Dataset Information

Maternal adiposity is associated with inflammatory gene expression in leukocytes at term human pregnancy: A pilot study.

ABSTRACT:

Background

Human labor is associated with an inflammatory process that takes place at the maternal-fetal interface, where leukocytes infiltrate and contribute to the local production of effector molecules such as cytokines, chemokines, MMPs, etc. This process may be altered by a low-grade chronic inflammation, characteristic of obesity, resulting in adverse pregnancy outcomes. In this cross-sectional pilot study, we analyzed the relationship between maternal adiposity and inflammation-related gene expression in leukocytes from six healthy women with term pregnancies without labor.

Methods

We estimated maternal adiposity and examined the relative expression of 211 inflammation-related genes in maternal peripheral blood leukocytes (MAT), placental intervillous blood leukocytes (PLA), and choriodecidual leukocytes (CHD) by real-time qPCR. Finally, we analyzed the correlation between maternal adiposity and gene expression.

Results

Participants' adiposity ranged from 27.6% to 61.1% (n = 6). The expression of 23 genes significantly differed (p < 0.05) in MAT, PLA, and CHD leukocytes, most of which code for chemokines and proinflammatory cytokines. Importantly, increasing maternal adiposity correlated (r > 0.7) mostly positively with the expression of genes related to activation, migration, infiltration, and proinflammation in MAT (36 genes) and PLA (31 genes). In contrast, in CHD leukocytes maternal adiposity correlated only negatively with seven genes, involved in migration and infiltration.

Conclusion

Our findings suggest that during term pregnancy, increased maternal adiposity may enhance the priming of peripheral leukocytes, while in choriodecidua it may alter leukocyte recruitment and proinflammatory activity. Maternal adiposity must be considered an important variable in further studies that analyze inflammation-related gene expression in pregnant women.

SUBMITTER: MacDonald-Ramos K

PROVIDER: S-EPMC8077112 | biostudies-literature |

REPOSITORIES: biostudies-literature

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