Objective: The present study was conducted to assess the changes in mucosal immunity and pulmonary function among participants in a 36-hour mixed task ultraendurance race.
Methods: Thirteen of the 20 race participants volunteered for the investigation (age 34±5 y). The event consisted of a mixture of aerobic, strong man, and military-style exercise. Participants had a pulmonary function test and gave a finger stick capillary blood sample and unstimulated saliva samples both before the event and upon dropout or completion. The blood sample was analyzed for hematocrit, and the saliva sample was analyzed for salivary flow rate, salivary alpha amylase, salivary immunoglobulin A (IgA), and IgA type 1.
Results: Significant differences were noted among the finishers and those who dropped out in salivary flow rate (P = .026), salivary IgA (P = .017), and peak expiratory flow (P = .05) measurements. Salivary flow rate and IgA for the race finishers were reduced from pre- to postrace, whereas the nonfinishers showed no change or small increases. No significant differences emerged for other variables.
Conclusions: Based on the results of the present investigation, finishing a 36-hour mixed task ultra-endurance event results in a decline in both pulmonary function and mucosal immunity compared with competitors who do not finish.
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http://dx.doi.org/10.1016/j.wem.2016.12.001 | DOI Listing |
J Immunol
January 2025
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
Macrophages are critical to maintaining and restoring tissue homeostasis during inflammation. The lipid metabolic state of macrophages influences their function and polarization, which is crucial to the resolution of inflammation. The contribution of lipid synthesis to proinflammatory macrophage responses is well understood.
View Article and Find Full Text PDFJ Immunol
February 2025
Division of Pulmonary, Critical Care and Sleep Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, United States.
The erythroblastic island (EBI) functions as a niche in which erythroblastic island macrophages (EBIMφs) are positioned within rings of erythroblasts, providing support and signals that orchestrate efficient erythropoiesis. We postulated burn injury impacts the EBI niche, given the nearly universal presence of anemia and inflammation in burn patients, and a divergent myeloid transcriptional signature that we observed in murine bone marrow following burn injury, in which granulocyte colony-stimulating factor (G-CSF) secretion broadly attenuated the expression of EBIMφ marker genes. Notably, we identified the heme-induced transcription factor Spi-C as a robust marker of EBIMφs in Spicigfp/igfp mice.
View Article and Find Full Text PDFSci Transl Med
March 2025
Department of Molecular Medicine, Scripps Research Institute, La Jolla, CA 92037, USA.
Interstitial lung disease (ILD) consists of a group of immune-mediated disorders that can cause inflammation and progressive fibrosis of the lungs, representing an area of unmet medical need given the lack of disease-modifying therapies and toxicities associated with current treatment options. Tissue-specific splice variants (SVs) of human aminoacyl-tRNA synthetases (aaRSs) are catalytic nulls thought to confer regulatory functions. One example from human histidyl-tRNA synthetase (HARS), termed HARS because the splicing event resulted in a protein encompassing the WHEP-TRS domain of HARS (a structurally conserved domain found in multiple aaRSs), is enriched in human lung and up-regulated by inflammatory cytokines in lung and immune cells.
View Article and Find Full Text PDFJ Immunol
February 2025
Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, United States.
Persistent systemic inflammation is associated with an elevated risk of cardiometabolic diseases. However, the characteristics of the innate and adaptive immune systems in individuals who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states.
View Article and Find Full Text PDFSci Adv
March 2025
Department of Radiation Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Lung cancer exhibits altered metabolism, influencing its response to radiation. To investigate the metabolic regulation of radiation response, we conducted a comprehensive, metabolic-wide CRISPR-Cas9 loss-of-function screen using radiation as selection pressure in human non-small cell lung cancer. Lipoylation emerged as a key metabolic target for radiosensitization, with lipoyltransferase 1 (LIPT1) identified as a top hit.
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