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Kathleen A. McPhillips

Researcher at Anschutz Medical Campus

Publications -  14
Citations -  2149

Kathleen A. McPhillips is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Inflammation & Apoptotic cell clearance. The author has an hindex of 9, co-authored 10 publications receiving 1932 citations.

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Cell-Surface Calreticulin Initiates Clearance of Viable or Apoptotic Cells through trans-Activation of LRP on the Phagocyte

TL;DR: It is demonstrated here that calreticulin acts as a second general recognition ligand by binding and activating LDL-receptor-related protein (LRP) on the engulfing cell, which creates an environment where "don't eat me" signals are rendered inactive and "eat me" signalling signals congregate together and signal for removal.
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Lovastatin Enhances Clearance of Apoptotic Cells (Efferocytosis) with Implications for Chronic Obstructive Pulmonary Disease

TL;DR: It is shown that lovastatin increased efferocytosis in vitro in an 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase-dependent manner, and suggest that statins may play an important therapeutic role in diseases where effercytosis is impaired and inflammation is dysregulated.
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Surfactant Proteins A and D Suppress Alveolar Macrophage Phagocytosis via Interaction with SIRPα

TL;DR: SP-A and SP-D tonically inhibit alveolar macrophage phagocytosis by binding SIRP alpha, which is essential for the resolution of acute pulmonary inflammation.
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Impaired apoptotic cell clearance in CGD due to altered macrophage programming is reversed by phosphatidylserine-dependent production of IL-4

TL;DR: Findings support the hypothesis that impaired PS exposure on dying cells results in defective macrophage programming, with consequent efferocytic impairment, which has important implications in understanding the underlying cause of enhanced inflammation in CGD.
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Impairment of Apoptotic Cell Engulfment by Pyocyanin, a Toxic Metabolite of Pseudomonas aeruginosa

TL;DR: These studies demonstrate that P. aeruginosa can manipulate the inflammatory microenvironment through inhibition of apoptotic cell engulfment, and suggest potential strategies to limit pulmonary inflammation in cystic fibrosis.