Abstract
Objective: We recently demonstrated that the biggest reduction of T cells in septic patients was produced in the γδ T subset. This depletion was directly proportional to the severity of the septic process, and it was associated with mortality. We hypothesized that microsporidia can harness the deficit of γδ T cells in septic patients to proliferate and contribute to the worsening of the sepsis. Methods: In this retrospective study, we analyzed anti-Encephalitozoon cuniculi antibody levels in sera from 46 septic patients, and compared them with a similar control group of healthy subjects. As a secondary objective we aimed to relate anti-E. cuniculi antibody levels with αβ and γδ T cells in these patients. Results: Forty-eight percent of septic patients were positive for IgE anti-E. cuniculi vs 13.0% of healthy subjects (OR: 3.67, CI95% 1.64-8.20, P=0.001). The frequency of αβ and CD56+ γδ T cell subsets decreased in septic patients with positive anti-E. cuniculi IgE antibodies. This decrease was more potent in the CD3+CD56+ γδ T cell subset. The genitourinary focus (urinary tract infections and pyelonephritis) produced a significant higher percentage of anti-E. cuniculi positive cases (11/13 (84.6%), OR=11.0, CI 95% 2.1-58.5, P=0.003). Conclusion: There was a greater level expression of IgE anti-E. cuniculi in septic patients, reaching almost 50% of positive. The presence of IgE anti-E. cuniculi in septic patients was related to a decrease of αβ and γδ T cells in peripheral blood. This decrease was more potent in the CD3+CD56+ γδ T cell subset. Microsporidia may be heavily involved in the physio-pathological evolution of sepsis.
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