Hospital San Juan de la Cruz

A dataset for the analysis of antibody response to glycan alpha-Gal in individuals with immune-mediated disorders.

Humans evolved by losing the capacity to synthesize the glycan Galα1-3Galβ1-(3)4GlcNAc-R (α-Gal), which resulted in the development of a protective response mediated by anti-α-Gal IgM/IgG/IgA antibodies against pathogens containing this modification on membrane proteins. As an evolutionary trade-off, humans can develop the alpha-Gal syndrome (AGS), a recently diagnosed disease mediated by anti-α-Gal IgE antibodies and associated with allergic reactions to mammalian meat consumption and tick bites. However, the anti-α-Gal antibody response may be associated with other immune-mediated disorders such as those occurring in patients with COVID-19 and Guillain-Barré syndrome (GBS). Here, we provide a dataset (209 entries) on the IgE/IgM/IgG/IgA anti-α-Gal antibody response in healthy individuals and patients diagnosed with AGS, tick-borne allergies, GBS and COVID-19. The data allows correlative analyses of the anti-α-Gal antibody response with factors such as patient and clinical characteristics, record of tick bites, blood group, age and sex. These analyses could provide insights into the role of anti-α-Gal antibody response in disease symptomatology and possible protective mechanisms.

Serum levels of anti-alphaGalactosyl antibodies predict survival and peritoneal dialysis-related enteric peritonitis rates in patients undergoing renal replacement therapy.

Anti-Galalpha1-3Gal antibodies (anti-alphaGal) represent a significant fraction of natural antibodies and were implicated in several disease states, yet their origin and physiological significance remain largely undisclosed. Under a prospective observational design, we estimated anti-alphaGal immunoglobulin G (IgG)/IgM and antipig hemolytic antibody (APA) levels in 133 patients starting dialysis therapy and again after a 1-year follow-up. We used baseline data to show correlations with demographic, nutritional, inflammatory, and anemia markers and analyzed their correlation with outcomes by using univariate and multivariate strategies of survival analysis. Serum anti-alphaGal and APA levels showed wide baseline variability, but remained relatively stable in time. Both were measurable in dialysate of peritoneal dialysis (PD) patients, showing close correlation to serum levels. We observed no association between levels of anti-alphaGal/APA and nutritional markers, but showed direct correlations of anti-alphaGal IgM (P = 0.005) and APA levels (P = 0.001) with tumor necrosis factor alpha (TNF-alpha) levels. High APA levels also were associated with severe anemia (P = 0.006). High baseline anti-alphaGal IgM (P = 0.03) and APA levels (P = 0.045) predicted later risk for enteric peritonitis in PD patients. Finally, univariate and multivariate analyses showed a consistent association between high baseline anti-alphaGal IgM (P = 0.014) and APA (P = 0.021) levels and global risk for mortality during follow-up. Anti-alphaGal IgM and APA levels at the start of dialysis therapy are significant predictors of later risk for mortality and, in PD patients, enteric peritonitis. Both correlate directly with TNF-alpha levels and, in the case of APA, severity of anemia in these patients.

Sustained decrease of serum anti-galactose alpha 1-3-galactose antibodies in baboons by removing aerobic gram-negative bacteria from the bowel.