Tabata Maruyama Dos Santos, Renato Fraga Righetti, Leandro do Nascimento Camargo, Edna Aparecida Leick, Silvia Fukuzaki, Elaine Cristina de Campos, Thiago Tafarel Galli, Beatriz Mangueira Saraiva-Romanholo, Luana Laura Sales da Silva, Jéssica Anastácia Silva Barbosa, Juliana Morelli Lopes Gonçalves João, Carla Máximo Prado, Bianca Goulart de Rezende, Christine Laure Marie Bourotte, Fernanda Degobbi Tenorio Quirino Dos Santos Lopes, Milton de Arruda Martins, Isabela M Bensenor, João Vitor de Oliveira Cirillo, Suellen Karoline Moreira Bezerra, Fabio José Alencar Silva, Marcela Souza Lima Paulo, Paulo A Lotufo, Iolanda de Fátima Lopes Calvo Tibério
{"title":"减少 VAChT 对哮喘模型中因接触铁微粒而引起的肺部变化的影响","authors":"Tabata Maruyama Dos Santos, Renato Fraga Righetti, Leandro do Nascimento Camargo, Edna Aparecida Leick, Silvia Fukuzaki, Elaine Cristina de Campos, Thiago Tafarel Galli, Beatriz Mangueira Saraiva-Romanholo, Luana Laura Sales da Silva, Jéssica Anastácia Silva Barbosa, Juliana Morelli Lopes Gonçalves João, Carla Máximo Prado, Bianca Goulart de Rezende, Christine Laure Marie Bourotte, Fernanda Degobbi Tenorio Quirino Dos Santos Lopes, Milton de Arruda Martins, Isabela M Bensenor, João Vitor de Oliveira Cirillo, Suellen Karoline Moreira Bezerra, Fabio José Alencar Silva, Marcela Souza Lima Paulo, Paulo A Lotufo, Iolanda de Fátima Lopes Calvo Tibério","doi":"10.1186/s12950-024-00399-6","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Pollution harms the health of people with asthma. The effect of the anti-inflammatory cholinergic pathway in chronic allergic inflammation associated to pollution is poorly understood.</p><p><strong>Methods: </strong>One hundred eight animals were divided into 18 groups (6 animals). Groups included: wild type mice (WT), genetically modified with reduced VAChT (VAChTKD), and those sensitized with ovalbumin (VAChTKDA), exposed to metal powder due to iron pelletizing in mining company (Local1) or 3.21 miles away from a mining company (Local2) in their locations for 2 weeks during summer and winter seasons. It was analyzed for hyperresponsivity, inflammation, remodeling, oxidative stress responses and the cholinergic system.</p><p><strong>Results: </strong>During summer, animals without changes in the cholinergic system revealed that Local1 exposure increased the hyperresponsiveness (%Rrs, %Raw), and inflammation (IL-17) relative to vivarium animals, while animals exposed to Local2 also exhibited elevated IL-17. During winter, animals without changes in the cholinergic system revealed that Local2 exposure increased the hyperresponsiveness (%Rrs) relative to vivarium animals. Comparing the exposure local of these animals during summer, animals exposed to Local1 showed elevated %Rrs, Raw, and IL-5 compared to Local 2, while in winter, Local2 exposure led to more IL-17 than Local1. Animals with VAChT attenuation displayed increased %Rrs, NFkappaB, IL-5, and IL-13 but reduced alpha-7 compared to animals without changes in the cholinergic system WT. Animals with VAChT attenuation and asthma showed increased the hyperresponsiveness, all inflammatory markers, remodeling and oxidative stress compared to animals without chronic lung inflammation. Exposure to Local1 exacerbated the hyperresponsiveness, oxidative stressand inflammation in animals with VAChT attenuation associated asthma, while Local2 exposure led to increased inflammation, remodeling and oxidative stress.</p><p><strong>Conclusions: </strong>Reduced cholinergic signaling amplifies lung inflammation in a model of chronic allergic lung inflammation. Furthermore, when associated with pollution, it can aggravate specific responses related to inflammation, oxidative stress, and remodeling.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":"21 1","pages":"24"},"PeriodicalIF":4.4000,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11223391/pdf/","citationCount":"0","resultStr":"{\"title\":\"Effect of VAChT reduction on lung alterations induced by exposure to iron particles in an asthma model.\",\"authors\":\"Tabata Maruyama Dos Santos, Renato Fraga Righetti, Leandro do Nascimento Camargo, Edna Aparecida Leick, Silvia Fukuzaki, Elaine Cristina de Campos, Thiago Tafarel Galli, Beatriz Mangueira Saraiva-Romanholo, Luana Laura Sales da Silva, Jéssica Anastácia Silva Barbosa, Juliana Morelli Lopes Gonçalves João, Carla Máximo Prado, Bianca Goulart de Rezende, Christine Laure Marie Bourotte, Fernanda Degobbi Tenorio Quirino Dos Santos Lopes, Milton de Arruda Martins, Isabela M Bensenor, João Vitor de Oliveira Cirillo, Suellen Karoline Moreira Bezerra, Fabio José Alencar Silva, Marcela Souza Lima Paulo, Paulo A Lotufo, Iolanda de Fátima Lopes Calvo Tibério\",\"doi\":\"10.1186/s12950-024-00399-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Pollution harms the health of people with asthma. The effect of the anti-inflammatory cholinergic pathway in chronic allergic inflammation associated to pollution is poorly understood.</p><p><strong>Methods: </strong>One hundred eight animals were divided into 18 groups (6 animals). Groups included: wild type mice (WT), genetically modified with reduced VAChT (VAChTKD), and those sensitized with ovalbumin (VAChTKDA), exposed to metal powder due to iron pelletizing in mining company (Local1) or 3.21 miles away from a mining company (Local2) in their locations for 2 weeks during summer and winter seasons. It was analyzed for hyperresponsivity, inflammation, remodeling, oxidative stress responses and the cholinergic system.</p><p><strong>Results: </strong>During summer, animals without changes in the cholinergic system revealed that Local1 exposure increased the hyperresponsiveness (%Rrs, %Raw), and inflammation (IL-17) relative to vivarium animals, while animals exposed to Local2 also exhibited elevated IL-17. During winter, animals without changes in the cholinergic system revealed that Local2 exposure increased the hyperresponsiveness (%Rrs) relative to vivarium animals. Comparing the exposure local of these animals during summer, animals exposed to Local1 showed elevated %Rrs, Raw, and IL-5 compared to Local 2, while in winter, Local2 exposure led to more IL-17 than Local1. Animals with VAChT attenuation displayed increased %Rrs, NFkappaB, IL-5, and IL-13 but reduced alpha-7 compared to animals without changes in the cholinergic system WT. Animals with VAChT attenuation and asthma showed increased the hyperresponsiveness, all inflammatory markers, remodeling and oxidative stress compared to animals without chronic lung inflammation. Exposure to Local1 exacerbated the hyperresponsiveness, oxidative stressand inflammation in animals with VAChT attenuation associated asthma, while Local2 exposure led to increased inflammation, remodeling and oxidative stress.</p><p><strong>Conclusions: </strong>Reduced cholinergic signaling amplifies lung inflammation in a model of chronic allergic lung inflammation. 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Effect of VAChT reduction on lung alterations induced by exposure to iron particles in an asthma model.
Introduction: Pollution harms the health of people with asthma. The effect of the anti-inflammatory cholinergic pathway in chronic allergic inflammation associated to pollution is poorly understood.
Methods: One hundred eight animals were divided into 18 groups (6 animals). Groups included: wild type mice (WT), genetically modified with reduced VAChT (VAChTKD), and those sensitized with ovalbumin (VAChTKDA), exposed to metal powder due to iron pelletizing in mining company (Local1) or 3.21 miles away from a mining company (Local2) in their locations for 2 weeks during summer and winter seasons. It was analyzed for hyperresponsivity, inflammation, remodeling, oxidative stress responses and the cholinergic system.
Results: During summer, animals without changes in the cholinergic system revealed that Local1 exposure increased the hyperresponsiveness (%Rrs, %Raw), and inflammation (IL-17) relative to vivarium animals, while animals exposed to Local2 also exhibited elevated IL-17. During winter, animals without changes in the cholinergic system revealed that Local2 exposure increased the hyperresponsiveness (%Rrs) relative to vivarium animals. Comparing the exposure local of these animals during summer, animals exposed to Local1 showed elevated %Rrs, Raw, and IL-5 compared to Local 2, while in winter, Local2 exposure led to more IL-17 than Local1. Animals with VAChT attenuation displayed increased %Rrs, NFkappaB, IL-5, and IL-13 but reduced alpha-7 compared to animals without changes in the cholinergic system WT. Animals with VAChT attenuation and asthma showed increased the hyperresponsiveness, all inflammatory markers, remodeling and oxidative stress compared to animals without chronic lung inflammation. Exposure to Local1 exacerbated the hyperresponsiveness, oxidative stressand inflammation in animals with VAChT attenuation associated asthma, while Local2 exposure led to increased inflammation, remodeling and oxidative stress.
Conclusions: Reduced cholinergic signaling amplifies lung inflammation in a model of chronic allergic lung inflammation. Furthermore, when associated with pollution, it can aggravate specific responses related to inflammation, oxidative stress, and remodeling.
期刊介绍：
Journal of Inflammation welcomes research submissions on all aspects of inflammation.
The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings.
Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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