Respir Investig. 2026 Sep 15;64(6):101515. doi: 10.1016/j.resinv.2026.101515. Online ahead of print.

ABSTRACT

The lung microbiome is increasingly recognized as an important factor in idiopathic pulmonary fibrosis (IPF) and hypersensitivity pneumonitis (HP), two interstitial lung diseases with overlapping clinical features but distinct underlying mechanisms and management. This systematic review, conducted in accordance with PRISMA guidelines, evaluated the current evidence regarding lung microbiome alterations in IPF and HP. A literature search was performed using PubMed as the primary database and supplemented by Google Scholar searches. The review protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO; CRD420261415180). Fourteen unique studies met the inclusion criteria, comprising 13 studies involving IPF and 2 studies involving HP, with one study overlapping between the two disease groups. Current evidence suggests that IPF is associated with increased bacterial burden, reduced microbial diversity, and enrichment of specific taxa, including Streptococcus and Staphylococcus, which have been linked to immune activation and fibrotic progression. In contrast, limited available evidence suggests that HP may exhibit a lower bacterial burden, with microbial patterns influenced predominantly by environmental exposures, including bacterial and fungal antigens from occupational and domestic sources. Emerging studies highlight host-microbiome and environment-microbiome interactions in disease progression. Overall, the current evidence supports a role for microbial dysbiosis in IPF, whereas microbiome alterations in HP appear to be more closely associated with environmental microbial exposures. However, conclusions regarding HP should be interpreted cautiously due to the limited number of studies. Further longitudinal and multi-omics studies are needed to clarify causality and identify robust microbial biomarkers for diagnosis and therapy.

PMID:42743786 | DOI:10.1016/j.resinv.2026.101515

Curr Probl Cancer. 2026 Sep 7;65:101333. doi: 10.1016/j.currproblcancer.2026.101333. Online ahead of print.

ABSTRACT

Heterogeneous tumor microenvironment (TME) in lung cancer plays a crucial role in disease progression and resistance to therapy. Despite advances in single-cell and bulk omics profiling, these methods often overlook spatial context, which is vital for understanding cell-cell interactions and regional heterogeneity. In recent years, spatial omics technologies-including spatial genomics, transcriptomics, proteomics, and metabolomics-have revolutionized the ability to map molecular landscapes while maintaining tissue architecture. These advancements have become essential components of next-generation lung cancer management. By providing unprecedented resolution in characterizing the lung cancer TME, spatial omics could reveal prognostic and predictive biomarkers and identify new therapeutic vulnerabilities. This review will provide the first critical evaluation of spatial multi-omics approaches for lung cancer prognosis. It will also assess various integration strategies for multi-omics data to explore the clinical translational potential of these tools for therapy selection and patient stratification. Therefore, a deeper understanding of spatial omics technologies and their application in lung cancer can significantly improve precision diagnostics and therapeutic decision-making.

PMID:42705130 | DOI:10.1016/j.currproblcancer.2026.101333