Short-term PM exposure induces transient lung injury and repair.

Exposure to fine atmospheric particulate matter (PM) is known to induce lung inflammation and injury; however, the way in which sophisticated endogenous lung repair and regenerative programs respond to this exposure remains unknown. In this study, we established a whole-body mouse exposure model to mimic real scenarios. Exposure to fine PM (PM with an aerodynamic diameter ≤ 2.

Cellular metabolic basis of altered immunity in the lungs of patients with COVID-19.

Metabolic pathways drive cellular behavior. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes lung tissue damage directly by targeting cells or indirectly by producing inflammatory cytokines. However, whether functional alterations are related to metabolic changes in lung cells after SARS-CoV-2 infection remains unknown.

LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.

Targeting airway goblet cell metaplasia is a novel strategy that can potentially reduce the chronic obstructive pulmonary disease (COPD) symptoms. Tumor suppressor liver kinase B1 (LKB1) is an important regulator of the proliferation and differentiation of stem/progenitor cells. In this study, we report that LKB1 expression was downregulated in the lungs of patients with COPD and in those of cigarette smoke-exposed mice.

Associations between CCL21 gene polymorphisms and susceptibility to rheumatoid arthritis: a meta-analysis.

Rheumatoid arthritis (RA) is a chronic systemic disorder characterized by the development through angiogenesis, which is dependent on endothelial cell activation, migration and proliferation and CCL21 plays an important role in this pathology. Currently, CCL21 gene polymorphism studies on rheumatoid arthritis are scarce and the results are diverse. This meta-analysis was performed to determine if CCL21 gene polymorphisms correlate with the risk of developing RA.