Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice

Bozinovski, Steven; Seow, Huei Jiunn; Chan, Sheau Pyng Jamie; Anthony, Desiree; McQualter, Jonathan L.; Hansen, Michelle; Jenkins, Brendan J.; Anderson, Gary P.; Vlahos, Ross

doi:10.1042/cs20140703

Cited by 75 publications

(63 citation statements)

References 50 publications

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“…Repeated GAS infection or intranasal vaccination stimulates an IgA/IgG antibody and Th17 cellular response in mice, which dramatically enhances neutrophil recruitment and myeloperoxidase antimicrobial activity during early infection . This is thought to be mediated by Th17 cell secretion of IL‐17A, which stimulates the production of chemokines and cytokines, promoting the recruitment and activation of polymorphonuclear leukocytes, such as neutrophils, as well as macrophages . Indeed, a neutralizing antibody against IL‐17A prevented GAS clearance from the NALT, likely because of impaired leukocyte infiltration.…”

Section: Innate Immune Response To Gas Pharyngitismentioning

confidence: 99%

“…SIC binds to and inhibits secreted AMPs IL-17A, which stimulates the production of chemokines and cytokines, promoting the recruitment and activation of polymorphonuclear leukocytes, such as neutrophils, as well as macrophages. 29,30 Indeed, a neutralizing antibody against IL-17A prevented GAS clearance from the NALT, 31 likely because of impaired leukocyte infiltration.…”

Section: Streptococcus Pyogenes F I G U R E 1 Interplay Between Immunmentioning

confidence: 99%

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Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Soderholm

Barnett

Sweet

et al. 2017

Journal of Leukocyte Biology

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Streptococcus pyogenes, the Group A Streptococcus (GAS), is the most common cause of bacterial pharyngitis in children and adults. Innate and adaptive host immune responses are fundamental for defense against streptococcal pharyngitis and are central to the clinical manifestation of disease. Host immune responses also contribute to the severe poststreptococcal immune diseases that constitute the major disease burden for this organism. However, until recently, little was known about the host responses elicited during infection. Cellular mediators of innate immunity used during host defense against GAS include epithelial cells, neutrophils, macrophages, and dendritic cells (DCs), which are reported to secrete a number of soluble inflammatory mediators, such as antimicrobial peptides (AMPs); eicosanoids, including PGE and leukotriene B4 (LTB ); chemokines; and proinflammatory cytokines. Th1 and Th17 responses play significant roles in adaptive immunity in both murine models of GAS pharyngitis and in human tonsil tissue. A number of inflammatory complications are associated with GAS pharyngitis, which can lead to chronic disease in patients. These include scarlet fever, tonsillar hypertrophy, and sleep apnea, as well as postinfectious sequelae, such as acute rheumatic fever (ARF), poststreptococcal glomerulonephritis, and guttate psoriasis (GP). This review aims to present the current state of knowledge on innate and adaptive immune responses elicited during GAS pharyngitis, mechanisms by which GAS evades these responses, the emerging role of the pharyngeal microbiota, and how the interplay among these factors can influence the outcome of infection and inflammation-related complications.

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Section: Innate Immune Response To Gas Pharyngitismentioning

confidence: 99%

Section: Streptococcus Pyogenes F I G U R E 1 Interplay Between Immunmentioning

confidence: 99%

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Soderholm

Barnett

Sweet

et al. 2017

Journal of Leukocyte Biology

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“…The components in the particulate phase can directly or indirectly damage lipids, proteins, the intracellular matrix, DNA, and organelles, thereby resulting in many diseases. There is increasing evidence from in vitro and in vivo studies that cigarette smoke extract (CSE) treatment can stimulate release and expression of inflammatory cytokines, such as interleukin (IL)-1alpha (Pauwels et al, 2011;Yang et al, 2014), IL-6 (Locati et al, 2001;Chen et al, 2012;Wang et al, 2015), IL-8 (Zhang et al, 2011;Wu et al, 2014), IL-17 (Zhang et al, 2011;Bozinovski et al, 2015) and IL-18 (Kang et al, 2007), and cause airway inflammation (Tamimi et al, 2012), lung inflammation (Tang et al, 2011;Izzotti and Pulliero, 2015), COPD (Zhang et al, 2011;Seys et al, 2015), emphysema (Xiong et al, 2011) and carcinogenesis (Chen et al, 2011a;Sobus and Warren, 2014).…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke extract-induced interleukin-6 expression is regulated by phospholipase D1 in human bronchial epithelial cells

Koo

Han

2016

J. Toxicol. Sci.

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-Cigarette smoking is known to be associated with various kinds of diseases, including atherosclerotic cardiovascular disease, cancer, and chronic obstructive pulmonary disease (COPD). Many of the diseases associated with cigarette smoking are also associated with changes in interleukin-6 (IL-6) expression. In this study, we investigated the role of phospholipase D1 (PLD1) in IL-6 expression induced by cigarette smoke extract (CSE). Treatment with CSE increased PLD1 and IL-6 expressions in human bronchial epithelial (BEAS-2B) cells. In addition, CSE treatment activated PLC, PKC, and MAPK pathway through the Gi protein-coupled receptor. Pertussis toxin (PTX, Gi protein-coupled receptor inhibitor), PAO (PLC inhibitor), Go6976 (PKC inhibitor) and SB203580 (p38MAPK inhibitor) decreased CSEinduced PLD1 expression. The results show that Gi protein, PLC, PKC, and p38MAPK act as upstream regulators of PLD1 in CSE-treated BEAS-2B cells. Moreover, PLD1 siRNA transfection decreased CSEinduced ATF2 phosphorylation and IL-6 expression. In addition, inhibitors of Gi protein, PLC, PKC, and p38MAPK, and ATF2 siRNA transfection decreased CSE-induced IL-6 expression, suggesting that CSEinduced IL-6 expression is regulated via Gi protein/PLC/PKC/p38MAPK/PLD1/ATF2 pathway. Taken together, the results suggest that PLD1 is an important regulator of IL-6 expression induced by CSE in BEAS-2B cells.

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“…50 In pathologies such as chronic obstructive pulmonary disease, cd T cells are present in the inflamed tissue, and they are an important source of IL-17A, which is a cytokine that regulates lung immunity and inflammation. 51 Taking this into account, we speculate that the inhibition of serine proteases (i.e. elastase) would reduce not only their own effect but also the action of the enzyme on cd T cells, thereby limiting a harmful immune response mediated by these T cells.…”

Section: Discussionmentioning

confidence: 99%

“…To control exacerbated proteolysis at sites of inflammation, the administration of therapeutic inhibitors of proteases has been tested as a therapy for a variety of inflammatory and infectious lung diseases . In pathologies such as chronic obstructive pulmonary disease, γδ T cells are present in the inflamed tissue, and they are an important source of IL‐17A, which is a cytokine that regulates lung immunity and inflammation . Taking this into account, we speculate that the inhibition of serine proteases (i.e.…”

Section: Discussionmentioning

confidence: 99%

Modulation of γδ T‐cell activation by neutrophil elastase

et al. 2017

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γδ T cells are non-conventional, innate-like T cells, characterized by a restricted T-cell receptor repertoire. They participate in protective immunity responses against extracellular and intracellular pathogens, tumour surveillance, modulation of innate and adaptive immune responses, tissue healing, epithelial cell maintenance and regulation of physiological organ function. In this study, we investigated the role of neutrophils during the activation of human blood γδ T cells through CD3 molecules. We found that the up-regulation of CD69 expression, and the production of interferon-γ and tumour necrosis factor-α induced by anti-CD3 antibodies was potentiated by neutrophils. We found that inhibition of caspase-1 and neutralization of interleukin-18 did not affect neutrophil-mediated modulation. By contrast, the treatment with serine protease inhibitors prevented the potentiation of γδ T-cell activation induced by neutrophils. Moreover, the addition of elastase to γδ T-cell culture increased their stimulation, and the treatment of neutrophils with elastase inhibitor prevented the effect of neutrophils on γδ T-cell activation. Furthermore, we demonstrated that the effect of elastase on γδ T cells was mediated through the protease-activated receptor, PAR1, because the inhibition of this receptor with a specific antagonist, RWJ56110, abrogated the effect of neutrophils on γδ T-cell activation.

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Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice

Cited by 75 publications

References 50 publications

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Cigarette smoke extract-induced interleukin-6 expression is regulated by phospholipase D1 in human bronchial epithelial cells

Modulation of γδ T‐cell activation by neutrophil elastase

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