The World Health Organization (WHO) has declared that Antimicrobial Resistance (AMR) is one of the top 10 global public health threats facing humanity.
Antibiotics are becoming increasingly ineffective as drug resistance spreads globally, leading to infections more difficult to treat and increased mortality. New antibacterial drugs are urgently needed – for example, to treat carbapenem-resistant gram-negative bacterial infections as identified in the WHO priority pathogen list.
The cost of AMR to national economies and their health systems is significant as it affects the productivity of patients or their caretakers through prolonged hospital stays and the need for more expensive and intensive care.
According to different reports, AMR is responsible for the death of around 1.27 million people/year and it is estimated to increase by 8-fold by 2050, reaching 10 million deaths/year.
Immunotherapies can be defined as a specific class of drugs that modulate the host immune system to fight disease.
In recent years, immunotherapies have been successfully used in cancer.
At Immunethep we believe that Immunotherapies can be a great approach to tackling infectious diseases. For this to become a reality it is essential to know the mechanisms through which the microbial attack our immune system.
For the past 10 years, we have been involved in the discovery of a virulence mechanism that is highly immunosuppressive and is shared by different bacteria. Our extensive R&D has been focused on the different steps of this mechanism and how to block it in a way that our immune system is able to respond to the infection.
The discovery of the immunosuppressive virulence mechanism was first made with Streptococcus agalactiae (Group B Streptococcus) and later confirmed for other four bacteria, namely: Staphylococcus aureus, Extra-intestinal pathogenic Escherichia coli (ExPEC), Klebsiella pneumoniae and Streptococcus pneumoniae.
With the discovery of the shared virulence mechanism, Immunethep realized that it could develop multivalent immunotherapies that could target simultaneously five different bacteria.
Moreover, as the virulence mechanism relies on the excretion of an immunosuppressive protein that is highly conserved amongst bacteria, the products developed to block this mechanism are not serotype-specific and can address all invasive serotypes of each bacteria.