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Influence of airway allergic inflammation on platelet infiltration in the lungs of mice consuming hyperlipidic diet or sucrose consumption: possible participation of gut microbiota

Grant number: 22/02840-5
Support Opportunities:Research Grants - Visiting Researcher Grant - International
Duration: September 05, 2022 - September 19, 2022
Field of knowledge:Biological Sciences - Pharmacology - General Pharmacology
Principal Investigator:Gabriel Forato Anhê
Grantee:Gabriel Forato Anhê
Visiting researcher: Yanira Riffo Vasquez
Visiting researcher institution: King's College London, England
Host Institution: Faculdade de Ciências Médicas (FCM). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:13/07607-8 - OCRC - Obesity and Comorbidities Research Center, AP.CEPID

Abstract

The allergic airway disease (AAD) is hallmarked by a predominant Th2 inflammatory response with eosinophil and neutrophils infiltration into the lung parenchyma. Landmark studies published by Dr Page and Dr Riffo-Vasquez collected evidence to support the notion that leukocyte recruitment to the lung induced by allergic inflammation is dependent on platelet-leukocyte interaction. In our laboratory we have gathered data showing that either a High Fat Diet (HFD) or a sucrose solution can exacerbate the AAD induced by ovalbumin in mice. Two experimental protocols recently performed in our laboratory suggest a potential participation of gut microbiota in this response. In the first protocol (Protocol 1), we have demonstrated that a pre-biotic enriched diet prevents the exacerbation of AAD induced by sucrose consumption. In a second protocol (protocol 2) we have found that a pharmacological inhibition NOD1 (a pattern recognition receptor that recognizes bacterial peptidoglycan fragments) inhibits the AAD exacerbation induced by HFD. We still do not known, however, if intake of HFD or liquid sucrose can exacerbate platelet infiltration into the lung parenchyma. Revealing the existence of this phenomenon would clarify the mechanisms by which HFD or sucrose can exacerbate the AAD. Samples of the protocol 1 and protocol 2 belong the projects funded by FAPESP (respectively, 2019/17953-7 and 2021/09365-8). During her visit, Dr Riffo-Vasquez will participate in experiments to elucidate if platelet infiltration into the lung is modulated by HFD or sucrose. The approach used to address this question will be the immuno-histochemistry to detect CD42b in lung sections. These experiments will greatly improve the publications resulting from these two projects. During her stay, we will also have the opportunity to discuss data of other projects related to AAD that are being currently developed in our laboratory. A regular project coordinated by Prof Gabriel Anhe in which the focus is the AAD after a transitory history of obesity (2020/13940-5). A PhD project developed in collaboration with Prof. Silvana Bordin in which we evaluate if sucrose consumption can modulate AAD in the offspring (PhD candidate Amanda Santos Cavalcante Proc. FAPESP 2021/06444-4, PPG-Farmacologia, UNICAMP). (AU)

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