Effects of combustible cigarettes and electronic nicotine delivery systems on immune cell‐driven inflammation: Evidences from diabetic patients and multiple low dose streptozotocin‐treated diabetic mice

Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS‐dependent modulation of immune cell‐driven infl...

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Vydané v:Journal of biochemical and molecular toxicology Ročník 38; číslo 9; s. e23841 - n/a
Hlavní autori: Kastratovic, Nikolina, Arsenijevic, Aleksandar, Harrell, Carl Randall, Mladenovic, Violeta, Djukic, Aleksandar, Volarevic, Ana, Jovanovic, Dalibor, Zdravkovic, Marija, Macut, Jelica Bjekic, Djonov, Valentin, Volarevic, Vladislav
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States Wiley Subscription Services, Inc 01.09.2024
Predmet:
Adult
Animals
Biological effects
Blood
CD3 antigen
CD4 antigen
Cell activation
Cigarettes
combustible cigarettes
Cytokines
Cytokines - blood
Cytokines - metabolism
Dendritic cells
Diabetes
Diabetes mellitus
Diabetes Mellitus, Experimental - immunology
Electronic cigarettes
Electronic Nicotine Delivery Systems
Female
Foxp3 protein
Helper cells
Humans
immune cells phenotypes
Immune system
Inflammasomes
Inflammation
Inflammation - immunology
Inflammatory response
inflammatory status
Leukocytes (neutrophilic)
Lymphocytes
Lymphocytes T
Macrophages
Male
Mice
Mice, Inbred C57BL
Middle Aged
Monocytes
Natural killer cells
Neutrophils
Nicotine
Streptozocin
diabetes mellitus
electronic nicotine delivery systems
immune cells phenotypes
combustible cigarettes
inflammatory status
ISSN:1095-6670, 1099-0461, 1099-0461
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Tagy: Pridať tag
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Abstract Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS‐dependent modulation of immune cell‐driven inflammation in DM patients who used ENDS (DMENDS), CCs (DMCC) or were non‐smokers (DMAIR), paving the way for the better understanding of ENDS‐induced biological effects. Multiple low dose streptozotocin (MLD‐STZ)‐induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD‐STZ‐induced DM. Pancreatic injury and inflammation were more severe in CC‐exposed than in ENDS‐exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF‐α, IFN‐γ and IL‐17‐producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3‐expressing, IL‐10‐producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF‐α and IL‐1β‐producing neutrophils and monocytes, TNF‐α and IFN‐γ‐producing T lymphocytes, NK and NKT cells were determined in the blood of DMCC patients, while total number of immunosuppressive, TGF‐β‐producing CD3 + CD4 + T cells was the highest in the blood of DMENDS patients. In conclusion, although both CC and ENDS aggravate on‐going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs. Both cigarettes (CCs) and electronic nicotine delivery systems (ENDS) modulate migration, activation and effector functions of immune cells, affecting progression of diabetes mellitus. Compared to ENDS, CCs more efficiently increase production of inflammatory cytokines in neutrophils, monocytes, T, NK and NKT cells and enhanced antigen‐presenting properties of dendritic cells, resulting in the aggravation of immune cell‐driven inflammation in diabetes.
AbstractList Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS‐dependent modulation of immune cell‐driven inflammation in DM patients who used ENDS (DMENDS), CCs (DMCC) or were non‐smokers (DMAIR), paving the way for the better understanding of ENDS‐induced biological effects. Multiple low dose streptozotocin (MLD‐STZ)‐induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD‐STZ‐induced DM. Pancreatic injury and inflammation were more severe in CC‐exposed than in ENDS‐exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF‐α, IFN‐γ and IL‐17‐producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3‐expressing, IL‐10‐producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF‐α and IL‐1β‐producing neutrophils and monocytes, TNF‐α and IFN‐γ‐producing T lymphocytes, NK and NKT cells were determined in the blood of DMCC patients, while total number of immunosuppressive, TGF‐β‐producing CD3 + CD4 + T cells was the highest in the blood of DMENDS patients. In conclusion, although both CC and ENDS aggravate on‐going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs. Both cigarettes (CCs) and electronic nicotine delivery systems (ENDS) modulate migration, activation and effector functions of immune cells, affecting progression of diabetes mellitus. Compared to ENDS, CCs more efficiently increase production of inflammatory cytokines in neutrophils, monocytes, T, NK and NKT cells and enhanced antigen‐presenting properties of dendritic cells, resulting in the aggravation of immune cell‐driven inflammation in diabetes.
Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS‐dependent modulation of immune cell‐driven inflammation in DM patients who used ENDS (DMENDS), CCs (DMCC) or were non‐smokers (DMAIR), paving the way for the better understanding of ENDS‐induced biological effects. Multiple low dose streptozotocin (MLD‐STZ)‐induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD‐STZ‐induced DM. Pancreatic injury and inflammation were more severe in CC‐exposed than in ENDS‐exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF‐α, IFN‐γ and IL‐17‐producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3‐expressing, IL‐10‐producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF‐α and IL‐1β‐producing neutrophils and monocytes, TNF‐α and IFN‐γ‐producing T lymphocytes, NK and NKT cells were determined in the blood of DMCC patients, while total number of immunosuppressive, TGF‐β‐producing CD3 + CD4 + T cells was the highest in the blood of DMENDS patients. In conclusion, although both CC and ENDS aggravate on‐going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs.
Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS‐dependent modulation of immune cell‐driven inflammation in DM patients who used ENDS (DM ENDS ), CCs (DM CC ) or were non‐smokers (DM AIR ), paving the way for the better understanding of ENDS‐induced biological effects. Multiple low dose streptozotocin (MLD‐STZ)‐induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD‐STZ‐induced DM. Pancreatic injury and inflammation were more severe in CC‐exposed than in ENDS‐exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF‐α, IFN‐γ and IL‐17‐producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3‐expressing, IL‐10‐producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF‐α and IL‐1β‐producing neutrophils and monocytes, TNF‐α and IFN‐γ‐producing T lymphocytes, NK and NKT cells were determined in the blood of DM CC patients, while total number of immunosuppressive, TGF‐β‐producing CD3 + CD4 + T cells was the highest in the blood of DM ENDS patients. In conclusion, although both CC and ENDS aggravate on‐going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs.
Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS-dependent modulation of immune cell-driven inflammation in DM patients who used ENDS (DM ), CCs (DM ) or were non-smokers (DM ), paving the way for the better understanding of ENDS-induced biological effects. Multiple low dose streptozotocin (MLD-STZ)-induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD-STZ-induced DM. Pancreatic injury and inflammation were more severe in CC-exposed than in ENDS-exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF-α, IFN-γ and IL-17-producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3-expressing, IL-10-producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF-α and IL-1β-producing neutrophils and monocytes, TNF-α and IFN-γ-producing T lymphocytes, NK and NKT cells were determined in the blood of DM patients, while total number of immunosuppressive, TGF-β-producing CD3 + CD4 + T cells was the highest in the blood of DM patients. In conclusion, although both CC and ENDS aggravate on-going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs.
Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS-dependent modulation of immune cell-driven inflammation in DM patients who used ENDS (DMENDS), CCs (DMCC) or were non-smokers (DMAIR), paving the way for the better understanding of ENDS-induced biological effects. Multiple low dose streptozotocin (MLD-STZ)-induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD-STZ-induced DM. Pancreatic injury and inflammation were more severe in CC-exposed than in ENDS-exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF-α, IFN-γ and IL-17-producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3-expressing, IL-10-producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF-α and IL-1β-producing neutrophils and monocytes, TNF-α and IFN-γ-producing T lymphocytes, NK and NKT cells were determined in the blood of DMCC patients, while total number of immunosuppressive, TGF-β-producing CD3 + CD4 + T cells was the highest in the blood of DMENDS patients. In conclusion, although both CC and ENDS aggravate on-going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs.Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have substituted CCs with electronic nicotine delivery systems (ENDS). Herewith, we compared CCs and ENDS-dependent modulation of immune cell-driven inflammation in DM patients who used ENDS (DMENDS), CCs (DMCC) or were non-smokers (DMAIR), paving the way for the better understanding of ENDS-induced biological effects. Multiple low dose streptozotocin (MLD-STZ)-induced mice model of DM was used to support clinical findings. Both CCs and ENDS aggravated MLD-STZ-induced DM. Pancreatic injury and inflammation were more severe in CC-exposed than in ENDS-exposed diabetic mice. CCs promoted activation of NLRP3 inflammasome, enhanced production of inflammatory cytokines in neutrophils, macrophages and remarkably improved antigen presenting capacity of dendritic cells which resulted in the expansion of TNF-α, IFN-γ and IL-17-producing Th1 and Th17 lymphocytes, NK and NKT cells. Compared to CCs, ENDS more intensively promoted expansion of FoxP3-expressing, IL-10-producing NK and NKT cells and triggered less intense systemic inflammatory response in diabetic animals. Similar findings were observed in DM patients. The highest numbers of inflammatory, TNF-α and IL-1β-producing neutrophils and monocytes, TNF-α and IFN-γ-producing T lymphocytes, NK and NKT cells were determined in the blood of DMCC patients, while total number of immunosuppressive, TGF-β-producing CD3 + CD4 + T cells was the highest in the blood of DMENDS patients. In conclusion, although both CC and ENDS aggravate on-going inflammation in DM, ENDS have weaker capacity to induce production of inflammatory cytokines in immune cells than CCs.
Author Mladenovic, Violeta
Djonov, Valentin
Volarevic, Ana
Kastratovic, Nikolina
Arsenijevic, Aleksandar
Volarevic, Vladislav
Djukic, Aleksandar
Jovanovic, Dalibor
Macut, Jelica Bjekic
Harrell, Carl Randall
Zdravkovic, Marija
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Keywords diabetes mellitus
electronic nicotine delivery systems
immune cells phenotypes
combustible cigarettes
inflammatory status
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Snippet Considering detrimental impacts of combustible cigarettes (CCs) on the exacerbation of diabetes mellitus (DM), a significant number of DM patients have...
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pubmed
crossref
wiley
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Publisher
StartPage e23841
SubjectTerms Adult
Animals
Biological effects
Blood
CD3 antigen
CD4 antigen
Cell activation
Cigarettes
combustible cigarettes
Cytokines
Cytokines - blood
Cytokines - metabolism
Dendritic cells
Diabetes
Diabetes mellitus
Diabetes Mellitus, Experimental - immunology
Electronic cigarettes
Electronic Nicotine Delivery Systems
Female
Foxp3 protein
Helper cells
Humans
immune cells phenotypes
Immune system
Inflammasomes
Inflammation
Inflammation - immunology
Inflammatory response
inflammatory status
Leukocytes (neutrophilic)
Lymphocytes
Lymphocytes T
Macrophages
Male
Mice
Mice, Inbred C57BL
Middle Aged
Monocytes
Natural killer cells
Neutrophils
Nicotine
Streptozocin
Title Effects of combustible cigarettes and electronic nicotine delivery systems on immune cell‐driven inflammation: Evidences from diabetic patients and multiple low dose streptozotocin‐treated diabetic mice
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjbt.23841
https://www.ncbi.nlm.nih.gov/pubmed/39235091
https://www.proquest.com/docview/3102310078
https://www.proquest.com/docview/3100919489
Volume 38
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