Dr Andrew Conway Morris

Follow @andymoz78

Patients who are admitted to intensive care are at high risk of complications from infection, both as the presenting pathology and developing as complications during their admission.  Pneumonia, a severe infection of the alveolar airspace, is both the commonest infective reason for admission and the commonest secondary infection acquired in the ICU.

Dr Conway Morris has demonstrated that patients in intensive care have impaired immune function, and has identified several defects in neutrophil anti-microbial functions.  These dysfunctions occur before patients develop secondary infections, and predict the risk of acquiring one.  This holds the promise of being able to prevent secondary infections by targeting immune dysfunction in at-risk patients.

One of the predominant drivers of this dysfunction  is the pro-inflammatory molecule C5a, a component of the complement cascade which is released in high concentrations in critically ill patients.  Dr Conway Morris demonstrated how C5a can drive impaired phagocytosis via phosphoinositide-3-kinase delta, and that this defect can be reversed using granulocyte-macrophage colony stimulating factor, which has led to a recent phase II clinical trial.  Using a phosphoproteomic technique developed in his lab, he has recently identified further defects in phagosomal maturation induced by C5a.  His current work focuses on understanding the signalling pathways which are activated when the neutrophil encounters a bacterial pathogen, how these are influenced by the inflammatory environment the cells are in and how this impairs antimicrobial responses.

Andrew is a practicing intensive care physician and clinician scientist whose research focuses on severe infections in intensive care patients.  He is interested in how the immune system fails in critical illness and how this leads to infections, most especially pneumonia.

His undertook degrees in medicine and biomedical science at the University of Glasgow before moving to Edinburgh where he completed a PhD in critical care immunology, identifying the complement component C5a as a key mediator in neutrophil dysfunction in critically ill patients.  After a period as a Clinical Lecturer in Intensive Care Medicine at the University of Edinburgh he moved to Cambridge to take up an NIHR Academic Clinical Lectureship, followed by a Wellcome Trust Clinical Research Career Development Fellowship.  He is currently an MRC Clinician Scientist in the Department of Medicine and Visiting Scientist in the Department of Pathology, where he works closely with Klaus Okkenhaug’s group in a shared lab space.  His group in the Department of Pathology seeks to understand the signalling pathways that underpin the neutrophil response to pathogens, and how these are disrupted in critical illness and sepsis.

Deputy Chair of the Infection Section, European Society of Intensive Care Medicine