Particulate matters induce acute exacerbation of allergic airway inflammation via the TLR2/NF-κB/NLRP3 signaling pathway

Dai, Mengyuan; Chen, Fang‐Fang; Wang, Yong; Wang, Muzi; Lv, Yunxiang; Liu, Rong‐Yu

doi:10.1016/j.toxlet.2019.12.013

Cited by 24 publications

(12 citation statements)

References 41 publications

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“…PM 2.5 exposure is also well documented to induce pulmonary inflammation, often characterized by the expression of several inflammatory markers, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 [6,7]. Ambient air pollution PM has also been shown to induce Tolllike receptor 2 (TLR2) expression and subsequent activation of the nuclear factor kappa B (NF-κB) transcription factor that accelerates the inflammatory response in both in vitro studies and in vivo exposures [8].…”

Section: Introductionmentioning

confidence: 99%

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

et al. 2021

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Background Exposure to traffic-generated emissions is associated with the development and exacerbation of inflammatory lung disorders such as chronic obstructive pulmonary disorder (COPD) and idiopathic pulmonary fibrosis (IPF). Although many lung diseases show an expansion of Proteobacteria, the role of traffic-generated particulate matter pollutants on the lung microbiota has not been well-characterized. Thus, we investigated the hypothesis that exposure to diesel exhaust particles (DEP) can alter commensal lung microbiota, thereby promoting alterations in the lung’s immune and inflammatory responses. We aimed to understand whether diet might also contribute to the alteration of the commensal lung microbiome, either alone or related to exposure. To do this, we used male C57Bl/6 mice (4–6-week-old) on either regular chow (LF) or high-fat (HF) diet (45% kcal fat), randomly assigned to be exposed via oropharyngeal aspiration to 35 μg DEP, suspended in 35 μl 0.9% sterile saline or sterile saline only (control) twice a week for 30 days. A separate group of study animals on the HF diet was concurrently treated with 0.3 g/day of Winclove Ecologic® Barrier probiotics in their drinking water throughout the study. Results Our results show that DEP-exposure increases lung tumor necrosis factor (TNF)-α, interleukin (IL)-10, Toll-like receptor (TLR)-2, TLR-4, and the nuclear factor kappa B (NF-κB) histologically and by RT-qPCR, as well as Immunoglobulin A (IgA) and Immunoglobulin G (IgG) in the bronchoalveolar lavage fluid (BALF), as quantified by ELISA. We also observed an increase in macrophage infiltration and peroxynitrite, a marker of reactive oxygen species (ROS) + reactive nitrogen species (RNS), immunofluorescence staining in the lungs of DEP-exposed and HF-diet animals, which was further exacerbated by concurrent DEP-exposure and HF-diet consumption. Histological examinations revealed enhanced inflammation and collagen deposition in the lungs DEP-exposed mice, regardless of diet. We observed an expansion of Proteobacteria, by qPCR of bacterial 16S rRNA, in the BALF of DEP-exposed mice on the HF diet, which was diminished with probiotic-treatment. Conclusions Our findings suggest that exposure to DEP causes persistent and sustained inflammation and bacterial alterations in a ROS-RNS mediated fashion, which is exacerbated by concurrent consumption of an HF diet.

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Section: Introductionmentioning

confidence: 99%

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

et al. 2021

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“…15, p. 353 and Chpt. 22, p. 475, as well as Hedbrant et al ( 2020 ) and Dai et al ( 2020 )]. Allergens— in the sense of external environmental factors —may directly act as exogenous DAMPs such as some metal allergens (e.g., nickel) (see Land ( 2018 ), Chpt.…”

Section: Damps As Major Integral Part Of the Exposome And Aop Conceptmentioning

confidence: 85%

“…15, p. 353]. This category of DAMPs was shown to trigger activation of the NLRP3 inflammasome associated with inflammasome-dependent proinflammatory processes (Moloudizargari et al 2019;Dai et al 2020) as well as, even more important, RCD in form of pyroptosis known to be associated with release of endogenous DAMPs [reviewed in Sarhan et al (2018)].…”

Section: Superimposition Of Noninfectious Environmental and Infectioumentioning

confidence: 99%

Role of Damage-Associated Molecular Patterns in Light of Modern Environmental Research: A Tautological Approach

Land

2020

Int J Environ Res

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Two prominent models emerged as a result of intense interdisciplinary discussions on the environmental health paradigm, called the "exposome" concept and the "adverse outcome pathway" (AOP) concept that links a molecular initiating event to the adverse outcome via key events. Here, evidence is discussed, suggesting that environmental stress/injury-induced damageassociated molecular patterns (DAMPs) may operate as an essential integrating element of both environmental health research paradigms. DAMP-promoted controlled/uncontrolled innate/adaptive immune responses reflect the key events of the AOP concept. The whole process starting from exposure to a distinct environmental stress/injury-associated with the presence/ emission of DAMPs-up to the manifestation of a disease may be regarded as an exposome. Clinical examples of such a scenario are briefly sketched, in particular, a model in relation to the emerging COVID-19 pandemic, where the interaction of noninfectious environmental factors (e.g., particulate matter) and infectious factors (SARS CoV-2) may promote SARS case fatality via superimposition of both exogenous and endogenous DAMPs. Article Highlights • This review is devoted to the first scientific attempt to integrate DAMP-controlled innate immune inflammatory and adaptive immune defense responses as well as DAMP-uncontrolled dysregulated pathological responses (acute and chronic human diseases) in the environmental health paradigm, called the "exposome" concept and the "adverse outcome pathway" (AOP) concept. • Evidence is discussed that DAMP-promoted controlled/uncontrolled innate immune/adaptive immune responses reflect the key events of the AOP concept. • The whole process starting from exposure to a distinct environmental stress/injury-associated with the presence/ emission of DAMPs-up to the manifestation of a disease may be regarded as an exposome. • Some exemplifying models of such a scenario are briefly sketched, including respiratory infections, autoimmune/ allergic diseases, organ fibrosis, and cancer. • In particular, a model in relation to the emerging COVID-19 pandemic is presented, where the interaction of noninfectious environmental factors (e.g., particulate matter) and infectious factors (SARS CoV-2) may promote SARS case fatality via superimposition of both exogenous and endogenous DAMPs.

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“…The synergistic effects of the inflammasome (the heterogeneous group of multiprotein complexes) and TLR signals are the main causes for cytokine release. Activation of inflammasome can cause autocatalysis and kinase activation, leading to the maturation of proinflammatory cytokines [9]. Once activated by microbial antigens, inflammasome and TLR signal transduction become activated through Myd88 and MAPK resulting in the translocation of NF‐κB with subsequent induction of inflammatory cytokines [10‐12].…”

Section: Introductionmentioning

confidence: 99%

Kupffer cell activation by different microbial lysates: Toll‐like receptor‐2 plays pivotal role on thromboxane A₂ production in mice and humans

Zhang¹,

Lin²,

Li³

et al. 2020

Eur J Immunol

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Thromboxane (TX) A 2 has been identified as an important intrahepatic vasoconstrictor upon Kupffer cell (KC) activation during infections such as spontaneous bacterial peritonitis (SBP). The study aimed to investigate the role of TLRs in the TXA 2 increase in liver nonparenchymal cells and their related mechanisms. Here, we identified TLR-2 as a common pathway for different microbials: microbial lysates including Gram-positive bacteria, Gram-negative bacteria, and fungi all increased TXA 2 secretion via activation of TLR-2 in human KCs, accompanied by increased expression and phosphorylation of Myd88related pathway. Of all TLR agonists, only TLR-1,-2, and-4 agonists increased TXA 2 in human KCs. These results were further confirmed by mouse liver nonparenchymal cells. Comparing the effects of TLR-1,-2, and-4 antagonists, only TLR-2 antagonist showed inhibitory effects with all tested microbial lysates. Pretreatment with TLR-2 antagonist in human KCs blocked the secretion of IL-10, CXCL-10, TNF-α, and IL-6 induced by Grampositive and Gram-negative bacterial stimulation. IL-23 and IL-1β were only induced by Gram-negative bacteria. Thus, TLR-2 might be a potential marker and an attractive target for future treatment of patients with SBP. In addition, IL-23 and IL-1β might distinguish early between Gram-positive and Gram-negative SBP.

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Particulate matters induce acute exacerbation of allergic airway inflammation via the TLR2/NF-κB/NLRP3 signaling pathway

Cited by 24 publications

References 41 publications

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

Role of Damage-Associated Molecular Patterns in Light of Modern Environmental Research: A Tautological Approach

Kupffer cell activation by different microbial lysates: Toll‐like receptor‐2 plays pivotal role on thromboxane A₂ production in mice and humans

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Particulate matters induce acute exacerbation of allergic airway inflammation via the TLR2/NF-κB/NLRP3 signaling pathway

Cited by 24 publications

References 41 publications

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

Role of Damage-Associated Molecular Patterns in Light of Modern Environmental Research: A Tautological Approach

Kupffer cell activation by different microbial lysates: Toll‐like receptor‐2 plays pivotal role on thromboxane A2 production in mice and humans

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Product

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Kupffer cell activation by different microbial lysates: Toll‐like receptor‐2 plays pivotal role on thromboxane A₂ production in mice and humans