Abstract
ObjectiveThe protein Hwp1, expressed on the pathogenic phase of Candida albicans, presents sequence analogy with the gluten protein gliadin and is also a substrate for transglutaminase. This had led to the suggestion that C. albicans infection (CI) may be a triggering factor for Celiac disease (CeD) onset. We investigated cross-immune reactivity between CeD and CI.MethodsSerum IgG levels against recombinant Hwp1 and serological markers of CeD were measured in 87 CeD patients, 41 CI patients, and 98 healthy controls (HC). IgA and IgG were also measured in 20 individuals from each of these groups using microchips sensitized with 38 peptides designed from the N-terminal of Hwp1.ResultsCI and CeD patients had higher levels of anti-Hwp1 (p=0.0005 and p=0.004) and anti-gliadin (p=0.002 and p=0.0009) antibodies than HC but there was no significant difference between CeD and CI patients. CeD and CI patients had higher levels of anti-transglutaminase IgA than HC (p=0.0001 and p=0.0039). During CI, the increase in anti-Hwp1 paralleled the increase in anti-gliadin antibodies. Microchip analysis showed that CeD patients were more reactive against some Hwp1 peptides than CI patients, and that some deamidated peptides were more reactive than their native analogs. Binding of IgG from CeD patients to Hwp1 peptides was inhibited by γIII gliadin peptides.ConclusionsHumoral cross-reactivity between Hwp1 and gliadin was observed during CeD and CI. Increased reactivity to Hwp1 deamidated peptide suggests that transglutaminase is involved in this interplay. These results support the hypothesis that CI may trigger CeD onset in genetically-susceptible individuals.
Highlights
Celiac disease (CeD), known as gluten-sensitive enteropathy, is a complex disorder where genetically-susceptible individuals develop signs of malabsorption and extra-intestinal manifestations after ingestion of cereals [1]
C. albicans infection (CI) and CeD patients had higher levels of anti-hyphal wall protein 1 (Hwp1) (p=0.0005 and p=0.004) and anti-gliadin (p=0.002 and p=0.0009) antibodies than healthy controls (HC) but there was no significant difference between CeD and CI patients
Microchip analysis showed that CeD patients were more reactive against some Hwp1 peptides than CI patients, and that some deamidated peptides were more reactive than their native analogs
Summary
The protein Hwp, expressed on the pathogenic phase of Candida albicans, presents sequence analogy with the gluten protein gliadin and is a substrate for transglutaminase. This had led to the suggestion that C. albicans infection (CI) may be a triggering factor for Celiac disease (CeD) onset. Data Availability Statement: All relevant data are within the paper and its Supporting Information files. Innobiochips provided support in the form of salary for author VS, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Innobiochips played an indirect role through the
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