Exposure to Ambient Particles Alters the Evolution of Macrophage Phenotype and Amplifies the Inducible Release of Eotaxin-1 in Allergen-Sensitized Mice

Zhang, Jiaxiang; Zeng, Xianlu; Li, Ye-Shan; Zhao, Wenxue; Chen, Zhongqi; Du, Qiang; Zhou, Fang; Ji, Ningfei; Huang, Mao

doi:10.1166/jbn.2019.2692

Cited by 14 publications

(7 citation statements)

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“…That study found that PM 2.5 may intensify asthma by intensifying M2 macrophages [39]. This is the first time that eotaxin-1 released by M2 macrophages was found to play a vital role in the pathogenesis of asthma [38]. The distribution of monocytes (monocytes being the predecessors of macrophages) in the present trial was essentially similar to the results of that prior trial.…”

Section: Plos Onesupporting

confidence: 80%

“…The group fed with L. paracasei HB89 had reduced inflammatory responses, and the histamine results shared the same trend. In 2018, Jiaxiang Zhang, et al Zhang et al, 2019 investigated immune cell changes in alveolar lavage fluid from allergic mice exposed to PM 2.5 [38]. The trial model was to apply stimulation with PM 2.5 continuously three days before sacrificing.…”

Section: Plos Onementioning

confidence: 99%

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Administration of Lactobacillus paracasei HB89 mitigates PM2.5-induced enhancement of inflammation and allergic airway response in murine asthma model

2020

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PM2.5 causes abnormal immune response and asthma in animals. In this study, a Balb/c mouse animal model was exposed to PM2.5 to induce asthma. Lactobacillus paracasei HB89 was fed at the same time, in order to observe whether L. paracasei HB89 mitigates respiratory tract allergies stimulated by PM2.5. The results showed that PM2.5 stimulated a significant increase in white blood cells and immunoglobulin (IgE) in OVA-induced allergic Balb/c mice, and IgE in the blood further triggered the release of histamine in the lung immune cells. This not only increased overall immune cell counts, but the lymphocyte counts also increased significantly, resulting in significant inhibitions of cytokines INF-r and TGF-β, and induction of IL-4, IL-5, IL-13 and IL-17a. After feeding with HB89, apart from the absence of observable changes in body weight, the total white blood cell count in the animal blood and IgE response were also be reduced; the proliferation of immune cells in the lungs caused by PM2.5 was slowed down; and histamine and cytokines INF-r and TGF-β were secreted in large quantities, but IL- 4, IL-5, IL-13, IL-17a were inhibited, which effectively reduced the possibility of asthma induction.

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Section: Plos Onesupporting

confidence: 80%

Section: Plos Onementioning

confidence: 99%

Administration of Lactobacillus paracasei HB89 mitigates PM2.5-induced enhancement of inflammation and allergic airway response in murine asthma model

2020

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“…PM 2.5 counteracts with IL-4-induced M2 polarization partially through mammalian target of rapamycin (mTOR) pathway, whereas in ovalbumin (OVA)-induced asthma, PM 2.5 aggravates allergic inflammation by activating M2 macrophages and subsequent Th2-related immune responses [21,30]. In addition, co-exposure to PM 2.5 and OVA notably promotes the levels of M2 marker YM-1, IL-4, and IL-13 in murine macrophages [31]. In apoE-deficient mice, the upregulation of TNF-α, IL-6, NOS2, IL-12, MRC1, and Arg-1 has been observed in PM 2.5 -exposed group, implying an activation of both M1 and M2 macrophages [32].…”

Section: Discussionmentioning

confidence: 99%

High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM2.5-Induced Lung Inflammation

Shi

Zhao

et al. 2019

Molecules

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PM2.5 is particulate matter with a diameter of 2.5 μm or less. Airway macrophages are the key players regulating PM2.5-induced inflammation. High molecular weight hyaluronan (HMW-HA) has previously been shown to exert protective effects on PM2.5-induced acute lung injury and inflammation. However, little is known about the detailed mechanism. In this study, we aimed to determine whether HMW-HA alleviates PM2.5-induced pulmonary inflammation by modulating macrophage polarization. The levels of M1 biomarkers TNF-α, IL-1β, IL-6, CXCL1, CXCL2, NOS2 and CD86, as well as M2 biomarkers IL-10, MRC1, and Arg-1 produced by macrophages were measured by ELISA, qPCR, and flow cytometry. In addition, the amount of M1 macrophages in lung tissues was examined by immunofluorescence of CD68 and NOS2. We observed a decline in PM2.5-induced M1 polarization both in macrophages and lung tissues when HMW-HA was administered simultaneously. Meanwhile, western blot analysis revealed that PM2.5-induced JNK and p38 phosphorylation was suppressed by HMW-HA. Furthermore, in vitro and in vivo studies showed that co-stimulation with HMW-HA and PM2.5 promoted the expression and release of IL-10, but exhibited limited effects on the transcription of MRC1 and ARG1. In conclusion, our results demonstrated that HMW-HA ameliorates PM2.5-induced lung inflammation by repressing M1 polarization through JNK and p38 pathways and promoting the production of pro-resolving cytokine IL-10.

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“…Previous studies indicated that PM 2.5 exposure significantly induced the inflammatory M1 polarization, which contributed to lung disorders [62,63]. In contrast, recent investigations demonstrated that PM 2.5 activated M2-polarization to exacerbate lung eosinophilia and allergic responses [64,65]. However, discrepancies and controversial results have emerged.…”

Section: Discussionmentioning

confidence: 99%

PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis

et al. 2020

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Background: Pneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM 2.5) is known to significantly contribute to respiratory diseases. PM 2.5-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM 2.5 exposure on molecular interactions between pneumococcus and macrophages. Results: PM 2.5 exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM 2.5-exposed pneumococcus-infected mouse model, PM 2.5 subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM 2.5 exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways. Conclusions: The effect of PM 2.5 exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.

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Exposure to Ambient Particles Alters the Evolution of Macrophage Phenotype and Amplifies the Inducible Release of Eotaxin-1 in Allergen-Sensitized Mice

Cited by 14 publications

References 0 publications

Administration of Lactobacillus paracasei HB89 mitigates PM2.5-induced enhancement of inflammation and allergic airway response in murine asthma model

Administration of Lactobacillus paracasei HB89 mitigates PM2.5-induced enhancement of inflammation and allergic airway response in murine asthma model

High Molecular Weight Hyaluronan Suppresses Macrophage M1 Polarization and Enhances IL-10 Production in PM2.5-Induced Lung Inflammation

PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis

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