CCL2, CCL3, CCL4, CCL5, CCL11, CXCL-8, and CXCL10. These small proteins, modulate the immune cells and propagate the inflammatory response, therefore playing a crucial role in the defense against pathogens, among them parasites [11], [12]. In particular, monocyte chemotactic protein 1 (also known as CCL2 or MCP-1) and IFN-inducible protein 10 (also known as CXCL10 or IP-10) have received particular attention by the researchers [13].

CXXL1O has been considered as a prototype chemokine of the C-X-C motif chemokines inducible by interferon (IFN)-γ [chemokines C-X-C motif ligand (CXCL9, CXCL10, CXCL11). These are associated with lymphocyte T helper (Th)1-mediated immune responses. Chemokines of the C–C family generally are chemoattractant for T lymphocytes, monocytes, and natural killer cells. Among these chemokines, monocyte chemoattractant protein 1 (MCP-l/CCL2) is a prototype of this family which plays an important role for the development of adaptive Th2 responses by driving the differentiation of Th0 cells to Th2 in vitro [14]. For these reasons, we aimed to study the serum levels of these chemokines to verify possible changes during infection, in relation to different clinical pictures, searching for a possible relation with a known marker of inflammation such as matrix metalloprotease-9 (MMP-9) [15].