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Investigating Immune Evasion in Bordetella spp. Respiratory Pathogens with Bruker’s CodePlex® Platform


Developing vaccines and therapies against infectious diseases is a formidable task. To establish durable immune protection, a comprehensive understanding of the immune system’s response to infectious agents is essential. This involves immune monitoring to assess and predict protective responses, alongside monitoring cytokine levels for potential toxicities.

Bordetella spp., respiratory bacterial pathogens, cause whooping cough—a persistent infection with high mortality rates in infants. Deciphering how Bordetella spp. eludes the immune system is a significant challenge. Unraveling these immunosuppression mechanisms holds promise for developing vaccines and therapies, addressing not only Bordetella spp. but also other mucosal invaders.

Decoding Immunosuppression Mechanisms with Cutting-Edge Proteomics

It is critical to understand the cellular mechanisms behind Bordetella spp.’s immunosuppression to effectively inform the development of vaccines and therapies to overcome Bordetella spp. and other mucosal pathogens. A recent study published in Cell Reports by researchers at the Louisiana State University Health Sciences Center Shreveport leveraged Bruker’s cutting-edge proteomic barcoding platform to shed light on the interplay between Bordetella spp. and the host immune system.

The core motiviation driving this study is the desire to understand Bordetella spp.’s immune evasion mechanisms. Researchers used Bruker’s CodePlex® bulk proteomics platform to assess T cell cytokine secretion profiles from mice infected with wild-type Bordetella bronchiseptica versus a mutant strain lacking the btrS pathway in order to understand how this specific pathway influences immunosuppression and contributes to Bordetella spp.’s overall strategy.

Critical Insights into Immune Response Dynamics Using CodePlex® Proteomic Barcoding Technology

Bruker’s CodePlex® Proteomic Barcoding platform played a crucial role in determining differences in cytokine secretions from T cells. The data revealed that the mutant bacteria triggered higher levels of specific cytokines compared to the wild-type, suggesting that Bordetella bronchiseptica suppresses pro-inflammatory T cell responses through btrS signaling.

The unique capabilities of CodePlex® allowed for a multiplexed cytokine analysis, providing insights into cytokine secretion mechanisms affected by wild-type versus mutant bacteria. This comprehensive approach, coupled with experiments exploring the transcriptome, flow cytometry, and immunostaining, unveiled the mechanisms used by Bordetella spp. respiratory pathogens. The authors also highlighted the critical role of eosinophils during bacterial infection and how btrS-mediated immunosuppression affects eosinophil functionality.

Implications for Future Research and Therapeutic Development

The identification of btrS-mediated immunosuppression and its impact on eosinophil functionality opens new avenues for future research. With these insights, researchers can explore ways to overcome immunosuppression or enhance eosinophil function, potentially leading to the development of vaccines and therapies against Bordetella spp. and other mucosal pathogens. CodePlex® technology plays a key role in guiding researchers toward practical solutions in the ongoing battle against infectious diseases.

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