ArticleRespiratory research2015
Cigarette smoke inhibits BAFF expression and mucosal immunoglobulin A responses in the lung during influenza virus infection.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Article
- Cannabis smoke suppresses antiviral immune responses to influenza A in mice.ERJ open research · 2023Article
- SARS-CoV-2 versus Influenza A Virus: Characteristics and Co-Treatments.Microorganisms · 2023Review
- BRD4 is involved in viral exacerbation of chronic obstructive pulmonary disease.Respiratory research · 2023Article
- Deep immune B and plasma cell repertoire in non-small cell lung cancer.Frontiers in immunology · 2023Article
- Modeling the effects of cigarette smoke extract on influenza B virus infections in mice.Frontiers in immunology · 2023Article
- In Vivo and In Vitro Studies of Cigarette Smoke Effects on Innate Responses to Influenza Virus: A Matter of Models?Viruses · 2022Review
- Review
- Teleost swim bladder, an ancient air-filled organ that elicits mucosal immune responses.Cell discovery · 2022Article
- MTMR14 Alleviates Chronic Obstructive Pulmonary Disease as a Regulator in Inflammation and Emphysema.Oxidative medicine and cellular longevity · 2022Article
- Differential serum interferon-β levels in autoimmune thyroid diseases.Archives of medical science : AMS · 2022Article
- Increased Methyl-CpG-Binding Domain Protein 2 Promotes Cigarette Smoke-Induced Pulmonary Hypertension.Frontiers in oncology · 2022Article
- Effects of Cigarette Smoking on Influenza Virus/Host Interplay.Pathogens (Basel, Switzerland) · 2021Review
- Cigarette smoke exposure attenuates the induction of antigen-specific IgA in the murine upper respiratory tract.Mucosal immunology · 2021Article
- Circ-RBMS1 Knockdown Alleviates CSE-Induced Apoptosis, Inflammation and Oxidative Stress via Up-Regulating FBXO11 Through miR-197-3p in 16HBE Cells.International journal of chronic obstructive pulmonary disease · 2021Article
- IgA Antibodies and IgA Deficiency in SARS-CoV-2 Infection.Frontiers in cellular and infection microbiology · 2021Review
- Long non-coding RNA maternally expressed gene regulates cigarette smoke extract induced lung inflammation and human bronchial epithelial apoptosis via miR-149-3p.Experimental and therapeutic medicine · 2021Article
- Exposure to low temperatures suppresses the production of B-cell activating factor via TLR3 in BEAS-2B cells.Biochemistry and biophysics reports · 2020Article
- Influenza in High-Risk Hosts-Lessons Learned from Animal Models.Cold Spring Harbor perspectives in medicine · 2020Review
- Particulate matter (PMEnvironmental pollution (Barking, Essex : 1987) · 2020Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt is incompletely understood how cigarette smoke (CS) exposure affects lung mucosal immune responses during viral respiratory infections. B cell activating factor belonging to the tumor necrosis factor family (BAFF) plays an important role in the induction of secretory immunoglobulin A (S-IgA) which is the main effector of the mucosal immune system. We therefore investigated the effects of CS exposure on BAFF expression and S-IgA responses in the lung during influenza virus infection.
methodsMice were exposed to CS and/or infected with influenza virus. Bronchoalveolar lavage fluid and lung compartments were analyzed for BAFF expression, influenza-specific S-IgA level and histological changes. Lung B cells were isolated and the activation-induced cytidine deaminase (Aicda) expression was determined. BEAS-2B cells were treated with CS extract (CSE), influenza virus, interferon beta or N-acetylcysteine and BAFF expression was measured.
resultsCS inhibited BAFF expression in the lung, particularly after long-term exposure. BAFF and S-IgA levels were increased during influenza virus infection. Three-month CS exposure prior to influenza virus infection resulted in reduced BAFF and S-IgA levels in the lung as well as augmented pulmonary inflammation on day 7 after infection. Prior CS exposure also caused decreased Aicda expression in lung B cells during infection. Neutralization of BAFF in the lung resulted in reduced S-IgA levels during influenza virus infection. CSE inhibited virus-mediated BAFF induction in a dose-dependent manner in BEAS-2B cells, while this inhibition of BAFF by CSE was prevented by pretreatment with the antioxidant N-acetylcysteine.
conclusionsOur findings indicate that CS may hinder early mucosal IgA responses in the lung during influenza virus infection through oxidative inhibition of BAFF, which might contribute to the increased incidence and severity of viral infections in smokers.
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