oxic mechanisms of cigarette smoke and heat-not-burn tobacco vapor inhalation on rheumatoid arthriti

Autor(es)

Heluany, Cintia Scucuglia ^[1] ; Scharf, Pablo ^[1] ; Schneider, Ayda Henriques ^[2] ; Donate, Paula Barbim ^[2] ; Pedreira Filho, Walter Dos Reis ^[3] ; de Oliveira, Tiago Franco ^[4] ; Cunha, Fernando Queiroz ^[2] ; Poliselli Farsky, Sandra Helena ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin & Toxicol Anal, Av Prof Lineu Prestes 580 BL13 B, BR-05508900 Sao Paulo, SP - Brazil

^[2] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Pharmacol, Sao Paulo - Brazil

^[3] Jorge Duprat Figueiredo Fdn Occupat Safety & Med, Minist Econ, Sao Paulo, SP - Brazil

^[4] Fed Univ Hlth Sci Porto Alegre, Dept Pharmacosci, Porto Alegre, RS - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Science of The Total Environment; v. 809, FEB 25 2022.
• Citações Web of Science: 0

Resumo

Tobacco combustion exposure worsens rheumatoid arthritis (RA). Non-combustible tobacco devices, as heat-not-burn tobacco (HNBT), are emerging as harm reduction to smokers by releasing nicotine and lower combustible tobacco products. Nevertheless, HNBT toxicity remains unclear. Hence, here we investigated the impacts of the tobacco combustible product (cigarette smoke; CS) or HNBT vapor exposures on antigen-induced arthritis (AIA) in C57BL/6 mice. Animals were exposed to airflow, HNBT vapor, or CS during 1 h/twice a day, under the Health Canada Intense (HCI) smoking regime, between days 14 to 20 after the first immunization. At day 21, 16 h after the last exposures, mice were i.a. challenged and the AIA effects were evaluated 24 h later. CS- or HNBT-exposed mice presented equivalent blood nicotine levels. CS exposure worsened articular symptoms, pulmonary inflammation, and expression of lung metallothioneins. Nevertheless, CS or HNBT exposures reduced lymphoid organs' cellularity, splenocyte proliferation and IL-2 secretion. Additional in vitro CS or HNBT exposures confirmed the harmful effects on splenocytes, which were partially mediated by the activation of nicotine/alpha 7nAchR pathway. Associated, data demonstrate the toxic mechanisms of CS or HNBT inhalation at HCI regime on RA, and highlight that further investigations are fundamental to assure the toxicity of emerging tobacco products on the immune system during specific challenges. (C) 2021 Elsevier B.V. All rights reserved. (AU)

• Processo FAPESP: 19/19573-7 - Efeitos da exposição ao vapor aquecido do tabaco sobre a Artrite Reumatóide
• Beneficiário: Sandra Helena Poliselli Farsky
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs
• Processo FAPESP: 17/26998-9 - Tabagismo e doenças articulares: investigação dos mecanismos de ação da hidroquinona e do aerossol gerado pelo tubo de tabaco (heatstick) na Artrite Reumatoide e na Osteoartrite
• Beneficiário: Cintia Scucuglia Heluany
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado