Impact of smoking on inflammation: overview of molecular mechanisms

Gonçalves, Reginaldo Bruno; Coletta, Ricardo D.; Silvério, Karina Gonzáles; Benevides, Luciana; Casati, Márcio Z.; Silva, João; Nociti, Francisco Humberto

doi:10.1007/s00011-011-0308-7

Cited by 253 publications

(203 citation statements)

References 112 publications

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“…Smoking activates the NF-κB pathway, which induces transcription of genes involved in immune regulation. 46 As a result, acute smoking exposure results in a systemic inflammatory response indicated by higher levels of leukocytes (neutrophils and macrophages) which release proinflammatory mediators such as TNF-α, IL-6 and hsCRP. 18,[47][48][49][50] The association of smoking and inflammation is also supported by epidemiologic studies which demonstrated a positive association of cigarettes per day with hsCRP, white blood cell count, and fibrinogen in univariate analyses.…”

Section: Inflammationmentioning

confidence: 99%

The Relationship Between Smoking Intensity and Subclinical Cardiovascular Injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

Rifai¹,

DeFillippis²,

McEvoy³

et al. 2017

Journal of Vascular Surgery

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Section: Inflammationmentioning

confidence: 99%

The Relationship Between Smoking Intensity and Subclinical Cardiovascular Injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

Rifai¹,

DeFillippis²,

McEvoy³

et al. 2017

Journal of Vascular Surgery

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“…The impact of smoking is not identical on different immune cells, and the adverse effect can be summarized as follows: inflammatory cells are recruited into the lungs but weaken the ability of those cells, and cell populations of some subtypes decrease and switch the immune response to a more harmful pattern. 7 On the other hand, immune cells play an important role in shaping the tumor microenvironment, which interacts with the tumor cells and can be involved in carcinogenesis, development, invasion, and metastasis of tumors. 8 Some antibody-based anticancer drugs that target immune-related receptors improve patients’ survival time to some extent, for example, ipilimumab targets cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), and nivolumab and lambrolizumab target the Programmed Death 1 (PD1) receptor and the PD1 ligand (PD-L1).…”

Section: Introductionmentioning

confidence: 99%

Smoker and non-smoker lung adenocarcinoma is characterized by distinct tumor immune microenvironments

et al. 2018

OncoImmunology

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Tobacco smoking causes DNA damages in epithelial cells and immune dysfunction in the lung, which collectively contribute to lung carcinogenesis and progression. However, potential mechanisms by which tumor-infiltrating immune cells contribute to lung cancer survival and their differential contributions in ever-smokers and never-smokers are not well studied. Here, we performed integrative analysis of 11 lung cancer gene-expression datasets, including 1,111 lung adenocarcinomas and 200 adjacent normal lung samples. Distinct pathways were altered in lung carcinogenesis in ever-smokers and never-smokers. Never-smoker patients had a better outcome than ever-smoker patients. We characterized compositional patterns of 21 types of immune cells in lung adenocarcinomas and revealed the complex association between immune cell composition and clinical outcomes. Interestingly, we found two subsets of immune cells, mast cells and CD4+ memory T cells, which had completely opposite associations with outcomes in resting and activated status. We further discovered that several chemokines and their associated receptors (e.g., CXCL11-CX3CR1 axis) were selectively altered in lung tumors in response to cigarette smoking and their abundances showed stronger correlation with fractions of these immune subsets in ever-smokers than never-smokers. The status switched from the resting to activated forms in mast cells and CD4+ memory T cells might manifest some important processes induced by cigarette smoking during tumor development and progression. Our findings suggested that aberrant activation of mast cells and CD4+ memory T cells plays crucial roles in cigarette smoking-induced immune dysfunction in the lung, which contributes to tumor development and progression.

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“…It seems that the molecular mechanism at least partially responsible for immunomodulating capabilities of smoking involves activation of inhibitor of IκB kinase (IKK), fosforylation of IκB (inhibitor of nuclear factor NF-κB), NF-κB nuclear translocation and histone acetylation (17,18,28). NF-κB is a key transcription factor regulating the expression of various proinflammatory cytokines and numerous studies have linked its activation to elevated cytokine expression in smokers (29). 20 other transcriptional factors regulated by smoking have been identified so far, including GATA, PAX5, Smad 3/4, AP-1, ISRE, ICSBP (30,31).…”

Section: Discussionmentioning

confidence: 99%

Different effect of smoking on genders in Crohn’s disease

Karczewski

Poniedziałek²,

Rzymski³

et al. 2015

Turk J Gastroenterol

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Background/Aims: Smoking is a well-established environmental risk factor in Crohn's disease (CD). The study was aimed to investigate possible gender differences in the effect of smoking on the course of CD, with a special focus on selected immune parameters such as Th1/Th2/Th17 cytokines and regulatory T cells (Tregs). Materials and Methods: A group of 55 adults with CD was enrolled to the study. The analysis of clinical, demographic and immunological characteristics of patients was performed according to their smoking status and gender. Values were considered significant when p≤0.05. Results: Patients who smoked, particularly females, more frequently suffered from a moderate-to-severe form of the disease, requiring glucocorticoid and immunosuppressive therapies. Smokers, particularly females, were also hospitalized and underwent surgeries more frequently than non-smokers. Cytometric analysis showed higher levels of serum proinflammatory cytokines and lower levels of peripheral Tregs in female smokers and former smokers, comparing to males from these subgroups.Conclusion: Presented results demonstrate that in all investigated subgroups, particularly however among current smokers and former smokers, female patients seemed to be more affected by CD. Females developed more severe form of the disease and experienced the onset earlier than men. The imbalance between pro-and anti-inflammatory factors observed in CD patients was also more distinct in female smokers and former smokers, comparing to males, and could substantially contribute to the severity of the disease. Exposure to smoking seems to be one of the environmental factors contributing to the gender differences in CD.

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Impact of smoking on inflammation: overview of molecular mechanisms

Abstract: Multiple mechanisms may be responsible for the association of smoking and inflammation, and the identification of potential therapeutic targets should guide future research.

Cited by 253 publications

References 112 publications

The Relationship Between Smoking Intensity and Subclinical Cardiovascular Injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

The Relationship Between Smoking Intensity and Subclinical Cardiovascular Injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

Smoker and non-smoker lung adenocarcinoma is characterized by distinct tumor immune microenvironments

Different effect of smoking on genders in Crohn’s disease

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