Professor University of California, Merced, California, United States
Disclosure(s):
Jennifer Manilay, PhD: No financial relationships to disclose
Introduction/Rationale: Populations with high pesticide exposure face elevated risks of immune and hematologic disorders, yet the mechanisms remain unclear. Pyraclostrobin (PYRA), a fungicide known to disrupt mitochondrial function, may alter hematopoietic and thymic processes. We hypothesized that PYRA induces mitochondrial stress leading to immune dysregulation in a sex-dependent manner.
Methods: Eight-week-old C57BL/6 mice were exposed to PYRA (10–100 mg/kg b.w.) for 14 or 30 days via intraperitoneal injection. Hematologic profiles were obtained by complete blood count, while flow cytometry assessed bone marrow progenitors, thymic and splenic cell populations.
Results: PYRA exposure at 10 mg/kg altered T lymphocyte populations in both differently, suggesting sex-specific immune modulation. Males showed increased MPP2 and decreased MPP3 frequencies, with reduced Lin⁻c-Kit⁺Sca1⁻ progenitors; females exhibited decreased ST-HSCs, increased GMP%, and decreased MEP%. Thymic analysis revealed increased total thymocyte counts in males, including CD8⁺SP cells, while females showed selective CD8⁺SP increases.
Conclusion: PYRA disrupts hematopoietic and thymic development in a sex-dependent manner, potentially through mitochondrial dysfunction. Ongoing gene expression analysis will clarify mitochondrial–hematopoietic interactions, enhancing understanding of pesticide-induced immune and marrow failure mechanisms.
