Neutrophils in respiratory viral infections

Abstract

Viral respiratory infections are a common cause of severe disease, especially in infants, people who are immunocompromised, and in the elderly. Neutrophils, an important innate immune cell, infiltrate the lungs rapidly after an inflammatory insult. The most well-characterized effector mechanisms by which neutrophils contribute to host defense are largely extracellular and the involvement of neutrophils in protection from numerous bacterial and fungal infections is well established. However, the role of neutrophils in responses to viruses, which replicate intracellularly, has been less studied. It remains unclear whether and, by which underlying immunological mechanisms, neutrophils contribute to viral control or confer protection against an intracellular pathogen. Furthermore, neutrophils need to be tightly regulated to avoid bystander damage to host tissues. This is especially relevant in the lung where damage to delicate alveolar structures can compromise gas exchange with life-threatening consequences. It is inherently less clear how neutrophils can contribute to host immunity to viruses without causing immunopathology and/or exacerbating disease severity. In this review, we summarize and discuss the current understanding of how neutrophils in the lung direct immune responses to viruses, control viral replication and spread, and cause pathology during respiratory viral infections.

Appeasing Pheromones against Bovine Respiratory Complex and Modulation of Immune Transcript Expressions

“…A higher amount of IL8 in the pheromone group than in the control group could have attracted more neutrophils to the sites of inflammation and thus could have promoted a quicker resolution of respiratory infections in the pheromone group. This hypothesis is supported by observations from multiple reports, where IL8 protective effects against respiratory infections-particularly bacterial infections as it is less clear for viral infections-were identified [40,44,45]. Moreover, administration of recombinant bovine IL8 was shown to also have positive effects on uterine health and milk production [46].…”

Interplay between Neutrophils, NETs and T-Cells in SARS-CoV-2 Infection—A Missing Piece of the Puzzle in the COVID-19 Pathogenesis?

“…PMN cells are present in the lungs during acute respiratory distress syndrome (ARDS), which can be caused by a wide variety of pathogens, including an array of viruses (for example, in influenza and CoVs2 infections), in addition to trauma and autoimmune disorders. Studies suggest that neutrophil recruitment to the lungs is associated with disease exacerbation in the course of viral infections [63,64].…”

Neutrophil Recruitment and Participation in Severe Diseases Caused by Flavivirus Infection

“…Neutrophil production of proinflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor- α (TNF-α), along with the release of ROS and other cytotoxic molecules, are important in initial phases of disease but may cause damage and tissue necrosis if uncontrolled [ 54 , 55 ]. Moreover, neutrophils are often involved in containing secondary bacterial infections associated with respiratory viral infections [ 56 ].…”

“…Studies of IAV infection in mice show that blockade of C5a minimized neutrophil recruitment to lungs and tissue injury [ 61 ] and blockade of IL-1β and IL-6 resulted in decreased neutrophil activation and chemotaxis to lungs [ 62 , 63 ]. RSV, Pneumonia virus (PVM) and IAV infections promote oxidative burst in murine neutrophils [ 56 , 64 , 65 ]. Complement and FcγRs receptors present in neutrophils recognize opsonized pathogens and trigger neutrophil effector functions.…”