Oral tissues are constantly exposed to damage from the mechanical effort of eating and from the invasion of foreign microorganisms such as bacteria, fungi, and virus. In healthy oral tissues, there is a balance between symbiotic bacteria and cells from the innate immune system, mainly neutrophils. When this balance is broken, inflammation appears and more immune cells are recruited to the gingiva. Neutrophils form a barrier against dysbiotic bacteria. However, when neutrophils are insufficient, bacteria thrive causing periodontitis, a chronic inflammatory disease that destroys the tooth‐supporting tissues or periodontium. Damage of periodontal tissues leads to tooth loss, and in severe cases, it can also affect systemic health by increasing a person's risk for atherosclerosis, rheumatoid arthritis, diabetes, and even cancer. The mechanisms neutrophil employ to keep a balance with bacteria in order to maintain healthy oral tissues is the focus of this chapter. We discuss how neutrophil antimicrobial functions keep bacteria at check and how some dysbiotic bacteria block neutrophils to promote an inflammatory state. Also, novel therapeutic approaches for periodontitis are discussed.
Part of the book: Role of Neutrophils in Disease Pathogenesis
Neutrophils, the most abundant leukocytes in blood, are relevant cells of both the innate and the adaptive immune system. Immunoglobulin (Ig) G antibody molecules are crucial activators of neutrophils. IgGs identify many types of pathogens via their two Fab portions and are in turn detected through their Fc portion by specific Fcγ receptors (FcγRs) on the membrane of neutrophils. Thus, antibodies bring the specificity of the adaptive immune response to the potent antimicrobial and inflammatory functions of neutrophils. Two types of FcγRs with several polymorphic variants exist on the human neutrophil. These receptors are considered to be redundant in inducing cell responses. Yet, new evidence presented in recent years on how the particular IgG subclass and the glycosylation pattern of the antibody modulate the IgG–FcγR interaction has suggested that a particular effector function may in fact be activated in response to a specific type of FcγR. In this chapter, we describe the main types of FcγRs on neutrophils and our current view on how particular FcγRs activate various signaling pathways to promote unique effector cell functions, including phagocytosis, activation of integrins, nuclear factor activation, and formation of neutrophil extracellular traps (NETs).
Part of the book: Neutrophils