Neutrophil homeostasis and inflammation: Novel paradigms from studying periodontitis

Publikation: Beitrag in FachzeitschriftÜbersichtsartikel (Review)BeigetragenBegutachtung

Beitragende

  • George Hajishengallis - , University of Pennsylvania (Autor:in)
  • Triantafyllos Chavakis - , Institut für Klinische Chemie und Laboratoriumsmedizin (Autor:in)
  • Evlambia Hajishengallis - , University of Pennsylvania (Autor:in)
  • John D. Lambris - , University of Pennsylvania (Autor:in)

Abstract

Once viewed as simply antibacterial effector cells packed with antimicrobials, neutrophils are now increasingly appreciated for their regulatory roles in immunity and inflammation. The homeostatic regulation of neutrophils is thus crucial for optimal operation of the immune system. An attractive model to understand mechanistically the role of neutrophils is periodontitis, an oral inflammatory disease that is particularly sensitive to neutrophil alterations in numbers or function. The recruitment and proper activation of neutrophils are largely dependent on leukocyte integrins and complement. This review discusses how these processes are affected by host genetic or microbial factors leading to the devel- opment of periodontitis. For instance, both hypo- and hyper-recruitment of neutrophils as a result of deficiencies in the expression of b2 integrins or their negative regulators, respectively, causes unwarranted IL-17-dependent inflammatory bone loss. Moreover, microbial hijacking of C5aR (CD88) signaling in neutrophils impairs their antimicrobial function while promoting destructive inflammatory responses. These studies not only support the concept that neutrophil homeostasis is key to periodontal health but also reveal promising, new therapeutic targets as discussed in the review.

Details

OriginalspracheEnglisch
Seiten (von - bis)539-548
Seitenumfang10
FachzeitschriftJournal of Leukocyte Biology
Jahrgang98
Ausgabenummer4
PublikationsstatusVeröffentlicht - Okt. 2015
Peer-Review-StatusJa

Externe IDs

researchoutputwizard legacy.publication#66909
researchoutputwizard legacy.publication#66226
Scopus 84943157037
PubMed 25548253

Schlagworte

Schlagwörter

  • Complement, Del-1, IL-17, Integrins, Leukocyte adhesion deficiency