Air pollution particles diminish bacterial clearance in the primed lungs of mice

Sigaud, Samuel; Goldsmith, Carroll-Ann; Zhou, Hongwei; Yang, Zhiping; Fedulov, Alexey V.; Imrich, Amy; Kobzik, Lester

doi:10.1016/j.taap.2007.04.014

Cited by 101 publications

(70 citation statements)

References 40 publications

(36 reference statements)

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“…27 Therefore, exposure to air pollutants, either through inhalation or ingestion, may induce inflammatory responses that are also evident in appendicitis. Alternatively, exposure to diesel exhaust has been shown to increase susceptibility to bacterial 28 and viral 29 pulmonary infections through impairment of microbial defence. 30 If air pollution similarly affects gastrointestinal immunity, exposure to pollutants may increase the risk of bacterial invasion resulting in appendicitis.…”

Section: Odds Ratio (95% Ci)mentioning

confidence: 99%

Effect of ambient air pollution on the incidence of appendicitis

Kaplan¹,

Dixon²,

Panaccione³

et al. 2009

Canadian Medical Association Journal

123

100

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Section: Odds Ratio (95% Ci)mentioning

confidence: 99%

Effect of ambient air pollution on the incidence of appendicitis

Kaplan¹,

Dixon²,

Panaccione³

et al. 2009

Canadian Medical Association Journal

123

100

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“…There are reports, however, of increased numbers of hospitalizations for respiratory disorders including infections on days of increased levels of PM (2). In support of these epidemiologic findings, several rodent models have shown PM exposure can increase susceptibility to infectious bacteria such as Listeria monocytogenes and Streptococcus pneumoniae (3,4).…”

mentioning

confidence: 93%

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Brant¹,

Fabisiak²

2008

Am J Respir Cell Mol Biol

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Particulate matter air pollution (PM) has been linked with chronic respiratory diseases. Real-life exposures are likely to involve a mixture of chemical and microbial stimuli, yet little attention has been paid to the potential interactions between PM components (e.g., Ni) and microbial agents on the development of inflammatory-like conditions in the lung. Using the Toll-like receptor (TLR)-2 agonist MALP-2 as a lipopeptide relevant to microbial colonization, we hypothesized that nickel sensitizes human lung fibroblasts (HLF) for microbial-driven chemokine release through modulation of TLR signaling pathways. NiSO 4 (200 mM) synergistically enhanced CXCL8, yet antagonized CXCL10 mRNA expression and protein release from HLF in response to MALP-2. RT 2 -PCR pathway-focused array results indicated that NiSO 4 exposure did not alter the expression of TLRs or their downstream signaling mediators, yet significantly increased the expression of cyclooxygenase 2 (COX-2). Moreover, when NiSO 4 was given in combination with MALP-2, there was an amplified induction of COX-2 mRNA and protein along with its metabolic product, PGE2, in HLF. The COX-2 inhibitor, NS-398, attenuated NiSO 4 and MALP-2-induced PGE2 and CXCL8 release and partially reversed the NiSO 4 -dependent inhibition of MALP-2-induced CXCL10 release from HLF. These data indicate that NiSO 4 alters the pattern of TLR-2-dependent chemokine release from HLF via a COX-2-mediated pathway. The quantitative and qualitative effects of NiSO 4 on microbial-driven chemokine release from HLF shed new light on how PM-derived metals can exacerbate respiratory diseases.Keywords: COX-2; nickel; inflammation; chemokines; fibroblasts Particulate matter air pollution (PM) is a contributing risk factor for many adverse health effects, including respiratory diseases (1). Real-life scenarios are likely to involve exposures not only to chemical stresses such as PM, but microbial stimuli as well. While much attention has been paid to microbial-driven inflammation in the lung, limited information is available regarding the potential interactions between PM exposures and microbial stress on respiratory function. There are reports, however, of increased numbers of hospitalizations for respiratory disorders including infections on days of increased levels of PM (2). In support of these epidemiologic findings, several rodent models have shown PM exposure can increase susceptibility to infectious bacteria such as Listeria monocytogenes and Streptococcus pneumoniae (3, 4).Recent evidence suggests that colonization with species originally considered commensal and not causing overt disease (e.g., Mycoplasma fermentans) also has the potential to interact with other stimuli and/or alter biological responses in infected host cells (5, 6). For example, we have previously shown that exposure of human lung fibroblast cells (HLF) to M. fermentans synergistically enhances the release of IL-6 by PM in the form of residual oil fly ash (ROFA) compared to either stimulus alone (7). It is well recognized t...

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“…It has also been demonstrated that nanoparticles can evade physical clearance mechanisms in humans, and enter or diffuse through cell membranes, leading to increased biodistribution and longer persistence in the body. In addition, it has been suggested repeatedly that the nanoparticle component of air pollution, such as particulate matter (PM 10 ), could be responsible for the increased susceptibility of individuals to respiratory infections in areas of high concentrations of air pollution by impacting the host response to the infection (3,4). However, no firm mechanistic understanding of this link has yet been demonstrated.…”

mentioning

confidence: 99%

Carbon Nanoparticles Inhibit the Antimicrobial Activities of the Human Cathelicidin LL-37 through Structural Alteration

Findlay

Pohl

Svoboda

et al. 2017

The Journal of Immunology

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Host defense peptides, also known as antimicrobial peptides, are key elements of innate host defense. One host defense peptide with well-characterized antimicrobial activity is the human cathelicidin, LL-37. LL-37 has been shown to be upregulated at sites of infection and inflammation and is regarded as one of the primary innate defense molecules against bacterial and viral infection. Human exposure to combustion-derived or engineered nanoparticles is of increasing concern, and the implications of nanomaterial exposure on the human immune response is poorly understood. However, it is widely acknowledged that nanoparticles can interact strongly with several immune proteins of biological significance, with these interactions resulting in structural and functional changes of the proteins involved. This study investigated whether the potent antibacterial and antiviral functions of LL-37 were inhibited by exposure to, and interaction with, carbon nanoparticles, together with characterizing the nature of the interaction. LL-37 was exposed to carbon black nanoparticles in vitro, and the antibacterial and antiviral functions of the peptide were subsequently assessed. We demonstrate a substantial loss of antimicrobial function when the peptide was exposed to low concentrations of nanomaterials, and we further show that the nanomaterial-peptide interaction resulted in a significant change in the structure of the peptide. The human health implications of these findings are significant, as, to our knowledge, this is the first evidence that nanoparticles can alter host defense peptide structure and function, indicating a new role for nanoparticle exposure in increased disease susceptibility.

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Air pollution particles diminish bacterial clearance in the primed lungs of mice

Cited by 101 publications

References 40 publications

Effect of ambient air pollution on the incidence of appendicitis

Effect of ambient air pollution on the incidence of appendicitis

Nickel Alterations of TLR2-Dependent Chemokine Profiles in Lung Fibroblasts Are Mediated by COX-2

Carbon Nanoparticles Inhibit the Antimicrobial Activities of the Human Cathelicidin LL-37 through Structural Alteration

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