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Genomic Profiling Reveals Distinct Routes To Complement Resistance in Klebsiella pneumoniae. | LitMetric

AI Article Synopsis

  • The serum complement system serves as a primary defense against bacteria, and some strains can resist its killing effects, which complicates treatment options for infections.
  • Research focused on four serum-resistant bacterial strains identified over 90 genes involved in complement resistance, with three genes common across all strains.
  • Deleting specific genes significantly impacted resistance, revealing that different strains use varied mechanisms to evade complement detection and attack.

Article Abstract

The serum complement system is a first line of defense against bacterial invaders. Resistance to killing by serum enhances the capacity of to cause infection, but it is an incompletely understood virulence trait. Identifying and characterizing the factors responsible for preventing activation of, and killing by, serum complement could inform new approaches to treatment of infections. Here, we used functional genomic profiling to define the genetic basis of complement resistance in four diverse serum-resistant strains (NTUH-K2044, B5055, ATCC 43816, and RH201207), and explored their recognition by key complement components. More than 90 genes contributed to resistance in one or more strains, but only three, , , and , were common to all four strains. Deletion of the antiterminator , which controls the expression of capsule and O side chains, resulted in dramatic complement resistance reductions in all strains. The murein lipoprotein gene promoted capsule retention through a mechanism dependent on its C-terminal lysine residue; its deletion led to modest reductions in complement resistance. Binding experiments with the complement components C3b and C5b-9 showed that the underlying mechanism of evasion varied in the four strains: B5055 and NTUH-K2044 appeared to bypass recognition by complement entirely, while ATCC 43816 and RH201207 were able to resist killing despite being associated with substantial levels of C5b-9. All and mutants bound C3b and C5b-9 in large quantities. Our findings show that, even among this small selection of isolates, adopts differing mechanisms and utilizes distinct gene sets to avoid complement attack.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7375759PMC
http://dx.doi.org/10.1128/IAI.00043-20DOI Listing

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