Microbial Bioactives

Microbial Bioactives | Online ISSN 2209-2161
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Perinatal Tobacco Exposure, Microbiome Dysbiosis, and Progressive Fibrosing Interstitial Lung Diseases: A Systematic Review

Abstract 1. Introduction 2. Materials and Methods 3. Results 4. Discussion 5. Limitations 6. Conclusion References

Zainab Nur-Eldeen Aziz 1*, Basil O. Saleh 1

 

 

+ Author Affiliations

Microbial Bioactives 5 (1) 1-8 https://doi.org/10.25163/microbbioacts.5110704

Submitted: 11 June 2022 Revised: 03 August 2022  Accepted: 12 August 2022  Published: 14 August 2022 


Abstract

Perinatal tobacco exposure has emerged as a significant environmental determinant capable of shaping long-term respiratory health through mechanisms that extend beyond direct toxic injury. Increasing evidence suggests that tobacco-related compounds disrupt early microbial colonization during critical developmental windows, thereby influencing immune maturation, inflammatory signaling, and pulmonary homeostasis across the lifespan. This systematic review and meta-analysis examined the relationship between prenatal and early postnatal tobacco exposure, microbiome dysbiosis, and susceptibility to progressive fibrosing interstitial lung diseases (PF-ILDs). Following PRISMA 2020 guidelines, studies published before January 2024 were systematically identified from PubMed, Scopus, Web of Science, and Embase. Eligible observational and experimental studies evaluating microbiome alterations, immune dysregulation, and fibrotic lung outcomes associated with tobacco exposure were included in qualitative and quantitative synthesis. The findings consistently demonstrated that perinatal tobacco exposure is associated with reduced microbial diversity, enrichment of pro-inflammatory taxa, altered immune responses, and impaired pulmonary development. Meta-analytic synthesis further revealed significant associations between microbial disruption and markers of fibrotic susceptibility, supporting a biologically plausible developmental pathway linking early-life exposure to later pulmonary vulnerability. Alterations in the gut–lung axis, persistent inflammatory activation, and dysregulated epithelial repair mechanisms emerged as central contributors to disease progression. Collectively, this review highlights microbiome dysbiosis as a potential intermediary mechanism connecting early tobacco exposure with progressive fibrotic lung disease and emphasizes the importance of early preventive interventions and microbiome-focused therapeutic strategies.

Keywords: Perinatal tobacco exposure; lung microbiome; developmental origins of disease; pulmonary fibrosis; PF-ILD; immune dysregulation; early-life exposure

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