Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

Kuroda, Etsushi; Ozasa, Koji; Temizoz, Burcu; Ohata, Keiichi; Koo, Christine X.; Kanuma, Tomohiro; Kusakabe, Takato; Kobari, Shingo; Horie, Masanori; Morimoto, Yasuo; Nakajima, Saeko; Kabashima, Kenji; Ziegler, Steven F.; Iwakura, Yoichiro; Ise, Wataru; Kurosaki, Tomohiro; Nagatake, Takahiro; Kunisawa, Jun; Takemura, Nobuyuki; Uematsu, Satoshi; Hayashi, Masayuki; Aoshi, Taiki; Kobiyama, Kouji; Coban, Cevayir; Ishii, Ken J.

doi:10.1016/j.immuni.2016.11.010

Cited by 114 publications

(145 citation statements)

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“…Indeed, BMDMs from Mrc1 −/− mice or BMDMs with Mrc1 knockdown mice displayed altered responses to M1 and M2 stimuli, suggesting that Mrc1 and miR-511-3p control macrophage polarization and activation, which might contribute to the protection of allergen-induced inflammatory responses. 45 However, although BMDMs are broadly used surrogates for analysis of macrophage polarization, it will be essential to validate these findings in cultured alveolar macrophages ( in vitro –differentiated alveolar macrophages) 46 and human lung macrophages. Intriguingly, we found that plasma levels of miR-511-3p were significantly lower in asthmatic patients compared with those in nonasthmatic subjects, regardless of allergic status, indicating that miR-511-3p can protect against asthma.…”

Section: Discussionmentioning

confidence: 99%

Mannose receptor modulates macrophage polarization and allergic inflammation through miR-511-3p

Zhou

Danh

Ishmael

et al. 2018

Journal of Allergy and Clinical Immunology

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Background Mannose receptor (MRC1/CD206) has been suggested to mediate allergic sensitization and asthma to multiple glycoallergens, including cockroach allergens. Objective We sought to determine the existence of a protective mechanism through which MRC1 limits allergic inflammation through its intronic miR-511-3p. Methods We examined MRC1-mediated cockroach allergen uptake by lung macrophages and lung inflammation using C57BL/6 wild-type (WT) and Mrc1−/− mice. The role of miR-511-3p in macrophage polarization and cockroach allergen–induced lung inflammation in mice transfected with adeno-associated virus (AAV)–miR-511-3p (AAV– cytomegalovirus–miR-511-3p–enhanced green fluorescent protein) was analyzed. Gene profiling of macrophages with or without miR-511-3p overexpression was also performed. Results Mrc1−/− lung macrophages showed a significant reduction in cockroach allergen uptake compared with WT mice, and Mrc1−/− mice had an exacerbated lung inflammation with increased levels of cockroach allergen–specific IgE and TH2/TH17 cytokines in a cockroach allergen–induced mouse model compared with WT mice. Macrophages from Mrc1−/− mice showed significantly reduced levels of miR-511-3 and an M1 phenotype, whereas overexpression of miR-511-3p rendered macrophages to exhibit a M2 phenotype. Furthermore, mice transfected with AAV–miR-511-3p showed a significant reduction in cockroach allergen–induced inflammation. Profiling of macrophages with or without miR-511-3p overexpression identified 729 differentially expressed genes, wherein expression of prostaglandin D2 synthase (Ptgds) and its product PGD2 were significantly downregulated by miR-511-3p. Ptgds showed a robust binding to miR-511-3p, which might contribute to the protective effect of miR-511-3p. Plasma levels of miR-511-3p were significantly lower in human asthmatic patients compared with nonasthmatic subjects. Conclusion These studies support a critical but previously unrecognized role of MRC1 and miR-511-3p in protection against allergen-induced lung inflammation.

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Section: Discussionmentioning

confidence: 99%

Mannose receptor modulates macrophage polarization and allergic inflammation through miR-511-3p

Zhou

Danh

Ishmael

et al. 2018

Journal of Allergy and Clinical Immunology

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“…The precise mechanism of iSALT formation remains unknown. CD11c‐positive alveolar macrophages are suggested to play a role in organizing iBALT through interleukin (IL)‐1α release . It has been also suggested that M1 macrophages activate medial vascular smooth muscle cells to organize adventitial TLO in a murine model of atherosclerosis .…”

Section: Discussionmentioning

confidence: 99%

Analysis of possible structures of inducible skin‐associated lymphoid tissue in lupus erythematosus profundus

Kogame

Yamashita

Hirata

et al. 2018

The Journal of Dermatology

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Lupus erythematosus profundus (LEP) is a variant of lupus erythematosus, involving the deep dermis and subcutaneous fat. LEP is characterized by the presence of lymphoid follicles (LF) and germinal centers (GC). However, it remains unknown whether these lymphoid structures correspond to the lymphoid tissues such as cutaneous tertiary lymphoid organs (TLO). Previously, we identified dynamically orchestrated cellular elements in murine contact dermatitis that resembled lymphoid structures, which we termed inducible skin-associated lymphoid tissues (iSALT). We subsequently reported structures analogous to iSALT in human secondary syphilis, suggesting that iSALT can also exist in humans. Here, we studied ectopic lymphoid tissues in the lesions of LEP by immunohistochemistry and compared their characteristics with those of TLO. We demonstrated that LF of LEP were composed of B-cell follicles intermingled with CXCL13-expressing cells, distinct aggregations of T cells, and some blood vessels expressing peripheral node addressin. These findings indicate that LF of LEP can be considered as a type of iSALT.

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“…Alum promotes the production of PGE2 in macrophages via inflammasome‐independent mechanisms favoring IgE production . More recently, it has been shown that aluminum salts kill alveolar macrophages, which subsequently release IL‐1α promoting the formation of tertiary lymphoid tissues in the lung that sustain type‐2 allergic immune responses after allergen exposure . Many different immunopotentiators have been analyzed in mouse models of allergy.…”

Section: Allergen‐specific Immunotherapymentioning

confidence: 99%

Mechanisms of immune regulation in allergic diseases: the role of regulatory T and B cells

Palomares

Akdiş

Martín‐Fontecha

2017

Immunological Reviews

263

300

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Allergy is a major public health problem with a high socio-economic impact. The number of allergic patients is expected to reach to four billion within two decades when the World's population reaches to 10 billion. Our knowledge on the molecular mechanisms underlying allergic diseases and allergen tolerance induction had significant advances during the last years. Nowadays, it is well accepted that the generation and maintenance of allergen-specific regulatory T cells (Tregs) and regulatory B cells (Bregs) and the involvement of their suppressive cytokines and surface molecules are essential for the induction of allergen tolerance. These mechanisms play essential roles for the restoration of healthy immune responses to allergens in allergen-specific immunotherapy (AIT) and healthy immune response during high-dose antigen exposure in beekeepers and cat owners. AIT remains as the only disease-modifying and curative treatment for allergic diseases and represents a perfect model to investigate the antigen-specific immune responses in humans. A large number of clinical trials demonstrated AIT as an effective treatment in many patients, but it still faces several drawbacks in relation to efficacy, safety, long duration, and patient adherence. Novel strategies to overcome these inconveniences, such as the development of novel adjuvants and alternative routes of administration are being developed. The better understanding of the molecular mechanism governing the generation of Treg and Breg cells during allergen tolerance might well open new avenues for alternative therapeutic interventions in allergic diseases and help better understanding of other immune-tolerance-related diseases.

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Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

Cited by 114 publications

References 51 publications

Mannose receptor modulates macrophage polarization and allergic inflammation through miR-511-3p

Mannose receptor modulates macrophage polarization and allergic inflammation through miR-511-3p

Analysis of possible structures of inducible skin‐associated lymphoid tissue in lupus erythematosus profundus

Mechanisms of immune regulation in allergic diseases: the role of regulatory T and B cells

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