The roles of NADPH oxidase in modulating neutrophil effector responses.

TitleThe roles of NADPH oxidase in modulating neutrophil effector responses.
Publication TypeJournal Article
Year of Publication2019
AuthorsZeng MY, Miralda I, Armstrong CL, Uriarte SM, Bagaitkar J
JournalMol Oral Microbiol
Volume34
Issue2
Pagination27-38
Date Published2019 04
ISSN2041-1014
KeywordsAnimals, Anti-Infective Agents, Apoptosis, Bacteria, Extracellular Traps, Granulomatous Disease, Chronic, Humans, Immunity, Innate, Inflammation, Mice, Mouth Mucosa, NADPH Oxidase 2, NADPH Oxidases, Neutrophils, Oxidative Stress, Periodontal Diseases, Reactive Oxygen Species, Respiratory Burst
Abstract

Neutrophils are phagocytic innate immune cells essential for killing bacteria via activation of a wide variety of effector responses and generation of large amounts of reactive oxygen species (ROS). Majority of the ROS in neutrophils is generated by activation of the superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Independent of their anti-microbial function, NADPH oxidase-derived ROS have emerged as key regulators of host immune responses and neutrophilic inflammation. Data from patients with inherited defects in the NADPH oxidase subunit alleles that ablate its enzyme function as well as mouse models demonstrate profound dysregulation of host inflammatory responses, neutrophil hyper-activation and tissue damage in response to microbial ligands or tissue trauma. A large body of literature now demonstrates how oxidants function as essential signaling molecules that are essential for the regulation of neutrophil responses during priming, degranulation, neutrophil extracellular trap formation, and apoptosis, independent of their role in microbial killing. In this review we summarize how NADPH oxidase-derived oxidants modulate neutrophil function in a cell intrinsic manner and regulate host inflammatory responses. In addition, we summarize studies that have elucidated possible roles of oxidants in neutrophilic responses within the oral mucosa and periodontal disease.

DOI10.1111/omi.12252
Custom 1

https://www.ncbi.nlm.nih.gov/pubmed/30632295?dopt=Abstract

Alternate JournalMol Oral Microbiol
PubMed ID30632295
PubMed Central IDPMC6935359
Grant ListP20 GM125504 / GM / NIGMS NIH HHS / United States
R01 DE024509 / DE / NIDCR NIH HHS / United States
R03 DE028031 / DE / NIDCR NIH HHS / United States

Weill Cornell Medicine Gale and Ira Drukier Institute for Children's Health 413 E. 69th Street New York, NY 10021