Scholarlink

Background <p>The pulmonary microbiome is increasingly recognized as a key determinant of pneumonia severity, yet its clinical implications remain incompletely understood. Disruption of microbial ecology, or dysbiosis, may impair host immune responses and exacerbate disease progression. This study aimed to characterize microbiome alterations associated with severe pneumonia and their correlation with host inflammatory and coagulative parameters.</p> Methods <p>In this multicenter, prospective observational cohort study conducted across nine hospitals in Shanghai (2021–2025), bronchoalveolar lavage fluid (BALF) samples from 306 patients with clinically diagnosed pulmonary infections were analyzed using metagenomic next-generation sequencing (mNGS). Patients were stratified into severe (<i>n</i> = 196) and non-severe (<i>n</i> = 110) groups using WHO-derived severe pneumonia criteria at the time of bronchoalveolar lavage (BAL). Microbial taxonomic profiles, diversity indices, co-occurrence networks, and correlations with clinical markers were comprehensively assessed using standard bioinformatic and statistical approaches.</p> Results <p>Severe pneumonia was associated with marked microbial dysbiosis, including reorganization of co-occurrence network topology with centrality shifting away from commensals toward opportunistic taxa in severe disease, characterized by reduced α-diversity, altered β-diversity, and enrichment of opportunistic Gram-negative pathogens including <i>Acinetobacter</i> and <i>Klebsiella</i>. In contrast, commensals such as <i>Rothia</i> and <i>Prevotella</i> were depleted. Co-occurrence network analysis revealed fragmentation of microbial interactions in severe cases, with centrality shifting from commensals to opportunists like <i>Corynebacterium striatum</i>. Shannon diversity negatively correlated with SOFA scores, and specific taxa positively associated with systemic inflammation (CRP, PCT) and coagulation abnormalities. Nearly all samples demonstrated polymicrobial infection, with distinct microbial patterns observed across monomicrobial and polymicrobial subgroups.</p> Conclusion <p>Our multicenter observational analysis suggests that severe pneumonia is associated with marked ecological disruption of the lower-airway microbiome, characterized by commensal loss, opportunist expansion, and fragmented interspecies networks, and with concurrent inflammatory and coagulative abnormalities. These hypothesis-generating findings warrant external validation in independent, multi-region cohorts and longitudinal sampling to test directionality and causality before informing clinical decision-making.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Airway microbiome dysbiosis in severe pneumonia: metagenomic evidence of pathogen expansion and commensal depletion

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月29日

查看全文
  • Yuhan Wang,
  • Yao Shen,
  • Jie Shen,
  • Jing Bi,
  • Jian Xu,
  • Tianchang Wei,
  • Ruilan Wang,
  • Xueling Wu,
  • Feng Li,
  • Jianwen Bai,
  • Zhijun Jie,
  • Dongni Hou,
  • Yuanlin Song

摘要

Background

The pulmonary microbiome is increasingly recognized as a key determinant of pneumonia severity, yet its clinical implications remain incompletely understood. Disruption of microbial ecology, or dysbiosis, may impair host immune responses and exacerbate disease progression. This study aimed to characterize microbiome alterations associated with severe pneumonia and their correlation with host inflammatory and coagulative parameters.

Methods

In this multicenter, prospective observational cohort study conducted across nine hospitals in Shanghai (2021–2025), bronchoalveolar lavage fluid (BALF) samples from 306 patients with clinically diagnosed pulmonary infections were analyzed using metagenomic next-generation sequencing (mNGS). Patients were stratified into severe (n = 196) and non-severe (n = 110) groups using WHO-derived severe pneumonia criteria at the time of bronchoalveolar lavage (BAL). Microbial taxonomic profiles, diversity indices, co-occurrence networks, and correlations with clinical markers were comprehensively assessed using standard bioinformatic and statistical approaches.

Results

Severe pneumonia was associated with marked microbial dysbiosis, including reorganization of co-occurrence network topology with centrality shifting away from commensals toward opportunistic taxa in severe disease, characterized by reduced α-diversity, altered β-diversity, and enrichment of opportunistic Gram-negative pathogens including Acinetobacter and Klebsiella. In contrast, commensals such as Rothia and Prevotella were depleted. Co-occurrence network analysis revealed fragmentation of microbial interactions in severe cases, with centrality shifting from commensals to opportunists like Corynebacterium striatum. Shannon diversity negatively correlated with SOFA scores, and specific taxa positively associated with systemic inflammation (CRP, PCT) and coagulation abnormalities. Nearly all samples demonstrated polymicrobial infection, with distinct microbial patterns observed across monomicrobial and polymicrobial subgroups.

Conclusion

Our multicenter observational analysis suggests that severe pneumonia is associated with marked ecological disruption of the lower-airway microbiome, characterized by commensal loss, opportunist expansion, and fragmented interspecies networks, and with concurrent inflammatory and coagulative abnormalities. These hypothesis-generating findings warrant external validation in independent, multi-region cohorts and longitudinal sampling to test directionality and causality before informing clinical decision-making.