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Updated: Feb 24, 2026

Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing
Published on: October 15, 2019
Association Between Dietary Index for Gut Microbiota and the Risk of Pelvic Inflammatory Disease: Mediating Role of
Yanjing Bao1,2, Xianyue Hu1,3, Tianyang Gao2,4
1The Second School of Clinical Medicine Southern Medical University Guangzhou People's Republic of China.
Abstract:
Recent studies suggest that an imbalance in the gut microbiota, known as dysbiosis, may affect inflammation. The Dietary Index for Gut Microbiota (DI-GM) is a new measure of dietary quality that reflects gut microbiota diversity and abundance. However, its association with pelvic inflammatory disease (PID) remains unclear. This study explored the relationship between DI-GM and the risk of developing PID. This cross-sectional study analyzed data from 4539 women aged 18-59 years obtained from the National Health and Nutrition Examination Survey (NHANES) database for the period of 2013-2018. To explore the association between DI-GM and PID, we employed weighted multivariable linear and logistic regression, restricted cubic splines (RCS), and subgroup analyses. Additionally, mediation analysis was conducted to assess the influence of anti- and pro-inflammatory dietary patterns, represented by the Dietary Inflammatory Index (DII), on the relationship between DI-GM and PID. Among the eligible participants, 255 (5.62%) had PID. A higher proportion of participants with lower DI-GM scores experienced PID. Multivariable logistic regression analysis revealed a negative association between DI-GM and the risk of PID, regardless of whether the independent variable was considered a continuous variable or in quartiles in the fully adjusted model (Model 3, continuous variable: OR = 0.87, 95% confidence interval (CI): 0.79-0.96, p = 0.012; Q3 vs. Q1: OR = 0.58, 95% CI = 0.36-0.94, p = 0.036; Q4 vs. Q1: OR = 0.55, 95% CI = 0.35-0.87, p = 0.017, p for trend = 0.018). The RCS curves demonstrated a non-linear relationship between the DI-GM scores and PID risk. Subgroup analyses indicated an inverse correlation between DI-GM and PID risk across various covariates. Mediation analysis showed that inflammatory dietary patterns accounted for 26.82% of the mediation proportion in the association between DI-GM and PID. These results indicate that higher DI-GM scores are correlated with a decreased risk of PID. Inflammatory dietary patterns may mediate the association between DI-GM and PID, suggesting that restoring gut homeostasis and health through dietary interventions may prevent or ameliorate PID.
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