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Causal Relationship Between Gut Microbiota and Pressure Ulcers: A Two-Sample Bidirectional Mendelian Randomisation
Pei Luo1, Liqing Jiang2, Hongmei Chen3
1Department of Thoracic Surgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi, China.
Background:
Pressure ulcers (PUs) remain a major clinical challenge, particularly among immobilized and critically ill patients. Accumulating evidence suggests that alterations in gut microbiota composition and diversity are associated with PUs. But until now, the causal association between them has been unclear.
Aim:
We conducted a two-sample Mendelian randomisation (MR) study to investigate the causal effect of gut microbiota on PUs.
Study Design:
Gut microbiota summary statistics were obtained from the MiBioGen Consortium (18,340 individuals, 24 cohorts, 211 taxa), and PU data were derived from the FinnGen biobank (354,567 Europeans; 1479 PU cases, 353,088 controls). Causal estimates were calculated using inverse variance weighted (IVW), weighted median, simple mode, weighted mode and MR-Egger methods, with sensitivity analyses including pleiotropy tests, Cochran's Q and leave-one-out analysis. MR Steiger's test was applied to infer directionality.
Results:
IVW analysis indicated protective effects of Clostridiaceae 1 (odds ratio, OR = 0.668, 95% confidence intervals (CI) = 0.455-0.982, p = 0.040), genus Coprococcus2 (OR = 0.508, 95% CI = 0.344-0.751, p = 0.001) and genus Gordonibacter (OR = 0.812, 95% CI = 0.676-0.976, p = 0.027) against PUs. While genus Anaerotruncus (OR = 1.729, 95% CI = 1.189-2.513, p = 0.004) and genus Christensenellaceae R7 (OR = 1.953, 95% CI = 1.087-3.508, p = 0.025) increased PUs' risk. Reverse MR suggested causal effects of PUs on five genera, including Butyrivibrio (OR = 0.887, 95% CI = 0.798-0.985, p = 0.026), Erysipelotrichaceae UCG003 (OR = 1.057, 95% CI = 1.004-1.113, p = 0.035), Eubacterium fissicatena group (OR = 0.898, 95% CI = 0.811-0.995, p = 0.040), Faecalibacterium (OR = 0.952, 95% CI = 0.908-0.999, p = 0.046) and Eubacterium oxidoreducens group (OR = 1.093, 95% CI = 1.001-1.194, p = 0.047). Sensitivity analysis supported the robustness of the findings, and Steiger's test confirmed directionality from gut microbiota to PUs.
Conclusion:
This MR study provides genetic evidence for a causal role of gut microbiota in PU risk, supporting the potential of microbiota-targeted interventions and offering new insights into PU pathogenesis and highlighting their particular relevance for prevention strategies in immobilized critical care patients.
Relevance To Clinical Practice:
The study provides epidemiological evidence for a gut-skin link in PUs and suggests personalised microbiota-based intervention strategies for critically bedridden patients.
Insights
This study used Mendelian randomization to investigate the causal link between gut microbiota and pressure ulcers (PUs). Certain gut bacteria like Coprococcus and Gordonibacter may protect against PUs, while others increase risk, suggesting microbiota-targeted interventions.
Area of Science:
- Genetics
- Microbiology
- Epidemiology
Background:
- Pressure ulcers (PUs) are a significant clinical problem, especially in immobilized patients.
- Alterations in gut microbiota composition are linked to PUs, but a causal relationship remains unclear.
Purpose of the Study:
- To investigate the causal effect of gut microbiota on the risk of developing pressure ulcers using a two-sample Mendelian randomization (MR) approach.
Main Methods:
- Utilized large-scale summary statistics for gut microbiota (MiBioGen Consortium) and pressure ulcer data (FinnGen biobank).
- Employed various MR methods (IVW, weighted median, etc.) and sensitivity analyses to assess causality and directionality.
Main Results:
- Identified specific gut bacteria with protective effects against PUs (e.g., Coprococcus, Gordonibacter) and those increasing risk (e.g., Anaerotruncus).
- Reverse MR indicated potential causal effects of PUs on certain gut genera.
- Sensitivity analyses confirmed the robustness of findings and directionality from gut microbiota to PUs.
Conclusions:
- Provides genetic evidence for a causal role of gut microbiota in PU development.
- Supports the potential for microbiota-targeted interventions in preventing PUs, particularly in critical care settings.
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