Celiac disease (CD) is now considered, more than a just gluten sensitivity enteropathy,
a multiple and systemic immune-mediate disorder triggered by the ingestion of
wheat gluten and related proteins. Following the discovery of a link between gluten and CD,
it was demonstrated that gliadin, one of the two principal protein groups comprising gluten,
plays a key role in CD. It has since become clear that the different and crucial roles of gliadin
in CD result from its ability to activate multiple signaling pathways that modulate CD pathology. Most
of these pathways involve the host innate and adaptive immune responses, but some pathways are activated
when gliadin interacts with the intestinal cellular compartment. The long pentraxin (PTX3), a marker of the
acute-phase inflammatory response, plays an important role in innate immunity and in modulation of the
adaptive immune response.
We investigated whether CD patients, considered as a model of gluten-sensitivity condition, have increased
PTX3 levels. Our data showed that PTX3 serum levels were high in active CD patients and serum levels of
PTX3 correlated with DGP IgA levels. We provide evidences that the bad compliance of GFD in patients 2
concurred with a pathological PTX3 concentration that could follow the improvement of both gastrointestinal
and extraintestinal symptoms. We hypothesized that PTX3 is able to modulate the innate response to gliadin
in CD and it could regulate the adaptive immune response.
It is also evidenced that a common “wooden horse” of CD and Non Celiac Gluten Sensitivity (NCGS) is the
ingestion of gluten and related toxic peptides. At the moment we don’t have adequate elements to suggest the
use of PTX3 in diagnosis of NCGS, but we are obliged to speculate about the possible role of PTX3 molecules
in NCGS pathogenesis.
The identified new strategies and uses of PTX3 could improve the management of gluten sensitivity conditions
in the next future.