Dr Paul Bowyer - Aspergillosis Study Day May 1st 2012
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Dr Paul Bowyer is the Principle Scientist at the National Aspergillosis Centre. This talk was given to a group of professionals allied to medicine who are attending an education & awareness day at the Centre. Dr Bowyer summarises our current understanding of the pathogenic processes that lead to an aspergillus infection.
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Dr Paul Bowyer - Aspergillosis Study Day May 1st 2012
- 1. Aspergillus Research – What's Coming Next? Paul Bowyer University of Manchester
- 2. The genus Aspergillus Discovered by Micheli in June 1729 The species A. fumigatus Diverged ~720,000 years ago
- 3. - the story so far.... IMMUNE RESPONSE! IRON CELL WALL With apologies to Hanabusa Itcho
- 4. - what we know about the disease
- 5. What the blind monks should really have been asking.... How big is it? Is it dangerous???
- 6. Thre real level of disease... Predominant At Risk Prevalence Annual burden risk groups population ABPA 1,5,6 Asthma 34,700,000 2.1% 729,000 (243 – 1,215) Cystic fibrosis 29,000 15% 4.300 Frequency of aspergillosis Frequency of aspergillosis SAFS 1,5 Severe asthma 3,470,000 33% 1,145,000 CPA 4 COPD, >13,600,000 1-10% 204,000 sarcoidosis, TB, ABPA, Invasive Aspergillosis >25000 /year Immune dysfunction Immune hyperactivity
- 7. - what we know about the fungus
- 8. The fundamental interconnectedness of all things... Multiple processes in fungal and human cells interact in complicated ways to cause disease In order to understand how disease occurs it is necessary to look at the whole elephant New techniques such as systems biology and high throughput sequencing are now used to do this. We are moving away from study of single genes or proteins towards studying all Simultaneously. - fungi produce about 10,000 proteins and human cells about 25,000
- 10. Candida protein networks involved in biofilm formation: Nobile et al. A Recently Evolved Transcriptional Network Controls Biofilm Development in Candida albicansCell 148:126-138
- 11. High throughput approaches used to determine global transcription, genetic polymorphisms and gene function. Systems biology is used to find patterns and networks... Condition Transcription factors Genes of interest
- 12. The drugs dont work: How is Aspergillosis treated now?? - does it work?? – will this change??
- 13. Global increase in drug resistance
- 14. Processes involved in drug resistance:
- 15. - what we know about the patient
- 16. 'New genetics' Previously: - look in families or do crosses and look at the progeny... Now: - follow DNA polymorphisms in populations, • sequence genomes
- 17. How does the immune system stop fungal disease? The innate immune response is a complex multicellular process. Meet the cells.... IMMUNE CELL: ROLE: DETECTS PATHOGENS, SNEAKS OFF AND PROGRAMS THE IMMUNE RESPONSE DENDRITIC CELL
- 18. IMMUNE CELL: ROLE: STOPS AND APPREHENDS KNOWN PATHOGENS MACROPHAGE IMMUNE CELL: ROLE: BRUTALLY ATTACKS THINGS NEUTROPHIL
- 19. How the immune system stops fungal disease: MACROPHAGE EPITHELIUM DENDRITIC CELL
- 20. How the immune system stops fungal disease: WHATS ALL THIS 'ERE THEN? MACROPHAGE EPITHELIUM I SAY CHAPS! DENDRITIC CELL
- 21. How the immune system stops fungal disease: OI! NOW THEN OI!! MACROPHAGE OI!!! EPITHELIUM DENDRITIC CELL NEUTROPHILS
- 22. Adaptive Immunity – changes may lead to allergy
- 23. Individuals with fungal disease have: Changes in genes that affect macrophage or dendritic cell ability to percieve the pathogen Changes in genes that affect the ability of cells to move to the point of infection Changes in genes that mediate chemical attack on the fungus
- 24. In conclusion: Our knowledge of the disease in various forms is increasing rapidly. The huge burden of fungal disease worldwide is becoming clear. Our ability to find genetic changes associated with disease has increased in recent years In fact a Manchester project will discover all of the variants associated with ABPA within one year... We may be able to pinpoint the important variants... Our knowledge of fungal systems is increasing. More than 50 genome sequences and transcriptomes have been determined. We are expecting to be able to pinpoint processes involved in disease.