Macrophage polarization in response to epigenetic modifiers during infection and inflammation

Patel, Urmi; Rajasingh, Sheeja; Samanta, Saheli; Cao, Thuy Giang Nguyen; Dawn, Buddhadeb; Rajasingh, Johnson

doi:10.1016/j.drudis.2016.08.006

Cited by 160 publications

(131 citation statements)

References 99 publications

(115 reference statements)

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“…It is notable that macrophages are the first line of defense against viral infection, and it has been indicated that they are critical for the defense against influenza virus infection [21][22][23]. Moreover, macrophages undergo specific differentiation programs, depending on the local environment [18]. Nevertheless, scant literature is available about the polarization states of AMs infected with influenza virus and exposed to AFB 1 or about the roles played by AFB 1 -induced polarization in viral infection.…”

Section: Introductionmentioning

confidence: 96%

“…The phenomenon of the existence of the two contrasting M1/M2 phenotypes is referred to as 'macrophage polarization'. Macrophage polarization can occur at any point in an inflammatory process [17]; multiple phenotypic markers, cytokines and growth factors, such as nitric oxide synthase (iNOS), TNF-α and interleukin 10 (IL-10), interact to determine the final polarization state [18]. Previous studies indicated that AFB 1 was immunotoxic to porcine alveolar macrophages (PAMs) and that AFB 1 leads to time-and dose-dependent decreases in the viability and phagocytic activity of PAMs [19]; furthermore, AFB 1 decreases proinflammatory cytokine levels and increases anti-inflammatory cytokine levels in macrophages [20].…”

Section: Introductionmentioning

confidence: 99%

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Low-Level Aflatoxin B1 Promotes Influenza Infection and Modulates a Switch in Macrophage Polarization from M1 to M2

Sun

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Swine influenza virus (SIV) is a major pathogen of both animals and humans. Afatoxin B1 (AFB₁) is one of the most common mycotoxins in feed and food. However, the central contribution of AFB₁ to SIV infection remains unclear. Methods: Here, TCID₅₀ assays, fluorescence-based quantitative real-time PCR, western blotting, immunofluorescence staining, histopathological examination, flow cytometry and scanning electron microscopy were performed to investigate the involvement and underlying mechanism of AFB₁ in SIV infection in vivo and in vitro using mouse models and porcine alveolar macrophage (PAM) models, respectively. Results: The in vivo study showed that low levels of AFB₁ promoted SIV infection and increased its severity, as demonstrated by the increased mRNA expression of viral matrix protein (M); by the increased protein expression of nucleoprotein (NP), matrix protein 1 and ion channel protein; and by animal weight loss, lung index and lung histologic damage. In addition, the increased occurrence of SIV infection accompanied by increases in the level of IL-10 in sera and lungs, in the spleen index and in the number of CD206-positive mouse alveolar macrophages but decreases in the level of TNF-α in sera and lungs, in the thymus index and in the number of CD80-positive mouse alveolar macrophages was observed in SIV-infected mice after low-level AFB₁ exposure. The in vitro study showed that low concentrations of AFB₁ promoted SIV infection, as demonstrated by the increases in viral titers and viral M mRNA and NP expression levels in SIV-infected PAMs as well as by the number of cells positive for NP protein expression. Furthermore, AFB₁ promoted the polarization of SIV-infected PAMs to the M1 phenotype at 8 hpi and to the M2 phenotype at 24 hpi, as measured by the increases in IL-10 expression and in the number of CD206-positive PAMs as well as by the morphological changes observed by scanning electron microscopy. The administration of the immune stimulant lipopolysaccharide (LPS) reversed the switch in PAM polarization from M2 to M1 and thereby counteracted the promotion of influenza virus infection induced by AFB₁. Conclusion: Our results are the first to confirm that low-level exposure to AFB₁ promotes SIV infection and modulates a switch in macrophage polarization from M1 to M2. The work reported here provides important data that point to a role for AFB₁ in SIV infection, and it opens a new field of study.

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Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Low-Level Aflatoxin B1 Promotes Influenza Infection and Modulates a Switch in Macrophage Polarization from M1 to M2

Sun

Liu

et al. 2018

Cell Physiol Biochem

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“…[5] By contrast, dysregulated production of these immune mediators by macrophages during prolonged inflammation is associated with different pathological conditions, such as autoimmune diseases, and cancers. [68] In the present study, both ULPF and ULLF showed no inhibitory effect on RAW 264.7 macrophages cell proliferation in graded concentrations (10, 30, 60 µg/mL). When assessed by MTT assay, this study revealed that both lectins and polysaccharides fractions from U. lacuta were weakly active on RAW cells proliferation promoting a weak cytotoxic effects even at 60 µg/mL.…”

Section: Determination Of Tnf-α Levelsmentioning

confidence: 82%

Immunomodulatory and Anti-Inflammatory Activities of Algerian Ulva Lactuca

Ameddah¹

2017

WJPR

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“…No fígado, o aumento no fluxo de ácidos graxos e citocinas também favorece a resistência insulínica e a maior secreção de triglicérides nas VLDL. A dislipidemia da resistência insulínica favorece um perfil pró-aterogênico (Patel et al, 2016).…”

Section: Tecido Adiposo E Produtos De Glicação Avançadaunclassified

“…Macrófagos peritoneais representam uma população heterogênea e associam-se a perfis funcionais distintos mediados pelo estímulo do microambiente (Ghosn et al, 2010;Chawla et al, 2012;Patel et al, 2016 (Rath et al, 2014).…”

Section: Figura 16 Concentração Urinária De Substâncias Reativas Ao unclassified

Albumina modificada por glicação avançada e resistência insulínica em ratos: foco no tecido adiposo periepididimal e nas ações da N-acetilcisteína

Silva¹

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À Dra. Vera Capelozi, pela maneira atenciosa na qual nos apresentou ao famoso retículo acoplado ao microscópio. Muito obrigada pela oportunidade e segurança em discutir conosco sobre as formas de análise histológica.Às Dra. Maristela Okamoto, Maria Heloísa Shimizu, Suely Kazue Marie no auxílio com importantes metodologias. Obrigada pela disponibilidade, prontidão e por tantos ensinamentos. Acrescento aqui o meu agradecimento à Vanessa Galdeno que, de maneira tão animada, partilhou o seu conhecimento sobre as TOP 10 vias enriquecidas após RNA-seq.Ao Dr. Isaac de Castro, pela imprescindível contribuição nas análises estatísticas deste trabalho.Aos colegas, Dr. Danilo Corrêa, Dra. Karina Thieme e Ms. Nelly Takashima, por vivenciarem comigo o mundo dos ratos, glicação e Nacetilcisteína, durante os exaustivos períodos de tratamento. Pelas discussões calorosas, "entre músculos, rins, fígado, macrófagos e tecido adiposo", acredito que todos se salvaram.À Claudia Souza, pois sem a sua paciência com tantas proformas, pedidos que se estendem em chegar ou são "perdidos" nas nuvens, auxílio nas prestações de conta, submissões de relatórios, as nossas vidas no laboratório seriam um pouco bagunçadas. Obrigada pelo afeto, conversas e preocupação diárias. Ainda bem que a temos por perto.Ao Dr. Diego Gomes, que me disse, dentre tantas coisas, algumas que nem de longe esquecerei. "Vai, eu injeto nos animais no domingo", "Eu te ensino, nega", "Vamos fazer cDNA juntos amanhã?", "Skype para treinar o intramuros?" Porque me sinto amparada e aquelas dúvidas de ontem serão todas resolvidas e musicadas na sua companhia. Solta o som... À Ms. Fernanda Fusco, nossa "Super-Fofa", pelos dias em que se mostrou ser uma fortaleza, exemplo de prestatividade, companheirismo e dedicação. O Sistema renina-angiotensina-aldosterona ganhou um tom lilás e uma identidade tão suave quanto a sua.À Ms. Juliana Tironi, por compartilhar a bancada, os protocolos, dias de experimentos que, muitas vezes, se misturavam a noite e por tantos "Meu", quando tudo chegava ao fim. Aos ratos Wistar e a N-acetilcisteína que nos uniram, as cores quentes e frias dos gráficos e a sua coragem em trilhar novos caminhos. À Ms. Maria Sílvia Lavrador, por dividir seus comportamentos tão ímpares, como clamar a todos os santos quando não encontra o seu pendrive ou por simplesmente vibrar pela banda da proteína que custou a aparecer no Western-blot. A minha trajetória, sem as nossas discussões sobre adipócitos iguais aos livros de histologia, polarização M1/M2, precisaria ser urgentemente reescrita e ganhar um novo sentido.À Dra. Milessa Afonso ou Tchura, sintam-se à vontade. Nossa empatia se deu no primeiro momento e soou como se já nos conhecêssemos. Isso é mágico! Não importa se São Paulo fica um pouco distante de New York, as nossas conquistas são diárias, nossas ligações são demoradas e a nossa amizade perdurará. Meu muito obrigada por estar sempre "aqui", filosofando sobre os macrófagos, reinventando protocolos e inspirando a todos ao seu redor.À Ms. Paula Ramos, que consegue...

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Macrophage polarization in response to epigenetic modifiers during infection and inflammation

Cited by 160 publications

References 99 publications

Low-Level Aflatoxin B1 Promotes Influenza Infection and Modulates a Switch in Macrophage Polarization from M1 to M2

Low-Level Aflatoxin B1 Promotes Influenza Infection and Modulates a Switch in Macrophage Polarization from M1 to M2

Immunomodulatory and Anti-Inflammatory Activities of Algerian Ulva Lactuca

Albumina modificada por glicação avançada e resistência insulínica em ratos: foco no tecido adiposo periepididimal e nas ações da N-acetilcisteína

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