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Objective <p>To investigate whether lung microbial composition differs between individuals with rheumatoid arthritis and pulmonary fibrosis (RA-PF) compared to those without fibrosis (RA-no-PF).</p> Methods <p>We enrolled 54 RA patients (22 RA-PF, 32 RA-no-PF) from rheumatology and pulmonary clinics. PF was defined by high-resolution computed tomography (HRCT) findings. Induced sputum was analyzed using 16&#xa0;S rRNA sequencing to identify the relative abundance of sputum bacteria. Taxonomic differences between groups were evaluated using three independent analytic approaches: Mann-Whitney U, DESeq2, and EdgeR, with false discovery rate correction. Logistic regression examined associations between <i>Lautropia</i> abundance and clinical variables.</p> Results <p>Individuals with RA-PF were older, more often male, and had a higher history of smoking than those with RA-no-PF. Alpha diversity was lower in RA-PF, while beta diversity did not differ between groups. Across the three analytic methods, <i>Lautropia</i> consistently showed decreased abundance in RA-PF compared to RA-no-PF. In multivariable models adjusting for age, sex, and smoking, RA-PF remained independently associated with undetectable levels of <i>Lautropia</i> (OR = 0.14, <i>p</i> = 0.023). Within RA-PF, when <i>Lautropia</i> was undetectable, there was no difference in pulmonary physiology but did show a trend towards more lung fibrosis.</p> Conclusion <p>Sputum <i>Lautropia</i> is significantly reduced in RA-PF, and its absence may correlate with more severe fibrosis. These findings support a potential role for the lung microbiome in the pathogenesis of pulmonary fibrosis and raise the possibility that commensal taxa such as <i>Lautropia</i> modulate fibrotic pathways. Longitudinal and mechanistic studies are needed to determine whether <i>Lautropia</i> depletion precedes fibrosis and whether microbial-directed approaches represent new therapeutic avenues in RA.</p>

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Sputum lautropia is decreased in rheumatoid arthritis-associated pulmonary fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月17日

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  • Timothy M. Wilson,
  • Brendan Allen,
  • J. Kirk Harris,
  • Kristine A. Kuhn,
  • Kevin D. Deane,
  • Stephen M. Humphries,
  • Joyce S. Lee,
  • Joshua J. Solomon,
  • M. Kristen Demoruelle

摘要

Objective

To investigate whether lung microbial composition differs between individuals with rheumatoid arthritis and pulmonary fibrosis (RA-PF) compared to those without fibrosis (RA-no-PF).

Methods

We enrolled 54 RA patients (22 RA-PF, 32 RA-no-PF) from rheumatology and pulmonary clinics. PF was defined by high-resolution computed tomography (HRCT) findings. Induced sputum was analyzed using 16 S rRNA sequencing to identify the relative abundance of sputum bacteria. Taxonomic differences between groups were evaluated using three independent analytic approaches: Mann-Whitney U, DESeq2, and EdgeR, with false discovery rate correction. Logistic regression examined associations between Lautropia abundance and clinical variables.

Results

Individuals with RA-PF were older, more often male, and had a higher history of smoking than those with RA-no-PF. Alpha diversity was lower in RA-PF, while beta diversity did not differ between groups. Across the three analytic methods, Lautropia consistently showed decreased abundance in RA-PF compared to RA-no-PF. In multivariable models adjusting for age, sex, and smoking, RA-PF remained independently associated with undetectable levels of Lautropia (OR = 0.14, p = 0.023). Within RA-PF, when Lautropia was undetectable, there was no difference in pulmonary physiology but did show a trend towards more lung fibrosis.

Conclusion

Sputum Lautropia is significantly reduced in RA-PF, and its absence may correlate with more severe fibrosis. These findings support a potential role for the lung microbiome in the pathogenesis of pulmonary fibrosis and raise the possibility that commensal taxa such as Lautropia modulate fibrotic pathways. Longitudinal and mechanistic studies are needed to determine whether Lautropia depletion precedes fibrosis and whether microbial-directed approaches represent new therapeutic avenues in RA.