Neutrophils cascading their way to inflammation
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TLDR
Current data suggest that neutrophil chemoattractants have unique functions in the recruitment of neutrophils into inflammatory sites in vivo, dictated by their distinct patterns of temporal and spatial expression.About:
This article is published in Trends in Immunology.The article was published on 2011-10-01 and is currently open access. It has received 486 citations till now. The article focuses on the topics: Innate immune system.read more
Citations
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Stretch-induced human myometrial cytokines enhance immune cell recruitment via endothelial activation.
TL;DR: The current in vitro study demonstrated that mechanical stretch directly induces secretion of multiple cytokines and chemokines by hTERT-HM cells, suggesting a putative mechanism for the leukocyte infiltrate into the uterus during labour and postpartum involution.
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The P2X1 Receptor Is Required for Neutrophil Extravasation during Lipopolysaccharide-Induced Lethal Endotoxemia in Mice
Blandine Maître,Stéphanie Magnenat,Véronique Heim,Catherine Ravanat,Richard J. Evans,Christian Gachet,Béatrice Hechler +6 more
TL;DR: A major role is revealed for the P2X1 receptor in LPS-induced lethal endotoxemia through its critical involvement in neutrophil emigration from venules through adoptive transfer of immunofluorescently labeled neutrophils from WT and P2x1−/− mice into WT mice.
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Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the Impairment of This Process during Sepsis.
TL;DR: Excessive ADAM17 sheddase activity during sepsis thus appears to undermine in a direct and indirect manner the necessary balance between intravascular adhesion and de-adhesion events that regulate neutrophil migration into sites of infection.
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The Regulatory Effects of Interleukin-4 Receptor Signaling on Neutrophils in Type 2 Immune Responses.
TL;DR: It is proposed for type 2 immune responses that neutrophils are, as in other immune responses, the first non-resident cells to arrive at a site of inflammation or infection, thereby guiding and attracting other innate and adaptive immune cells; however, as soon as the type 2 cytokines IL-4 and IL-13 predominate, neutrophil recruitment, chemotaxis, and effector functions are rapidly shut off byIL-4/IL-13-mediated IL- 4R
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Tristetraprolin (TTP) coordinately regulates primary and secondary cellular responses to proinflammatory stimuli.
TL;DR: TTP‐promoted decay of transcripts encoding chemokines and other proinflammatory mediators is thus a critical post‐transcriptional regulatory mechanism in the response of secondary cells, such as fibroblasts, to TNF released from primary immune cells.
References
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Getting to the site of inflammation: the leukocyte adhesion cascade updated
TL;DR: This Review focuses on new aspects of one of the central paradigms of inflammation and immunity — the leukocyte adhesion cascade.
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The Nature of Small-Airway Obstruction in Chronic Obstructive Pulmonary Disease
James C. Hogg,Fanny Chu,Soraya Utokaparch,Ryan Woods,W. Mark Elliott,Liliana Buzatu,Ruben M. Cherniack,Robert M. Rogers,Frank C. Sciurba,Harvey O. Coxson,Peter D. Paré +10 more
TL;DR: Progression of COPD is associated with the accumulation of inflammatory mucous exudates in the lumen and infiltration of the wall by innate and adaptive inflammatory immune cells that form lymphoid follicles, coupled to a repair or remodeling process that thickens the walls of these airways.
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How neutrophils kill microbes
TL;DR: Killing was previously believed to be accomplished by oxygen free radicals and other reactive oxygen species generated by the NADPH oxidase, and by oxidized halides produced by myeloperoxidase, but this is incorrect.
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Monocyte emigration from bone marrow during bacterial infection requires signals mediated by chemokine receptor CCR2
Natalya V. Serbina,Eric G. Pamer +1 more
TL;DR: In blood, Ccr2−/− monocytes could traffic to sites of infection, demonstrating that CCR2 is not required for migration from the circulation into tissues, and determining the frequency of Ly6Chi monocytes in the circulation.
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Neutrophils, from marrow to microbes.
TL;DR: Neutrophils are produced in the bone marrow from stem cells that proliferate and differentiate to mature neutrophils fully equipped with an armory of granules that contain proteins that enable the neutrophil to deliver lethal hits against microorganisms, but also to cause great tissue damage.