The ability of neutrophils to carry out chemotaxis in response to low chemoattractant concentrations, but arrest their motility when exposed to higher concentrations of the same substance, has fascinated investigators for years. By analyzing the temporal characteristics of the morphological responses, corresponding to chemotaxis and cell arrest, we have recently discovered that the choice between them is made by transduction of the continuous binding process into either single or multiple stimuli within defined time intervals, initiating chemotaxis or cell arrest, respectively. Both experimental and theoretical lines of evidence are presented to support the validity of this unique mechanism.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0167-4889(94)00197-m | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The IclR-family transcriptional regulator XyrR controls flotation, motility, antibiotic production and virulence in sp. ATCC 39006.
Front Microbiol
January 2025
Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
The opportunistic pathogen sp. ATCC 39006 (S39006) is a rod-shaped, motile, Gram-negative bacterium that produces a 𝛽-lactam antibiotic (a carbapenem) and a bioactive red-pigmented tripyrrole antibiotic, prodigiosin. It is also the only known enterobacterium that naturally produces intracellular gas vesicles (GVs), enabling cells to float in static water columns.
View Article and Find Full Text PDFBiological activities observed in living systems occur as the output of which nanometer-, submicrometer-, and micrometer-sized structures and tissues non-linearly and dynamically behave through chemical reaction networks, including the generation of various molecules and their assembly and disassembly. To understand the essence of the dynamic behavior in living systems, simpler artificial objects that exhibit cell-like non-linear phenomena have been recently constructed. However, most objects exhibiting cell-like dynamics have been found through trial-and-error experiments, and there are no strategies for designing them as molecular systems.
View Article and Find Full Text PDFREDD1-dependent GSK3β signaling in podocytes promotes canonical NF-κB activation in diabetic nephropathy.
J Biol Chem
January 2025
Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania 17033. Electronic address:
Increasing evidence supports the role of an augmented immune response in the early development and progression of renal complications caused by diabetes. We recently demonstrated that podocyte-specific expression of stress response protein regulated in development and DNA damage response 1 (REDD1) contributes to activation of the pro-inflammatory transcription factor NF-κB in the kidney of diabetic mice. The studies here were designed to define the specific signaling events whereby REDD1 promotes NF-κB activation in the context of diabetic nephropathy.
View Article and Find Full Text PDFKnockout or treatment with an antagonist of formyl peptide receptor 1 protects mice from sepsis by inhibiting inflammation.
Cytokine
January 2025
Department of Gastroenterology, General Hospital of Ningxia Medical University (The First Clinical Medical College of Ningxia Medical University), 750004 Yinchuan, China.
Background: Sepsis is an infection-related systemic inflammation with high mortality rates. Activation of formyl peptide receptor 1 (FPR1) in immune cells can promote their chemotaxis and inflammatory response, which imbalances immune response during the process of sepsis. FPR1 blockade did diminish systemic inflammatory response during bacterial infection.
View Article and Find Full Text PDFOrgan-specific microenvironments drive divergent T cell evolution in acute graft-versus-host disease.
Sci Transl Med
January 2025
Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
Tissue-specific T cell immune responses play a critical role in maintaining organ health but can also drive immune pathology during both autoimmunity and alloimmunity. The mechanisms controlling intratissue T cell programming remain unclear. Here, we leveraged a nonhuman primate model of acute graft-versus-host disease (aGVHD) after allogeneic hematopoietic stem cell transplantation to probe the biological underpinnings of tissue-specific alloimmune disease using a comprehensive systems immunology approach including multiparameter flow cytometry, population-based transcriptional profiling, and multiplexed single-cell RNA sequencing and TCR sequencing.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!