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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
TLRs are abundant on the surfaces of macrophages and dendritic cells. Among the cytokines that are frequently up-regulated in response to TLR engagement is IL-12. One of the effector functions of this cytokine is the activation of natural killer (NK) cells. NK cells are lymphocytes that lack the specificity of T or B cells. They play an especially important role in the early response to many pathogens, prior to the full activation of an adaptive response. Once activated, they serve as an early source of IFN-γ. This important cytokine is a powerful activator of phagocytes, and it increases their ability to kill ingested parasites through the production of reactive oxygen and nitrogen molecules (Figure 4.15), a phenomenon known as the respiratory burst. Such activation is crucial to the early containment of a protozoan infection prior to the initiation of an adaptive response.
Macrophages and Their Potential Role in Hyperreactive Airways Disease
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
The IgE-antigen complexes used in rat experiments by Dessaint and colleagues98 and referred to earlier in this chapter (see Section III) activated rat peritoneal macrophage generation of oxygen metabolites and also activated these cells to release lysosomal enzymes. Superoxide anion, one product of the metabolism of oxygen by macrophages, is directly injurious to alveolar epithelial cells.99 Importantly, the respiratory burst of asthmatic macrophages cultured in vitro is increased compared to that of macrophages from nonasthmatics.100 These observations have been confirmed by Kelly and colleagues,30 who retrieved macrophages by BAL from 22 patients with stable asthma. Measurement of cell respiratory burst was increased approximately fourfold on these subjects compared to controls.
Cellular and Molecular Interactions in the Induction of Inflammation in Rheumatic Diseases
Published in Thomas F. Kresina, Monoclonal Antibodies, Cytokines, and Arthritis, 2020
Enhanced monocyte phagocytosis occurs via complement and Fc receptors (FcγR), which are increased during maturation induced by such inflammatory stimuli as IFN-γ (102). However, the reported absence of IFN-γ in the rheumatoid synovium suggested other mechanisms of augmented FcγR expression and phagocytosis. In this regard, another cytokine, TGF-β, has recently been shown to selectively augment the expression of FcγRIII, an important receptor for immunophagocytosis (103). During FcγR-mediated phagocytosis, monocytes as well as neutrophils experience an oxidative burst that causes the release of reactive oxygen species (102,104). The initial product of the respiratory burst, superoxide anion (O2–), is formed at the membrane of monocytes by NADPH oxidase and is converted by superoxide dismutase (SOD) to H2O2. This H2O2 subsequently forms toxic hypohalous acids with potent oxidizing potential. These products can be extremely toxic to adjacent cells and tissues if released to the external milieu (105).
Legacy and emerging per- and polyfluoroalkyl substances suppress the neutrophil respiratory burst
Published in Journal of Immunotoxicology, 2023
Drake W. Phelps, Anika I. Palekar, Haleigh E. Conley, Giuliano Ferrero, Jacob H. Driggers, Keith E. Linder, Seth W. Kullman, David M. Reif, M. Katie Sheats, Jamie C. DeWitt, Jeffrey A. Yoder
Recently, laboratories here reported that larval zebrafish can be used as a screening tool to identify compounds that suppress one component of innate immune function, the respiratory burst (Phelps et al. 2020). The respiratory burst is a critical function of neutrophils and macrophages involving the rapid production of reactive oxygen species (ROS), which have microbicidal properties and act as second messengers in signal transduction, further amplifying immune responses (Dupré-Crochet et al. 2013; Herb and Schramm 2021). In neutrophils, the respiratory burst is preceded by degranulation (Manara et al. 1991), and ROS production is dependent upon the activities of myeloperoxidase (MPO) and NADPH oxidase (Dahlgren et al. 2019), indicating that measuring the respiratory burst can serve as a broad readout of neutrophil function. Mutations in MPO, NADPH oxidase, or upstream kinases (e.g. protein kinase C [PKC]) have been linked to immunosuppression and an increased susceptibility to infection (Klebanoff 1970; Drutman et al. 2020; Neehus et al. 2021, 2022; Yu et al. 2023).
Screening the immunotoxicity of different food preservative agents on the model organism Galleria mellonella L. (Lepidoptera: Pyralidae) larvae
Published in Drug and Chemical Toxicology, 2023
Emine Duman Erbaş, Rehemah Gwokyalya, Hülya Altuntaş, Bilal Kutrup
Additionally, the reduced number of granulocytes after force-feeding with SB, SNi, and SNa could also be related to increased toxicity of the food additives, which induce granulocyte-targeted apoptosis. Moreover, the possibility that granulocytes in circulation reduced due to food preservative-induced respiratory burst cannot be ruled out. Previous research has shown that the respiratory burst pathway involving NADPH oxidase activity is activated during phagocytosis of foreign agents by hemocytes. Superoxide production has also been shown to be critical for effective microbial killing by both neutrophils and hemocytes (Reeves et al.2002, Bergin et al.2005). Yet, treating G. mellonella larvae with potassium nitrate, which is a food preservative, increased SOD enzyme activity in the larval hemolymph (Maguire et al.2017). Accordingly, we argue that food preservatives may have induced a respiratory burst in the G. mellonella larval granulocytes due to increased concentration of superoxide anions leading to low granulocyte counts.
How to recognize inborn errors of immunity in a child presenting with a malignancy: guidelines for the pediatric hemato-oncologist
Published in Pediatric Hematology and Oncology, 2023
Jutte van der Werff ten Bosch, Eva Hlaváčková, Charlotte Derpoorter, Ute Fischer, Francesco Saettini, Sujal Ghosh, Roula Farah, Delfien Bogaert, Rabea Wagener, Jan Loeffen, Chris M Bacon, Simon Bomken
To rule out antibody deficiency, measuring immunoglobulin levels including subclasses of IgG, is indispensable.59,60 The evaluation of specific antibodies such as isohemaglutinin and the titers of common postvaccination serum antibodies is crucial.64 Specific postvaccination antibody responses to nonconjugated polysaccharide pneumococcal vaccine or Salmonella enterica subsp. Typhi Vi antigen capsular polysaccharide enables in vivo evaluation of specific antibody responses.59 This test might be difficult at diagnosis. Finally, a variety of other tests can be helpful in well-selected cases, like the assessment of telomere length, neutrophil respiratory burst for chronic granulomatous disease (CGD), or in vitro evaluation of signaling pathways such as JAK-STAT or Toll like receptor pathways.