Building on a decade of pre-clinical research, the “HAP2” project is proposing a complete reappraisal of the physiopathology of HAP, whereby HAP is not induced by the contamination of the respiratory tracts by exogenous pathogens, but results from a dysbiosis between a dysfunctional commensal bacteria and a dampened immunity in hospitalised patients. This reappraisal is a game-changer in the prevention and treatment of this dramatic condition, departing from the prevailing “one-fits-all” approach towards achieving truly personalised treatment of infectious diseases.
The frequent treatment failures currently observed with antimicrobial therapy can thus be explained by a further reduction of bacterial diversity and metabolic functions within treatment. The development and validation of targeted host-directed immunotherapies able to restore the lost functions of the microbiome and of the mucosal immunity holds great promise for patients care and will minimize, or even ultimately replace antibiotics – which are currently the sole therapies to date. Moreover, these approaches can offer new opportunity of therapies in infections caused by multiple drug resistant bacteria, and help solve the worldwide challenge of antibiotic resistance.
