Bordetella pertussis (PRN) Quantitation Kit

Bordetella pertussis is a gram-negative rod that infects the airways, and it plays many virulence genes in its interaction with respiratory epithelial cells. Such virulence molecules allow the bacteria to latch on to and attack epithelial cells, interrupt normal breathing and lead to serious illness or death. Pertactin, or PRN is a non-fimbrial agglutinogen that all virulent Bordetella pertussis strains generate. It is on the cell's outer membrane and a member of the autotransporter family. PRN comes from the prn gene as a precursor polypeptide. When hydrolysed, it turns into a 63,000 Da-molecular weight protein encoding an arginine-glycine-aspartic acid tripeptide. PRN contributes to multiple pathways in B. pertussis development: (1) Adhesion: PRN assists B. pertussis to stick to host cells, so that bacteria can enter ciliated epithelial cells of respiratory mucosa and alveolar macrophages, making B. pertussis invasive. (2) Immune evasion: PRN helps B. pertussis evade neutrophil clearance. (3) Immunomodulation: An immunomodulatory agent that will force you to avoid the body's immune system.

PRN is very immunogenic and induces protective antibodies, and an antigenic component of acellular pertussis vaccines. Studies have found that PRN in combination or single dose vaccines increases vaccine efficacy in large proportions. In multi-component aPV, PRN is considered an essential antigen. Phagocytosis mediated by PRN antibodies plays a vital role in immunity against Bordetella pertussis. Multivariate analysis has revealed that low PRN antibody levels are associated with susceptibility to infection, while high PRN antibody levels confer greater protection. In the era of aPV immunization, an increasing number of countries have detected strains that do not express functional PRN protein, known as PRN-deficient strains. These strains may have emerged as a result of selective pressure induced by aPV use. Research has shown that in vaccinated populations, the risk of contracting pertussis from PRN-deficient strains is higher than from PRN-expressing strains.

Figure 1. Model for various roles of antibodies against antigens in acellular pertussis vaccine
(Source: Ma L, et al. 2021)

The authors have come up with the following molecular scenarios to explain the formation of PRN deficient variants of Bordetella pertussis: (1) Insertion of IS481 sequences; (2) Inversion of the prn promoter; (3) Single nucleotide polymorphisms in the prn gene that add premature stop codons; (4) Partially deletion of the prn gene; (5) Replacement of the deleted parts of the prn gene with additional DNA fragments. Genetic sequencing has revealed 13 different PRN genotypes, demonstrating the protein's polymorphic nature. Mutations causing PRN deficiency can arise independently in various B. pertussis lineages. Similar selective pressures within populations, particularly vaccination strategies, may lead to the establishment of PRN-deficient strains in specific communities, potentially resulting in outbreaks and epidemics. Some regions exhibit circulating strain genotypes that differ from national epidemic strains, suggesting that PRN-deficient strains resulting from B. pertussis genotype changes may have regional specificity. The prevalence and outbreaks of PRN-deficient strains are thus considered a result of natural selection, driven by both bacterial mutations and host population immunity levels.

B. pertussis (PRN) Quantitation Kit
PRN Quantitation Kit
Pertactin Quantitation Kit