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<p>Microsporidia are obligate intracellular pathogens that pose a significant threat to immunocompromised individuals, with <i>Encephalitozoon intestinalis</i> a primary source of gastrointestinal infections. Honey contains well-documented antimicrobial and immunomodulatory properties and exhibits diverse bioactive compounds that may affect host–pathogen interactions. In this in vitro study, we investigated the effects of flower honey (FH), pine honey (PH), and chestnut honey (CHH) on the proliferation of <i>E. intestinalis</i> spores using a HEK-293 epithelial host cell model. Cytotoxicity was first evaluated using the XTT assay to determine non-cytotoxic concentrations, ensuring that potential antiparasitic effects were independent of host cell toxicity. The spore burden was subsequently quantified by quantitative real-time polymerase chain reaction, and morphological alterations were assessed using trichrome staining. FH demonstrated a pronounced dose-dependent inhibitory effect on spore proliferation. The three highest non-cytotoxic concentrations (1.25% w/v, 0.6% w/v, and 0.3% w/v) reduced spore numbers by 58.4%, 50.1%, and 28.7%, respectively (<i>p</i> &lt; 0.05). On the other hand, PH exhibited a concentration-dependent dual response: 5% w/v inhibited spore proliferation, while lower concentrations promoted parasite growth. A similar pattern was seen for CHH, where concentrations of 1.25% w/v and 0.6% w/v significantly increased spore proliferation by 21.7% and 49.9%, respectively (<i>p</i> &lt; 0.05). However, no significant increase was observed at 2.5% w/v. LC-HRMS profiling revealed that FH is particularly enriched in phenolic compounds, suggesting that compositional differences among honey types may explain their divergent biological effects. These findings suggest that the antimicrosporidial efficacy of honey is source- and concentration-dependent. Additional research is required to clarify the underlying molecular mechanisms.</p>

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Inhibitory and proliferative effects of floral-source-specific honeys on Encephalitozoon intestinalis: A comparative in vitro study

  • 期刊论文

  • 发表日期：

    2026年7月6日

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  • Derya Gül Gülpinar,
  • Zübeyda Akın Polat,
  • Ülfet Çetinkaya

摘要

Microsporidia are obligate intracellular pathogens that pose a significant threat to immunocompromised individuals, with Encephalitozoon intestinalis a primary source of gastrointestinal infections. Honey contains well-documented antimicrobial and immunomodulatory properties and exhibits diverse bioactive compounds that may affect host–pathogen interactions. In this in vitro study, we investigated the effects of flower honey (FH), pine honey (PH), and chestnut honey (CHH) on the proliferation of E. intestinalis spores using a HEK-293 epithelial host cell model. Cytotoxicity was first evaluated using the XTT assay to determine non-cytotoxic concentrations, ensuring that potential antiparasitic effects were independent of host cell toxicity. The spore burden was subsequently quantified by quantitative real-time polymerase chain reaction, and morphological alterations were assessed using trichrome staining. FH demonstrated a pronounced dose-dependent inhibitory effect on spore proliferation. The three highest non-cytotoxic concentrations (1.25% w/v, 0.6% w/v, and 0.3% w/v) reduced spore numbers by 58.4%, 50.1%, and 28.7%, respectively (p < 0.05). On the other hand, PH exhibited a concentration-dependent dual response: 5% w/v inhibited spore proliferation, while lower concentrations promoted parasite growth. A similar pattern was seen for CHH, where concentrations of 1.25% w/v and 0.6% w/v significantly increased spore proliferation by 21.7% and 49.9%, respectively (p < 0.05). However, no significant increase was observed at 2.5% w/v. LC-HRMS profiling revealed that FH is particularly enriched in phenolic compounds, suggesting that compositional differences among honey types may explain their divergent biological effects. These findings suggest that the antimicrosporidial efficacy of honey is source- and concentration-dependent. Additional research is required to clarify the underlying molecular mechanisms.