PhD Scientific Days 2024

Poster Session J - Pathological and Oncological Sciences 1.

Immune system organs and intestinal tumors morphological features in tolerant and susceptible to hypoxia mice after azoxymethane administration and dextran sulfate sodium consumption

Text of the abstract

Introduction

Organisms are divided according to hypoxia resistance as tolerant (T) or susceptible (S), based on HIF-1 expression. Differences in HIF-1 levels may influence inflammation, inflammatory bowel disease development, and colorectal cancer (CRC) progression due to dextran sodium sulfate (DSS) and azoxymethane (AOM) effect.

Aims

To investigate a morphological features of the colon, mesenteric lymph nodes, thymus, and spleen, as well as the lymphocyte subpopulation composition in CRC induced by AOM administration and DSS consumption in male C57BL/6 mice with different hypoxia tolerance.

Methods

Male C57BL/6 mice (n=50) were examined to hypoxia tolerance in decompression chamber. After assessing gasping time on altitude 10 000 m, colorectal cancer was induced by AOM. Tissues were collected on the 141st day for tumor area and lymphocyte subpopulations analysis.

Result

Tumors were detected in the colon's distal part in 24% T and 80% S to hypoxia animals. Microscopic analysis revealed tumors in 41% T and 80% S mice, with S mice larger tumor areas. No metastases were detected in lymph nodes. In S mice there was an increase in the number of cytotoxic T-lymphocytes and B-lymphocytes in blood. Only in S mice the absolute and relative numbers of B-lymphocytes and NK cells, the absolute number of cytotoxic T-lymphocytes increased in mesenteric lymph nodes.

Conclusion

The severity of CRC induced by AOM and DSS varied depending on hypoxia tolerance. S animals demonstrated larger tumor areas and a higher frequency of adenocarcinomas. S mice demonstrated certain immune cells in blood and lymph nodes higher levels, therefore, contributing stronger immune response to CRC.

Funding

This work was supported by the Russian Science Foundation Grant No. 23-25-00294.