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SUMMARY:Invasive Salmonella infections in animal models and man: castles o
 f cards\, roundabouts\, vaccines and disease  - Dr Piero Mastroeni\, Depar
 tment of Veterinary Medicine\, University of Cambridge
DTSTART:20151111T160000Z
DTEND:20151111T170000Z
UID:TALK60011@talks.cam.ac.uk
CONTACT:Fiona Roby
DESCRIPTION:The principle forms of invasive Salmonella infections\, typhoi
 d fever and invasive nontyphoidal Salmonella disease (iNTS)\, are both cha
 racterized by intracellular growth and extracellular systemic spread of ba
 cteria belonging to different serovars of Salmonella enterica. \n\nAnimal 
 models have provided many insights into those host-pathogen relationships 
 that control invasive Salmonella infections. Immunological or genetic mani
 pulations of B- and T-cell mediated immunity\, signaling pathways\, cytoki
 ne networks and phagocyte effector functions modulate host resistance/susc
 eptibility and have provided solid information on which immunological effe
 ctors control and eliminate the disease. These models have also enabled us
  to test different classes of vaccines and determine which ones are likely
  to induce the highest level of protection in other animal species and in 
 humans.\n\nThe higher incidence of invasive Salmonella disease in patients
  with genetic immunodeficiencies\, individuals carrying specific immune ge
 ne alleles and patients with comorbidities (e.g. malaria\,  severe anaemia
 \, HIV)\, indicates common resistance/susceptibility traits between mice a
 nd humans. iNTS and typhoid fever are often inferred to be immunologically
  similar. It would therefore be reasonable to assume that the determinants
  of resistance/susceptibility to these diseases are similar and require in
 vocation of humoral and cellular immunity. However\, evidence from host su
 sceptibility and risk factor associations provides a far more complex scen
 ario. \n\nThe presence of comorbidities in endemic area poses serious chal
 lenges to disease prevention by undermining those element of the innate im
 mune response that are the foundations upon which vaccines build resistanc
 e. There are currently large gaps in our knowledge of the mechanisms that 
 control Salmonella infections is humans and we still do not fully understa
 nd of how comorbidities\, alone or in combination\, impair immunity. \n\nA
  major challenge ahead is to link risk factors/comorbidities with specific
  immunological/functional defects that determine increased susceptibility 
 to infections in endemic areas. This will provide a rational pathway to de
 velop approaches and tools to restore such defects in individuals with hig
 h risk of contracting disease.\n
LOCATION:Lecture Theatre 2\, Department of Veterinary Medicine
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