Increased Respiratory Burst and Increased Expression of Complement Receptor-3 (CD11b/CD18) and of IL-8 Receptor-A in Neutrophil Granulocytes from Newborns after Vaginal Delivery

Neonatology ◽  
2003 ◽  
Vol 83 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Peter Gessler ◽  
Clemens Dahinden
Keyword(s):  
Vaginal Delivery ◽  
Respiratory Burst ◽  
Neutrophil Granulocytes ◽  
Complement Receptor ◽  
Complement Receptor 3

scholarly journals β-Glucan enhances complement-mediated hematopoietic recovery after bone marrow injury

Blood ◽  
2006 ◽  
Vol 107 (2) ◽  
pp. 835-840 ◽  
Author(s):  
Daniel E. Cramer ◽  
Daniel J. Allendorf ◽  
Jarek T. Baran ◽  
Richard Hansen ◽  
Jose Marroquin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Serum ◽  
Complement Receptor ◽  
Dependent Manner ◽  
Complement Receptor 3 ◽  
Total Body ◽  
Stimulating Factor ◽  
Sublethal Irradiation ◽  
Classic Pathway

AbstractMyelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony-stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b). In the present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPCs) and the role of complement (C) and complement receptor 3 (CR3) in BM injury/repair. We demonstrate here that stroma-iC3b tethers HPCs via the inserted (I) domain of HPC complement receptor 3 (CR3, CD11b/CD18, Mac-1). Following irradiation, stroma-iC3b was observed in the presence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2-/- mice, implicating a role for antibody (Ab) and the classic pathway of C activation. Furthermore, a novel role for soluble yeast β-glucan, a ligand for the CR3 lectin-like domain (LLD), in the priming of CR3+ HPC is suggested. Soluble yeast β-glucan could enhance the proliferation of tethered HPCs, promote leukocyte recovery following sublethal irradiation, and increase the survival of lethally irradiated animals following allogeneic HPC transplantation in a CR3-dependent manner. Taken together, these observations suggest a novel role for C, CR3, and β-glucan in the restoration of hematopoiesis following injury. (Blood. 2006;107:835-840)

scholarly journals Activated microglia desialylate their surface, stimulating complement receptor 3‐mediated phagocytosis of neurons

Glia ◽  
2019 ◽  
Vol 68 (5) ◽  
pp. 989-998 ◽  
Author(s):  
David H. Allendorf ◽  
Mar Puigdellívol ◽  
Guy C. Brown
Keyword(s):  
Complement Receptor ◽  
Activated Microglia ◽  
Complement Receptor 3

Role of complement and Fcγ receptors in the protective activity of the long pentraxin PTX3 against Aspergillus fumigatus

Blood ◽  
2010 ◽  
Vol 116 (24) ◽  
pp. 5170-5180 ◽  
Author(s):  
Federica Moalli ◽  
Andrea Doni ◽  
Livija Deban ◽  
Teresa Zelante ◽  
Silvia Zagarella ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Alternative Pathway ◽  
Complement Receptor ◽  
Protective Activity ◽  
Opsonic Activity ◽  
Reactive Protein ◽  
Complement Receptor 3 ◽  
Dependent Pathway

AbstractPentraxin 3 (PTX3) is a soluble pattern recognition molecule playing a nonredundant role in resistance against Aspergillus fumigatus. The present study was designed to investigate the molecular pathways involved in the opsonic activity of PTX3. The PTX3 N-terminal domain was responsible for conidia recognition, but the full-length molecule was necessary for opsonic activity. The PTX3-dependent pathway of enhanced neutrophil phagocytic activity involved complement activation via the alternative pathway; Fcγ receptor (FcγR) IIA/CD32 recognition of PTX3-sensitized conidia and complement receptor 3 (CR3) activation; and CR3 and CD32 localization to the phagocytic cup. Gene targeted mice (ptx3, FcR common γ chain, C3, C1q) validated the in vivo relevance of the pathway. In particular, the protective activity of exogenous PTX3 against A fumigatus was abolished in FcR common γ chain-deficient mice. Thus, the opsonic and antifungal activity of PTX3 is at the crossroad between complement, complement receptor 3-, and FcγR-mediated recognition. Because short pentraxins (eg, C-reactive protein) interact with complement and FcγR, the present results may have general significance for the mode of action of these components of the humoral arm of innate immunity.

Factor H facilitates adherence of Neisseria gonorrhoeae to complement receptor 3 on eukaryotic cells

2010 ◽  
Vol 47 (13) ◽  
pp. 2246-2246
Author(s):  
Sarika Agarwal ◽  
Sanjay Ram ◽  
Jutamas Ngampasutadol ◽  
Sunita Gulati ◽  
Peter F. Zipfel ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Factor H ◽  
Eukaryotic Cells ◽  
Complement Receptor ◽  
Complement Receptor 3

Complement receptor 3-like immunoreactivity in the light green cells and the canopy cells of the pond snail, Lymnaea stagnalis

2000 ◽  
Vol 865 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Dai Hatakeyama ◽  
Iori Ito ◽  
Satoshi Kojima ◽  
Yutaka Fujito ◽  
Etsuro Ito
Keyword(s):  
Lymnaea Stagnalis ◽  
Pond Snail ◽  
Complement Receptor ◽  
Complement Receptor 3 ◽  
Light Green

Neutrophil labeling with [99mTc]-technetium stannous colloid is complement receptor 3-mediated and increases the neutrophil priming response to lipopolysaccharide

2006 ◽  
Vol 33 (3) ◽  
pp. 433-439 ◽  
Author(s):  
Hayley Gallagher ◽  
Stuart C. Ramsay ◽  
Jodie Barnes ◽  
Jacqueline Maggs ◽  
Nathan Cassidy ◽  
...  
Keyword(s):  
Complement Receptor ◽  
Complement Receptor 3 ◽  
Neutrophil Priming

scholarly journals Cranial irradiation mediated spine loss is sex-specific and complement receptor-3 dependent in male mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Joshua J. Hinkle ◽  
John A. Olschowka ◽  
Tanzy M. Love ◽  
Jacqueline P. Williams ◽  
M. Kerry O’Banion
Keyword(s):  
Quality Of Life ◽  
Dendritic Spine ◽  
Cranial Irradiation ◽  
Common Mechanism ◽  
Complement Receptor ◽  
Spine Density ◽  
Male Mice ◽  
Activation Markers ◽  
Complement Receptor 3

AbstractCranial irradiation is the main therapeutic treatment for primary and metastatic malignancies in the brain. However, cranial radiation therapy produces long-term impairment in memory, information processing, and attention that contribute to a decline in quality of life. The hippocampal neural network is fundamental for proper storage and retrieval of episodic and spatial memories, suggesting that hippocampal signaling dysfunction could be responsible for the progressive memory deficits observed following irradiation. Previous rodent studies demonstrated that irradiation induces significant loss in dendritic spine number, alters spine morphology, and is associated with behavioral task deficits. Additionally, the literature suggests a common mechanism in which synaptic elimination via microglial-mediated phagocytosis is complement dependent and associated with cognitive impairment in aging as well as disease. We demonstrate sexual dimorphisms in irradiation-mediated alterations of microglia activation markers and dendritic spine density. Further, we find that the significant dendritic spine loss observed in male mice following irradiation is microglia complement receptor 3 (CR3)-dependent. By identifying sex-dependent cellular and molecular factors underlying irradiation-mediated spine loss, therapies can be developed to counteract irradiation-induced cognitive decline and improve patient quality of life.

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