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Kwa, A. L. H.

Publications and source records attributed to Kwa, A. L. H..

2 recordsLinked to original sources

Layered phage therapy exploits capsule-loss escape and altered antibiotic susceptibility in CG23 hypervirulent Klebsiella pneumoniae

The rise of drug-resistant Klebsiella pneumoniae infections is prompting a re-evaluation of phage therapy as an alternative treatment. Phage therapy has achieved successful outcomes, yet important limitations persist, including the rapid emergence of phage resistance and the time required to source suitable phages. Combining multiple phages into a phage cocktail based on genetic diversity, morphology or distinct infection mechanisms is a common strategy to mitigate resistance. Phage pairing based on these criteria neither mitigates nor delays the emergence of resistance, using CG23 hypervirulent Klebsiella pneumoniae (hvKp) EC0675 as a model. In CG23 Kp strains, resistance arises through disruption of the capsular biosynthetic pathway, leading to capsule impairment and global cross-resistance to all capsule-active phages. Combining phages active against encapsulated wild-type bacteria with those active against capsule-deficient escape mutants can overcome this constraint, improving bacterial suppression in vitro and reducing bacterial burdens across multiple organs in a mouse systemic infection model. In parallel, phage-driven capsule loss increased susceptibility of hvKp EC0675 to selected antibiotics targeting the bacterial envelope or cell wall in vitro. These findings highlight the contribution of capsule-associated resistance to phage cross-resistance in the CG23 Kp strains examined, and support further evaluation of phage combinations targeting both wild-type bacteria and resistant derivatives, including their use alongside selected antibiotics, informing future clinical translation.

microbiology↗

Human MAIT cell cytolytic effector proteins synergize to overcome carbapenem resistance in Escherichia coli

Mucosa-associated invariant T (MAIT) cells are abundant antimicrobial T cells in humans, and recognize antigens derived from the microbial riboflavin biosynthetic pathway presented by the MHC-Ib-related protein (MR1). However, the mechanisms responsible for MAIT cell antimicrobial activity are not fully understood, and the efficacy of these mechanisms against antibiotic resistant bacteria has not been explored. Here, we show that MAIT cells mediate MR1-restricted antimicrobial activity against E. coli clinical strains in a manner dependent on the activity of cytolytic proteins, but independent of production of pro-inflammatory cytokines or induction of apoptosis in infected cells. The combined action of the pore-forming antimicrobial protein granulysin and the serine protease granzyme B released in response to TCR-mediated recognition of MR1-presented antigen is essential to mediate control against both cell-associated and free-living E. coli. Furthermore, MAIT cell-mediated bacterial control extend to multidrug-resistant E. coli primary clinical isolates additionally resistant to carbapenems, a class of last resort antibiotics. Notably, high levels of granulysin and granzyme B in the MAIT cell secretomes directly damage bacterial cells by increasing their permeability, rendering initially resistant E. coli susceptible to the bactericidal activity of carbapenems. These findings define the role of cytolytic effector proteins in MAIT cell-mediated antimicrobial activity, and indicate that granulysin and granzyme B synergize to restore carbapenem bactericidal activity and overcome carbapenem resistance in E. coli. One Sentence SummaryPotent antimicrobial activity of human MAIT cells overcomes carbapenem-resistance in control of Escherichia coli

immunology↗