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Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
Cigarette smoke condensate affects monocyte interaction with endothelium
I Giunzioni1, A Bonomo1, E Bishop2
1Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, via Balzaretti 9, 20133 Milan, Italy.
Insights
Cigarette smoke condensate (CSC) affects human monocyte (HM) behavior, potentially worsening atherosclerosis. While CSC can decrease HM migration, it also triggers factors that amplify inflammatory cell recruitment and transmigration through the endothelium.
Area of Science:
- Cardiovascular Biology
- Immunology
- Atherosclerosis Research
Background:
- Monocyte adhesion and transmigration into the endothelium are key processes in atherosclerotic plaque development.
- Cigarette smoke is a known risk factor for atherosclerosis, but its precise impact on monocyte-endothelial interactions is not fully understood.
Purpose of the Study:
- To investigate the effects of cigarette smoke condensate (CSC) on human monocyte (HM) chemotaxis and transmigration across endothelial cells (ECs).
- To elucidate the molecular mechanisms underlying CSC's influence on monocyte behavior and endothelial interactions in atherogenesis.
Main Methods:
- Assessed human monocyte (HM) chemotaxis and transmigration through endothelial cell (EC) monolayers using cigarette smoke condensate (CSC).
- Analyzed the expression of key molecules including Rac 1 GTPase, VCAM1, ICAM1, integrins, TLR4, MCP1, IL8, IL1beta, and TNFalfa.
- Utilized conditioned media from CSC-exposed HMs and neutralizing antibodies for mechanistic studies.
Main Results:
- CSC pre-treatment reduced HM chemotaxis and transmigration, linked to decreased Rac 1 GTPase expression.
- Direct CSC exposure increased HM transmigration, stimulating EC VCAM1/ICAM1 and monocyte integrin expression.
- CSC-conditioned medium significantly enhanced HM transmigration, mediated by HM-released factors like MCP1 and IL8, and increased expression of TLR4, IL1beta, and TNFalfa.
Conclusions:
- CSC exerts dual effects: it can impair monocyte migratory capacity but also induces HMs to release factors that amplify inflammatory cell recruitment and transmigration.
- These complex interactions between CSC, monocytes, and endothelium can exacerbate the atherosclerotic process.
Objective:
Circulating monocytes adhere to the endothelium and migrate into the intima contributing to atherosclerotic plaque growth. Cigarette smoke is a risk factor for atherosclerosis, but it is not completely known how it affects monocyte behavior in atherogenesis.
Methods:
We studied the effects of cigarette smoke condensate (CSC) on human monocytes (HM) chemotaxis and transmigration through an endothelial cell (EC) monolayer.
Results:
Pre-treatment with CSC caused a decrease in HM chemotaxis and transmigration (-55% and -18% vs control, p < 0.05, respectively), paralleled by a reduced expression of Rac 1 GTPase. On the contrary, direct exposure of both HM and EC to CSC increased (+23% vs control, p < 0.05) HM transmigration, paralleled by a strong stimulation of VCAM1 and ICAM1 expression by ECs, and by a slight increase in monocyte integrin expression. An enhancement of monocyte transmigration was obtained after the exposure of both HM and EC to medium conditioned by HM previously incubated with CSC (+265% vs control, p < 0.001). CSC showed a stimulatory effect on the expression by HM of TLR4, MCP1, IL8, IL1beta, and TNFalfa, which was ablated by pre treatment with PDTC. Incubation with neutralizing antibodies against both MCP1 or IL8 completely abolished the CSC-conditioned medium induced HM transmigration.
Conclusions:
CSC induces HM to release chemotactic factor(s), which amplify the recruitment and transmigration of inflammatory cells through EC, but CSC may also reduce HM migratory capacity. Therefore, exposure to CSC affects monocyte behavior and interaction with the endothelium, thus potentially facilitating and/or further aggravating the atherogenic process.
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