Microtubules are in a dynamic equilibrium of polymerization and depolymerization. In monocytes and macrophages, microtubules bind endotoxin and partly regulate inflammatory events such as cytokine production. To characterize the morphologic differences between alveolar macrophage and blood monocyte microtubules after LPS stimulation, cells were examined by immunofluorescent microscopy and laser confocal microscopy. Fresh monocytes contained an average of 26 microtubules per cell which significantly increased to 31 microtubules per cell following a 30-min exposure to LPS (P < 0.001). Using a nocodazole-based assay of microtubule dynamic instability, the half-life of fresh unstimulated human monocyte microtubules was approximately 18 s and extended to 26 s following a 30-min exposure to LPS. In vitro maturation of monocytes for 18 h increased microtubule stability but not number. Compared to monocytes, alveolar macrophage microtubules were longer, more numerous, and much more stable. These results suggest that alveolar macrophage microtubules are more numerous and stable than blood monocyte microtubules and that LPS causes an increase in monocyte microtubule number and stability.
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http://dx.doi.org/10.1165/ajrcmb.16.2.9032118 | DOI Listing |
Unlabelled: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. ( ) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during infection and the variation of the response in different macrophage subtypes remain obscure.
View Article and Find Full Text PDFRespir Investig
January 2025
Department of Respiratory Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki, 852-8501, Japan.
Sargramostim, a recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSF) inhalation therapy, was recently approved for pharmaceutical use in Japan and shows promise as a treatment for autoimmune pulmonary alveolar proteinosis (APAP). For APAP patients with severe respiratory failure due to advanced lung fibrosis, lung transplantation is also a treatment option; however, APAP may recur after the procedure. Here, we report a case of successful sargramostim inhalation therapy for post-transplant APAP relapse in a patient who underwent living lung transplantation owing to severe fibrosis.
View Article and Find Full Text PDFSci Rep
January 2025
Harbin Medical University, Harbin, Heilongjiang Province, China.
Interstitial lung disease (ILD) is known to be a major complication of systemic sclerosis (SSc) and a leading cause of death in SSc patients. As the most common type of ILD, the pathogenesis of idiopathic pulmonary fibrosis (IPF) has not been fully elucidated. In this study, weighted correlation network analysis (WGCNA), protein‒protein interaction, Kaplan-Meier curve, univariate Cox analysis and machine learning methods were used on datasets from the Gene Expression Omnibus database.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China. Electronic address:
Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.
View Article and Find Full Text PDFFront Immunol
January 2025
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Introduction: AE and whether the inhibition of the MyD88 inflammatory pathway can enhance Ghrelin expression to collaboratively modulate AE progression remains unclear.
Methods: In this study, we evaluated Ghrelin serum levels and changes in TLR4/MyD88/NF-κB pathway proteins and inflammatory factors in AE patients and mouse models at different stages of infection (-4, -8, and -12 weeks). Additionally, we administered the MyD88 inhibitor TJ-M2010-5 intraperitoneally to infected mice to evaluate alterations in inflammation and Ghrelin levels, as well as disease progression.
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