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Current Allergy and Asthma Reports

Erschienen in:

01.05.2021 | Allergies and the Environment (T Moran, Section Editor)

Role of Innate Immune System in Environmental Lung Diseases

verfasst von: Marissa A. Guttenberg, Aaron T. Vose, Robert M. Tighe

Erschienen in: Current Allergy and Asthma Reports | Ausgabe 5/2021

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Abstract

The lung mucosa functions as a principal barrier between the body and inhaled environmental irritants and pathogens. Precise and targeted surveillance mechanisms are required at this lung-environment interface to maintain homeostasis and preserve gas exchange. This is performed by the innate immune system, a germline-encoded system that regulates initial responses to foreign irritants and pathogens. Environmental pollutants, such as particulate matter (PM), ozone (O₃), and other products of combustion (NO₂, SO₃, etc.), both stimulate and disrupt the function of the innate immune system of the lung, leading to the potential for pathologic consequences.

Purpose of review

The purpose of this review is to explore recent discoveries and investigations into the role of the innate immune system in responding to environmental exposures. This focuses on mechanisms by which the normal function of the innate immune system is modified by environmental agents leading to disruptions in respiratory function.

Recent findings

This is a narrative review of mechanisms of pulmonary innate immunity and the impact of environmental exposures on these responses. Recent findings highlighted in this review are categorized by specific components of innate immunity including epithelial function, macrophages, pattern recognition receptors, and the microbiome. Overall, the review supports broad impacts of environmental exposures to alterations to normal innate immune functions and has important implications for incidence and exacerbations of lung disease.

Summary

The innate immune system plays a critical role in maintaining pulmonary homeostasis in response to inhaled air pollutants. As many of these agents are unable to be mitigated, understanding their mechanistic impact is critical to develop future interventions to limit their pathologic consequences.

Riera Romo M, Pérez-Martínez D, Castillo Ferrer C. Innate immunity in vertebrates: an overview. Immunology. 2016;148:125–39.PubMedPubMedCentralCrossRef

Bauer RN, Diaz-Sanchez D, Jaspers I. Effects of air pollutants on innate immunity: the role of Toll-like receptors and nucleotide-binding oligomerization domain-like receptors. J Allergy Clin Immunol. 2012;129:26.CrossRef

Estrella B, Naumova EN, Cepeda M, Voortman T, Katsikis PD, Drexhage HA. Effects of air pollution on lung innate lymphoid cells: review of in vitro and in vivo experimental studies. Int J Environ Res Public Health. 2019. https://doi.org/10.3390/ijerph16132347.

Shi R, Su WW, Zhu ZT, Guan MY, Cheng KL, Fan WY, et al. Regulation effects of naringin on diesel particulate matter-induced abnormal airway surface liquid secretion. Phytomedicine. 2019. https://doi.org/10.1016/j.phymed.2019.153004.

Vargas Buonfiglio LG, Mudunkotuwa IA, Abou Alaiwa MH, Vanegas Calderón OG, Borcherding JA, Gerke AK, et al. Effects of coal fly ash particulate matter on the antimicrobial activity of airway surface liquid. Environ Health Perspect. 2017. https://doi.org/10.1289/EHP876.

Kim B-G, Lee P-H, Lee S-H, Park C-S, Jang A-S. Impact of ozone on claudins and tight junctions in the lungs. Environ. Toxicol. [Internet]. John Wiley and Sons Inc.; 2018 Jul 1 [cited 2020 Oct 28];33(7):798–806. Available from: https://doi.org/10.1002/tox.22566

Faber SC, McNabb NA, Ariel P, Aungst ER, McCullough SD. Exposure effects beyond the epithelial barrier: transepithelial induction of oxidative stress by diesel exhaust particulates in lung fibroblasts in an organotypic human airway model. Toxicol. Sci. [Internet]. Oxford University Press; 2020 Sep 1 [cited 2021 Feb 11];177(1):140–55. Available from: https://pubmed.ncbi.nlm.nih.gov/32525552/

Martin PJ, Héliot A, Trémolet G, Landkocz Y, Dewaele D, Cazier F, et al. Cellular response and extracellular vesicles characterization of human macrophages exposed to fine atmospheric particulate matter. Environ. Pollut. [Internet]. Elsevier Ltd; 2019 Nov 1 [cited 2020 Nov 20];254. Available from: https://doi.org/10.1016/j.envpol.2019.07.101

9.••

Singh Gangwar R, Vinayachandran V, Rengasamy P, et al. Differential contribution of bone marrow-derived infiltrating monocytes and resident macrophages to persistent lung inflammation in chronic air pollution exposure. Sci Rep. 2020;10:14348 This study explores the composition and source of pulmonary macrophages and how they are modified following chronic particulate matter exposure. This has implications for understanding how distinct macrophage populations can drive chronic inflammation associated with prolonged exposure to air pollution.CrossRef

10.

Bowatte G, Lodge CJ, Knibbs LD, Lowe AJ, Erbas B, Dennekamp M, et al. Traffic-related air pollution exposure is associated with allergic sensitization, asthma, and poor lung function in middle age. J Allergy Clin Immunol Mosby Inc. 2017;139(1):122-129.e1.

11.

Tashiro H, Kasahara DI, Osgood RS, Brown T, Cardoso A, Cho Y, et al. Sex differences in the impact of dietary fiber on pulmonary responses to ozone. Am J Respir Cell Mol Biol. 2020;62:503–12.PubMedPubMedCentralCrossRef

12.••

Cho Y, Abu-Ali G, Tashiro H, Brown TA, Osgood RS, Kasahara DI, et al. Sex differences in pulmonary responses to ozone in mice role of the microbiome. Am J Respir Cell Mol Biol. 2019;60:198–208 Explores the microbiome in O₃-induced airway disease suggesting that microbiome-mediate regulation are sex-dependent. Furthermore, microbiome effects on O₃ responses can be transferred by raising pups of one sex with bedding from adult mice of the opposite sex.PubMedPubMedCentralCrossRef

13.

Mutlu EA, Comba IY, Cho T, Engen PA, Yazıcı C, Soberanes S, et al. Inhalational exposure to particulate matter air pollution alters the composition of the gut microbiome. Environ. Pollut. [Internet]. Elsevier Ltd; 2018 Sep 1 [cited 2021 Feb 11];240:817–30. Available from: https://pubmed.ncbi.nlm.nih.gov/29783199/

14.

Anenberg SC, Henze DK, Tinney V, et al. Estimates of the global burden of ambient PM2:5, ozone, and NO2 on asthma incidence and emergency room visits. Environ Health Perspect. 2018. https://doi.org/10.1289/EHP3766.

15.

Halonen JI, Lanki T, Tiittanen P, Niemi JV, Loh M, Pekkanen J. Ozone and cause-specific cardiorespiratory morbidity and mortality. J Epidemiol Community Health. 2010;64:814–20.PubMedCrossRef

16.

Holst GJ, Pedersen CB, Thygesen M, Brandt J, Geels C, Bønløkke JH, et al. Air pollution and family related determinants of asthma onset and persistent wheezing in children: nationwide case-control study. BMJ. 2020. https://doi.org/10.1136/bmj.m2791.

17.

Chatkin J, Correa L, Santos U. External environmental pollution as a risk factor for asthma. Clin Rev Allergy Immunol. 2021;1:18.

18.

Tiotiu AI, Novakova P, Nedeva D, Chong-Neto HJ, Novakova S, Steiropoulos P, et al. Impact of air pollution on asthma outcomes. Int J Environ Res Public Health. 2020;17:1–29.CrossRef

19.

Medina-Ramón M, Zanobetti A, Schwartz J. The effect of ozone and PM10 on hospital admissions for pneumonia and chronic obstructive pulmonary disease: a national multicity study. Am J Epidemiol. 2006;163:579–88.PubMedCrossRef

20.

Wang M, Aaron CP, Madrigano J, et al. Association between long-term exposure to ambient air pollution and change in quantitatively assessed emphysema and lung function. JAMA - J Am Med Assoc. 2019;322:546–56.CrossRef

21.

Doiron D, de Hoogh K, Probst-Hensch N, Fortier I, Cai Y, De Matteis S, et al. Air pollution, lung function and COPD: results from the population-based UK Biobank study. Eur Respir J. 2019. https://doi.org/10.1183/13993003.02140-2018.

22.

Elbarbary M, Oganesyan A, Honda T, Kelly P, Zhang Y, Guo Y, et al. Ambient air pollution, lung function and COPD: cross-sectional analysis from the WHO Study of AGEing and adult health wave 1. BMJ Open Respir Res. 2020. https://doi.org/10.1136/bmjresp-2020-000684.

23.

Duan R-R, Hao K, Yang T. Air pollution and chronic obstructive pulmonary disease. Chronic Dis Transl Med. 2020;6:260–9.PubMedPubMedCentral

24.

Szczesniak R, Rice JL, Brokamp C, et al. Influences of environmental exposures on individuals living with cystic fibrosis. Expert Rev Respir Med. 2020;14:737–48.PubMedCrossRef

25.

Brugha R, Edmondson C, Davies JC. Outdoor air pollution and cystic fibrosis. Paediatr Respir Rev. 2018;28:80–6.PubMed

26.

Farhat SCL, Almeida MB, Silva-Filho LVRF, Farhat J, Rodrigues JC, Braga ALF. Ozone is associated with an increased risk of respiratory exacerbations in patients with cystic fibrosis. Chest. 2013;144:1186–92.PubMedPubMedCentralCrossRef

27.

Thurston GD, Balmes JR, Garcia E, et al. Outdoor air pollution and new-onset airway disease: an official American Thoracic Society workshop report. In: Ann. Am. Thorac. Soc. American Thoracic Society; 2020. p. 387–98.

28.

Georas SN, Rezaee F. Epithelial barrier function: at the front line of asthma immunology and allergic airway inflammation. J Allergy Clin Immunol. 2014;134:509–20.PubMedPubMedCentralCrossRef

29.••

Huff RD, Carlsten C, Hirota JA. An update on immunologic mechanisms in the respiratory mucosa in response to air pollutants. J Allergy Clin Immunol. 2019;143:1989–2001 An excellent review of the mechanisms of airway epithelial responses to air pollution.PubMedCrossRef

30.

Kesic MJ, Meyer M, Bauer R, Jaspers I. Exposure to ozone modulates human airway protease/antiprotease balance contributing to increased influenza A infection. PLoS One. 2012. https://doi.org/10.1371/journal.pone.0035108.

31.

Bromberg PA. Mechanisms of the acute effects of inhaled ozone in humans. Biochim Biophys Acta - Gen Subj. 2016;1860:2771–81.CrossRef

32.

Garantziotis S, Li Z, Potts EN, et al. Hyaluronan mediates ozone-induced airway hyperresponsiveness in mice. J Biol Chem. 2009;284:11309–17.PubMedPubMedCentralCrossRef

33.

Tighe RM, Garantziotis S. Hyaluronan interactions with innate immunity in lung biology. Matrix Biol. 2019;78–79:84–99.PubMedCrossRef

34.

Uhlson C, Harrison K, Allen CB, Ahmad S, White CW, Murphy RC. Oxidized phospholipids derived from ozone-treated lung surfactant extract reduce macrophage and epithelial cell viability. Chem Res Toxicol. 2002;15:896–906.PubMedCrossRef

35.

Almstrand AC, Voelker D, Murphy RC. Identification of oxidized phospholipids in bronchoalveolar lavage exposed to low ozone levels using multivariate analysis. Anal Biochem. 2015;474:50–8.PubMedPubMedCentralCrossRef

36.

Voter KZ, Whitin JC, Torres A, Morrow PE, Cox C, Tsai Y, et al. Ozone exposure and the production of reactive oxygen species by bronchoalveolar cells in humans. Inhal Toxicol. 2001;13:465–83.PubMedCrossRef

37.

Zhang S, Huo X, Zhang Y, Huang Y, Zheng X, Xu X. Ambient fine particulate matter inhibits innate airway antimicrobial activity in preschool children in e-waste areas. Environ Int. 2019;123:535–42.PubMedCrossRef

38.

Chen X, Liu J, Zhou J, Wang J, Chen C, Song Y, et al. Urban particulate matter (PM) suppresses airway antibacterial defence. Respir Res. 2018. https://doi.org/10.1186/s12931-017-0700-0.

39.

Luan X, Belev G, Tam JS, et al. Cystic fibrosis swine fail to secrete airway surface liquid in response to inhalation of pathogens. Nat Commun. 2017. https://doi.org/10.1038/s41467-017-00835-7.

40.

Celebi Sözener Z, Cevhertas L, Nadeau K, Akdis M, Akdis CA. Environmental factors in epithelial barrier dysfunction. J Allergy Clin Immunol. 2020;145:1517–28.PubMedCrossRef

41.

Michaudel C, Mackowiak C, Maillet I, et al. Ozone exposure induces respiratory barrier biphasic injury and inflammation controlled by IL-33. J Allergy Clin Immunol. 2018;142:942–58.PubMedCrossRef

42.

Smyth T, Veazey J, Eliseeva S, Chalupa D, Elder A, Georas SN. Diesel exhaust particle exposure reduces expression of the epithelial tight junction protein tricellulin. Part Fibre Toxicol. 2020. https://doi.org/10.1186/s12989-020-00383-x.

43.

Chen CM, Wu ML, Ho YC, Gung PY, Tsai MH, Orekhov AN, et al. Exposure to zinc oxide nanoparticles disrupts endothelial tight and adherens junctions and induces pulmonary inflammatory cell infiltration. Int J Mol Sci. 2020. https://doi.org/10.3390/ijms21103437.

44.

Dye JA, Adler KB. Effects of cigarette smoke on epithelial cells of the respiratory tract. Thorax. 1994;49:825–34.PubMedPubMedCentralCrossRef

45.

Strzelak A, Ratajczak A, Adamiec A, Feleszko W. Tobacco smoke induces and alters immune responses in the lung triggering inflammation, allergy, asthma and other lung diseases: a mechanistic review. Int J Environ Res Public Health. 2018. https://doi.org/10.3390/ijerph15051033.

46.

Brant TCS, Yoshida CT, Carvalho TS, et al. Mucociliary clearance, airway inflammation and nasal symptoms in urban motorcyclists. Clinics. 2014;69:867–70.PubMedPubMedCentralCrossRef

47.

Özler GS, Akoğlu E. Impairment of nasal mucociliary clearance time in wood industry workers. Eur Arch Oto-Rhino-Laryngology. 2020;277:493–6.CrossRef

48.

Cooper DM, Loxham M. Particulate matter and the airway epithelium: the special case of the underground? Eur Respir Rev. 2019. https://doi.org/10.1183/16000617.0066-2019.

49.

Wang J, Huang J, Wang L, Chen C, Yang D, Jin M, et al. Urban particulate matter triggers lung inflammation via the ROS-MAPK- NF-κB signaling pathway. J Thorac Dis. 2017;9:4398–412.PubMedPubMedCentralCrossRef

50.

Salvi SS, Nordenhall C, Blomberg A, Rudell B, Pourazar J, Kelly FJ, et al. Acute exposure to diesel exhaust increases IL-8 and GRO-α production in healthy human airways. Am J Respir Crit Care Med. 2000;161:550–7.PubMedCrossRef

51.

Reynolds PR, Wasley KM, Allison CH. Diesel particulate matter induces receptor for advanced glycation end-products (RAGE) expression in pulmonary epithelial cells, and RAGE signaling influences NF-κB-mediated inflammation. Environ Health Perspect. 2011;119:332–6.PubMedCrossRef

52.

Devlin RB, McKinnon KP, Noah T, Becker S, Koren HS. Ozone-induced release of cytokines and fibronectin by alveolar macrophages and airway epithelial cells. Am J Physiol - Lung Cell Mol Physiol. 1994. https://doi.org/10.1152/ajplung.1994.266.6.l612.

53.

Tripathi P, Deng F, Scruggs AM, Chen Y, Huang SK. Variation in doses and duration of particulate matter exposure in bronchial epithelial cells results in upregulation of different genes associated with airway disorders. Toxicol Vitr. 2018;51:95–105.CrossRef

54.

Bowers EC, McCullough SD, Morgan DS, Dailey LA, Diaz-Sanchez D. ERK1/2 and p38 regulate inter-individual variability in ozone-mediated IL-8 gene expression in primary human bronchial epithelial cells. Sci Rep. 2018;8:1–11.CrossRef

55.

Bauer RN, Müller L, Brighton LE, Duncan KE, Jaspers I. Interaction with epithelial cells modifies airway macrophage response to ozone. Am J Respir Cell Mol Biol. 2015;52:285–94.PubMedPubMedCentralCrossRef

56.

Bartemes KR, Kita H. Dynamic role of epithelium-derived cytokines in asthma. Clin Immunol. 2012;143:222–35.PubMedPubMedCentralCrossRef

57.

Zhou B, Comeau MR, De Smedt T, Liggitt HD, Dahl ME, Lewis DB, et al. Thymic stromal lymphopoietin as a key initiator of allergic airway inflammation in mice. Nat Immunol. 2005;6:1047–53.PubMedCrossRef

58.

Wang YH, Angkasekwinai P, Lu N, et al. IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC-activated Th2 memory cells. J Exp Med. 2007;204:1837–47.PubMedPubMedCentralCrossRef

59.

Kondo Y, Yoshimoto T, Yasuda K, Futatsugi-yumikura S, Morimoto M, Hayashi N, et al. Administration of IL-33 induces airway hyperresponsiveness and goblet cell hyperplasia in the lungs in the absence of adaptive immune system. Int Immunol. 2008;20:791–800.PubMedCrossRef

60.

Ying S, O’Connor B, Ratoff J, et al. Thymic stromal lymphopoietin expression is increased in asthmatic airways and correlates with expression of Th2-attracting chemokines and disease severity. J Immunol. 2005;174:8183–90.PubMedCrossRef

61.

Wang W, Li Y, Lv Z, Chen Y, Li Y, Huang K, et al. Bronchial allergen challenge of patients with atopic asthma triggers an alarmin (IL-33, TSLP, and IL-25) response in the airways epithelium and submucosa. J Immunol. 2018;201:2221–31.PubMedCrossRef

62.

Liew FY, Girard JP, Turnquist HR. Interleukin-33 in health and disease. Nat Rev Immunol. 2016;16:676–89.PubMedCrossRef

63.

De Grove KC, Provoost S, Braun H, Blomme EE, Teufelberger AR, Krysko O, et al. IL-33 signalling contributes to pollutant-induced allergic airway inflammation. Clin Exp Allergy. 2018;48:1665–75.PubMedCrossRef

64.

Robbins PD, Morelli AE. Regulation of immune responses by extracellular vesicles. Nat Rev Immunol. 2014;14:195–208.PubMedPubMedCentralCrossRef

65.

Clay CC, Maniar-Hew K, Gerriets JE, Wang TT, Postlethwait EM, Evans MJ, et al. Early life ozone exposure results in dysregulated innate immune function and altered microRNA expression in airway epithelium. PLoS One. 2014. https://doi.org/10.1371/journal.pone.0090401.

66.

Bartel S, La Grutta S, Cilluffo G, et al. Human airway epithelial extracellular vesicle miRNA signature is altered upon asthma development. Allergy Eur J Allergy Clin Immunol. 2020;75:346–56.CrossRef

67.

Patial S, Saini Y. Lung macrophages: current understanding of their roles in Ozone-induced lung diseases. Crit Rev Toxicol. 2020;50:310–23.PubMedPubMedCentralCrossRef

68.

Laskin DL, Malaviya R, Laskin JD. Role of macrophages in acute lung injury and chronic fibrosis induced by pulmonary toxicants. Toxicol Sci. 2019;168:287–301.PubMedCrossRef

69.

Bekki K, Ito T, Yoshida Y, et al. PM2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways. Environ Toxicol Pharmacol. 2016;45:362–9.PubMedCrossRef

70.

Raji H, Riahi A, Borsi SH, Masoumi K, Khanjani N, Ahmadiangali K, et al. Acute effects of air pollution on hospital admissions for asthma, copd, and bronchiectasis in Ahvaz, Iran. Int J COPD. 2020;15:501–14.CrossRef

71.

Kilburg-Basnyat B, Reece SW, Crouch MJ, et al. Specialized pro-resolving lipid mediators regulate ozone-induced pulmonary and systemic inflammation. Toxicol Sci. 2018;163:466–77.PubMedPubMedCentralCrossRef

72.

Epelman S, Lavine KJ, Randolph GJ. Origin and functions of tissue macrophages. Immunity. 2014;41:21–35.PubMedPubMedCentralCrossRef

73.

Gordon S, Plüddemann A. Tissue macrophages: heterogeneity and functions. BMC Biol. 2017. https://doi.org/10.1186/s12915-017-0392-4.

74.

Patel VI, Metcalf JP. Airway macrophage and dendritic cell subsets in the resting human lung. Crit Rev Immunol. 2018;38:303–31.PubMedPubMedCentralCrossRef

75.

Schyns J, Bureau F, Marichal T. Lung interstitial macrophages: past, present, and future. J Immunol Res. 2018. https://doi.org/10.1155/2018/5160794.

76.

Tighe RM, Misharin AV, Jakubzick CV, et al. Improving the quality and reproducibility of flow cytometry in the lung. An official American Thoracic Society workshop report. Am J Respir Cell Mol Biol. 2019;61:150–61.PubMedPubMedCentralCrossRef

77.

Mould KJ, Moore CM, McManus SA, McCubbrey AL, McClendon JD, Griesmer CL, et al. Airspace macrophages and monocytes exist in transcriptionally distinct subsets in healthy adults. Am J Respir Crit Care Med. 2020. https://doi.org/10.1164/rccm.202005-1989oc.

78.

Novak CM, Tighe RM, Ballinger MN. What is ‘normal’ when examining myeloid cells in human airways? Am J Respir Crit Care Med. 2020. https://doi.org/10.1164/rccm.202010-3932ed.

79.

Lavrich KS, Speen AM, Ghio AJ, Bromberg PA, Samet JM, Alexis NE. Macrophages from the upper and lower human respiratory tract are metabolically distinct. Am J Physiol - Lung Cell Mol Physiol. 2018;315:L752–64.PubMedPubMedCentralCrossRef

80.

Hume PS, Gibbings SL, Jakubzick CV, Tuder RM, Curran-Everett D, Henson PM, et al. Localization of macrophages in the human lung via design-based stereology. Am J Respir Crit Care Med. 2020;201:1209–17.PubMedPubMedCentralCrossRef

81.

Venosa A, Malaviya R, Gow AJ, Hall L, Laskin JD, Laskin DL. Protective role of spleen-derived macrophages in lung inflammation, injury, and fibrosis induced by nitrogen mustard. Am J Physiol - Lung Cell Mol Physiol. 2015;309:L1487–98.PubMedPubMedCentralCrossRef

82.

Francis M, Guo G, Kong B, Abramova EV, Cervelli JA, Gow AJ, et al. Regulation of lung macrophage activation and oxidative stress following ozone exposure by Farnesoid X receptor. Toxicol Sci. 2020;177:441–53.PubMedCrossRef

83.

Choudhary I, Vo T, Paudel K, Patial S, Saini Y. Compartment-specific transcriptomics of ozone-exposed murine lungs reveals sex- and cell type-associated perturbations relevant to mucoinflammatory lung diseases. Am J Physiol Cell Mol Physiol. 2021;320:L99–L125.CrossRef

84.•

Birukova A, Cyphert-Daly J, Cumming RI, Yu YR, Gowdy KM, Que LG, et al. Sex modifies acute ozone-mediated airway physiologic responses. Toxicol Sci. 2019;169:499–510 Explores the impact of sex as a variable in acute O3-induced lung injury and airway hyperresponsiveness. Identifiese that O3-induced airway hyperresponsiveness was elevated in male mice, but not in female mice. Alternatively, female mice exhibited increased airspace inflammation.PubMedPubMedCentralCrossRef

85.

Venosa A, Malaviya R, Choi H, Gow AJ, Laskin JD, Laskin DL. Characterization of distinct macrophage subpopulations during nitrogen mustard-induced lung injury and fibrosis. Am J Respir Cell Mol Biol. 2016;54:436–46.PubMedPubMedCentralCrossRef

86.

Becker S, Madden MC, Newman SL, Devlin RB, Koren HS. Modulation of human alveolar macrophage properties by ozone exposure in vitro. Toxicol Appl Pharmacol. 1991;110:403–15.PubMedCrossRef

87.

Thimmulappa RK, Chattopadhyay I, Rajasekaran S. Oxidative stress mechanisms in the pathogenesis of environmental lung diseases. In: Chakraborti S, Parinandi NL, Ghosh R, Ganguly NK, Chakraborti T, editors. Oxidative Stress Lung Dis. Singapore: Springer; 2019. p. 103–37.

88.

Gawda A, Majka G, Nowak B, Śróttek M, Walczewska M, Marcinkiewicz J. Air particulate matter SRM 1648a primes macrophages to hyperinflammatory response after LPS stimulation. Inflamm Res. 2018;67:765–76.PubMedPubMedCentralCrossRef

89.

Shahbaz MA, Martikainen MV, Rönkkö TJ, Komppula M, Jalava PI, Roponen M. Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro. Environ Res. 2021. https://doi.org/10.1016/j.envres.2020.110244.

90.

Oakes JL, O’Connor BP, Warg LA, et al. Ozone enhances pulmonary innate immune response to a toll-like receptor-2 agonist. Am J Respir Cell Mol Biol. 2013;48:27–34.PubMedPubMedCentralCrossRef

91.

Li Z, Potts EN, Piantadosi CA, Foster WM, Hollingsworth JW. Hyaluronan fragments contribute to the ozone-primed immune response to lipopolysaccharide. J Immunol. 2010;185:6891–8.PubMedPubMedCentralCrossRef

92.

Hollingsworth JW, Maruoka S, Li Z, Potts EN, Brass DM, Garantziotis S, et al. Ambient ozone primes pulmonary innate immunity in mice. J Immunol. 2007;179:4367–75.PubMedCrossRef

93.

Fu H, Liu X, Li W, Zu Y, Zhou F, Shou Q, et al. PM2.5 exposure induces inflammatory response in macrophages via the TLR4/COX-2/NF-κB pathway. Inflammation. 2020;43:1948–58.PubMedCrossRef

94.

de Souza Xavier Costa N, Ribeiro Júnior G, Dos Santos Alemany AA, et al. Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury. Sci Rep. 2020. https://doi.org/10.1038/s41598-020-72130-3.

95.

Li Z, Potts-Kant EN, Garantziotis S, Foster WM, Hollingsworth JW. Hyaluronan signaling during ozone-induced lung injury requires TLR4, MyD88, and TIRAP. PLoS One. 2011. https://doi.org/10.1371/journal.pone.0027137.

96.

Frush BW, Li Z, Stiles JV, Cotter SF, Shofer SL, Foster WM, et al. Ozone primes alveolar macrophage–derived innate immunity in healthy human subjects. J Allergy Clin Immunol. 2016;138:1213-1215.e1.PubMedPubMedCentralCrossRef

97.•

Hussain S, Johnson CG, Sciurba J, et al. TLR5 participates in the TLR4 receptor complex and promotes MyD88-dependent signaling in environmental lung injury. Elife. 2020. https://doi.org/10.7554/eLife.50458This study highlights a role for TLR5 signaling in environmental lung disease. Supports that TLR5 is required for TLR4 signaling and biases to MyD88 signaling via direct interactions between TLR5 and TLR4.

98.

Martin CJ, Peters KN, Behar SM. Macrophages clean up: efferocytosis and microbial control. Curr Opin Microbiol. 2014;17:17–23.PubMedCrossRef

99.

Underhill DM, Goodridge HS. Information processing during phagocytosis. Nat Rev Immunol. 2012;12:492–502.PubMedPubMedCentralCrossRef

100.

Karavitis J, Kovacs EJ. Macrophage phagocytosis: effects of environmental pollutants, alcohol, cigarette smoke, and other external factors. J Leukoc Biol. 2011;90:1065–78.PubMedPubMedCentralCrossRef

101.

Soukup JM, Becker S. Human alveolar macrophage responses to air pollution particulates are associated with insoluble components of coarse material, including particulate endotoxin. Toxicol Appl Pharmacol. 2001;171:20–6.PubMedCrossRef

102.

Sweeney S, Grandolfo D, Ruenraroengsak P, Tetley TD. Functional consequences for primary human alveolar macrophages following treatment with long, but not short, multiwalled carbon nanotubes. Int J Nanomedicine. 2015;10:3115–29.PubMedPubMedCentral

103.

Doran AC, Yurdagul A Jr, Tabas I. Efferocytosis in health and disease. Nat Rev Immunol. 2020;20:254–67.PubMedCrossRef

104.

Grabiec AM, Denny N, Doherty JA, et al. Diminished airway macrophage expression of the Axl receptor tyrosine kinase is associated with defective efferocytosis in asthma. J Allergy Clin Immunol. 2017;140:1144-1146.e4.PubMedCrossRef

105.••

Hodge MX, Reece SW, Madenspacher JH, Gowdy KM. In vivo assessment of alveolar macrophage efferocytosis following ozone exposure. J Vis Exp. 2019;2019:60109 Describes a protocol for in vivo assessment of macrophage-induced efferocytosis in rodents to facilitate assessment of efferocytosis in genetically modified animals and under distinct exposure conditions.

106.

West CE, Jenmalm MC, Prescott SL. The gut microbiota and its role in the development of allergic disease: a wider perspective. Clin Exp Allergy. 2015;45:43–53.PubMedCrossRef

107.

McCumber AW, Kim YJ, Isikhuemhen OS, Tighe RM, Gunsch CK. The environment shapes swine lung bacterial communities. Sci Total Environ. 2021. https://doi.org/10.1016/j.scitotenv.2020.143623.

108.

Ege MJ, Mayer M, Normand A-C, Genuneit J, Cookson WOCM, Braun-Fahrländer C, et al. Exposure to environmental microorganisms and childhood asthma. N Engl J Med. 2011;364:701–9.PubMedCrossRef

109.

Noverr MC, Falkowski NR, McDonald RA, McKenzie AN, Huffnagle GB. Development of allergic airway disease in mice following antibiotic therapy and fungal microbiota increase: role of host genetics, antigen, and interleukin-13. Infect Immun. 2005;73:30–8.PubMedPubMedCentralCrossRef

110.

Noverr MC, Huffnagle GB. The “microflora hypothesis” of allergic diseases. Clin Exp Allergy. 2005;35:1511–20.PubMedCrossRef

111.

Trompette A, Gollwitzer ES, Yadava K, et al. Gut microbiota metabolism of dietary fiber influences allergic airway disease and hematopoiesis. Nat Med. 2014;20:159–66.PubMedCrossRef

112.

Ghebre MA, Pang PH, Diver S, et al. Biological exacerbation clusters demonstrate asthma and chronic obstructive pulmonary disease overlap with distinct mediator and microbiome profiles. J Allergy Clin Immunol. 2018;141:2027-2036.e12.PubMedPubMedCentralCrossRef

113.

Durack J, Lynch SV, Nariya S, et al. Features of the bronchial bacterial microbiome associated with atopy, asthma, and responsiveness to inhaled corticosteroid treatment. J Allergy Clin Immunol. 2017;140:63–75.PubMedCrossRef

114.•

Dickson RP, Erb-Downward JR, Falkowski NR, Hunter EM, Ashley SL, Huffnagle GB. The lung microbiota of healthy mice are highly variable, cluster by environment, and reflect variation in baseline lung innate immunity. Am J Respir Crit Care Med. 2018;198:497–508 Demonstrates the importance of the microbiome in regulating innate immune responses as defined by inflammatory cytokine production and how these effects can be altered by environmental conditions that regulate the microbiome.PubMedPubMedCentralCrossRef

115.

Gibson PG, Yang IA, Upham JW, et al. Effect of azithromycin on asthma exacerbations and quality of life in adults with persistent uncontrolled asthma (AMAZES): a randomised, double-blind, placebo-controlled trial. Lancet. 2017;390:659–68.PubMedCrossRef

116.

Lopes dos Santos Santiago G, Brusselle G, Dauwe K, Deschaght P, Verhofstede C, Vaneechoutte D, et al. Influence of chronic azithromycin treatment on the composition of the oropharyngeal microbial community in patients with severe asthma. BMC Microbiol. 2017;17:109.PubMedPubMedCentralCrossRef

117.

Mishra V, DiAngelo SL, Silveyra P. Sex-specific IL-6-associated signaling activation in ozone-induced lung inflammation. Biol Sex Differ. 2016;7:1–22.CrossRef

118.

Osgood RS, Kasahara DI, Tashiro H, Cho Y, Shore SA. Androgens augment pulmonary responses to ozone in mice. Physiol Rep. 2019. https://doi.org/10.14814/phy2.14214.

119.

Fuentes N, Nicoleau M, Cabello N, Montes D, Zomorodi N, Chroneos ZC, et al. 17β-Estradiol affects lung function and inflammation following ozone exposure in a sex-specific manner. Am J Physiol - Lung Cell Mol Physiol. 2019;317:L702–16.PubMedPubMedCentralCrossRef

120.

Fuentes N, Cabello N, Nicoleau M, Chroneos ZC, Silveyra P. Modulation of the lung inflammatory response to ozone by the estrous cycle. Physiol Rep. 2019. https://doi.org/10.14814/phy2.14026.

121.

Fuentes N, Roy A, Mishra V, Cabello N, Silveyra P. Sex-specific microRNA expression networks in an acute mouse model of ozone-induced lung inflammation. Biol Sex Differ. 2018. https://doi.org/10.1186/s13293-018-0177-7.

122.

Cabello N, Mishra V, Sinha U, Diangelo SL, Chroneos ZC, Ekpa NA, et al. Sex differences in the expression of lung inflammatory mediators in response to ozone. Am J Physiol - Lung Cell Mol Physiol. 2015;309:L1150–63.PubMedPubMedCentralCrossRef

123.

Rebuli ME, Speen AM, Martin EM, Addo KA, Pawlak EA, Glista-Baker E, et al. Wood smoke exposure alters human inflammatory responses to viral infection in a sex-specific manner: a randomized, placebo-controlled study. Am J Respir Crit Care Med. 2019;199:996–1007.PubMedPubMedCentralCrossRef

124.••

McCullough SD, Bowers EC, On DM, Morgan DS, Dailey LA, Hines RN, et al. Baseline chromatin modification levels may predict interindividual variability in ozone-induced gene expression. Toxicol Sci. 2016;150:216–24 Identified that the chromatin structure of human epithelial cells from individual donors exhibited specific responses to in vitro O3 exposure. This highlights that individual variability in exposure responses can be predicted by an individual's chromatin modification.PubMedCrossRef

125.

Ladd-Acosta C, Feinberg JI, Brown SC, Lurmann FW, Croen LA, Hertz-Picciotto I, et al. Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health. Environ Int. 2019;126:363–76.PubMedPubMedCentralCrossRef

Titel: Role of Innate Immune System in Environmental Lung Diseases
verfasst von: Marissa A. Guttenberg
Aaron T. Vose
Robert M. Tighe
Publikationsdatum: 01.05.2021
Verlag: Springer US
Erschienen in: Current Allergy and Asthma Reports / Ausgabe 5/2021
Print ISSN: 1529-7322
Elektronische ISSN: 1534-6315
DOI: https://doi.org/10.1007/s11882-021-01011-0

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Springer Medizin

Role of Innate Immune System in Environmental Lung Diseases

Abstract

Purpose of review

Recent findings

Summary

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Springer Medizin

Abstract

Purpose of review

Recent findings

Summary

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