CO2 is not only a waste produce of metabolism, but is an important signalling molecule
that can affect multiple processes including inflammation, wound healing and muscle function
(9th March 2021) The findings presented in a collection of PAPERS published in the Royal Society Journal; Interface Focus on 12th February, following a Dec 2019 international scientific meeting titled ‘Carbon dioxide detection in biological systems’ show a better understanding of molecular basis of CO2 detection and its downstream signalling and physiological effects. This, first of its kind meeting, discussed common themes of carbon dioxide sensing between plant and animal kingdoms as well as clinical challenges posed by hypercapnia (elevated blood carbon dioxide levels). Findings presented around the ‘CO2 in immunity and inflammation’ theme highlighted the ‘double-edged sword’ effects of hypercapnia (HC) which are detrimental in the context of chronic lung diseases and infection but may be beneficial in the context of inflammation.
Speaking about the findings presented, Dr Eoin Cummins, Assistant Professor in Physiology, UCD School of Medicine and a co-organiser and speaker at the Dec 2019 Theo Murphy International Scientific Meeting said ‘Rising Carbon dioxide (CO2) levels in the atmosphere are a current topic of intense discussion on account of the link between CO2 and climate change. However, CO2 levels in the body are normally 125 times greater than those in the atmosphere and can rise further in disease. Most cells in the body consume oxygen (O2) and produce CO2 to survive. Much is known about how oxygen is sensed by cells and how the cell adapts to low oxygen. However, in marked contrast relatively little is understood about how CO2 is sensed by cells and the effects this has on cell function.”
“In the past CO2 was considered simply a waste product of metabolism but recent work has highlighted the important role that CO2 plays as a signalling molecule affecting multiple processes including inflammation, wound healing, muscle function, mitochondrial activity and as a risk factor in serious lung diseases, such as COPD” continued Dr Cummins.
Also speaking about the literature review relating to the effects of increased CO2 on immune cells, David Phelan, PhD Researcher, UCD School of Medicine said ‘In our laboratory we are examining the evidence for CO2-dependent regulation of key cellular processes, including inflammatory signalling, transcriptional changes, mitochondrial function and pH change. It is our hope that a better understanding of how CO2 signals can reduce the adverse consequences of elevated CO2 in lung disease patients and may provide new therapeutic opportunities for uncontrolled inflammation.”
The findings presented in this collection of papers published in the Royal Society Journal; Interface Focus underline the need for further understanding of the impact of elevated CO2 on critically ill patients and how enhancing knowledge of the physiological effects of CO2 could lead to the preservation of life. The review concludes by noting that clinicians must tightly control HC to provide any clinical benefit and that researchers might target future work in this area towards small molecules that underlie these pathways.
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