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Hanson, K.

Publications and source records attributed to Hanson, K..

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Infection drives localised and individualised antibody repertoires, whereas immunisation promotes repertoire convergence in pig

Respiratory viruses elicit mucosal and systemic immunity, yet how tissue compartmentalisation and exposure route shape B cell repertoires remain unclear. Using the pig model, we characterised antibody repertoires in bronchoalveolar lavage, tracheobronchial lymph nodes, spleen, and blood following intranasal infection with pandemic influenza virus (pH1N1) or porcine respiratory coronavirus (PRCV), and after intramuscular PRCV immunisation. Infection induced highly compartmentalised responses, with antigen-associated clones enriched in lung, lymph nodes and spleen but with limited presentation in blood. These clones were largely private, indicating individualised responses, and displayed tissue-specific diversity. The similar tissue distributions between pH1N1 and PRCV infections suggest a conserved spatial organisation, although differential lymph node involvement indicates pathogen-specific effects. In contrast, intramuscular immunisation generated more convergent, public repertoires in blood, characterised by reduced clonal size diversity. Monoclonal antibody analysis revealed functional heterogeneity and limited overlap with bulk repertoires. Together, these findings show that despite stable germline usage, functional antibody responses are shaped by the route of antigen exposure, clonal selection, and host specific factors, resulting in distinct repertoire architectures between infection and immunisation. Author summaryRespiratory viruses such as influenza and coronaviruses infect the airways and lungs, where they trigger immune responses that help the body fight infection. Most studies of immunity rely on blood, although many immune cells function in tissues like the lungs. Therefore, we may be missing important parts of the immune response. We used pigs, a large animal model that closely resembles humans in respiratory biology and is naturally infected with influenzas and coronaviruses, to investigate how immune responses are shaped by infection compared with intramuscular vaccination. We examined B cells in lungs, nearby lymph nodes, spleen, and blood after infection with influenza or a porcine coronavirus and compared these with responses after vaccination. We found that infection generates distinct, individual immune responses in the lung and lymphoid organs. Vaccination by injection led to more similar responses across animals, mostly in the blood. This suggests the way the immune system encounters an antigen influences the response generated. We also showed that antibodies with similar binding properties can behave very differently in their ability to neutralise viruses. Our findings show that infection and vaccination shape immunity in fundamentally different ways, with important implications for designing vaccines that better protect against respiratory diseases.

immunology↗

Intestinal tissue response to Shiga toxin exposure

Shiga toxin (Stx) is produced by some pathogenic strains of E. coli. To study the impact of Stx on the human intestine we utilized human intestinal organoids (HIOs) and human intestinal enteroids (HIEs) grown as human intestinal enteroid monolayers (HIEMs) in transwells. To establish optimal experimental conditions, HIEMs were grown with or without mesenchymal cells added to the basolateral wells to recapitulate the interactions between the intestinal epithelium and underlying mesenchyme. Monolayer barrier integrity was determined through transepithelial electrical resistance (TEER) readings. Apical saline was used on the apical surface since growth medium caused uneven development of the TEER. Medium used for epithelial cells contains added growth factors, while mesenchymal medium lacks these growth factors. We have shown that mesenchymal cells can maintain the epithelial monolayer in medium lacking growth factors suggesting they produce these factors. Furthermore, growth factors produced by mesenchymal cells need to buildup in the medium over time, since daily medium changes were not as effective as medium changes performed every three days. We have also shown that addition of growth factors is toxic to mesenchymal cells. Epithelial cells were more resistant to Stx2 than the mesenchymal cells, and mesenchymal cells contributed to epithelial cell death. Epithelial cells tolerated luminal exposure better than basolateral exposure. These studies demonstrate the importance of understanding tissue interactions in a disease state when using in vitro and in vitro models. ImportanceThese studies have cemented the need for complex cell culture models when studying host-pathogen interactions. Common animal models such as mice are resistant to E. coli O157:H7 infections and intestinal delivery of Stx2, while humans appear to be sensitive to both. It has been proposed that in humans, STEC-mediated intestinal damage destroys the intestinal barrier and allows basolateral access to Stx2. In mice, there is no epithelial damage, therefore they are resistant to epithelial delivery of Stx2, while remaining sensitive to Stx2 injection. Our studies show that like mice, the human epithelial layer is quite resistant to Stx2, and it is the sensitivity of the mesenchymal cells that kills the epithelial cells. We have shown that Stx2 is transported through the intact epithelium without causing damage to the resistant epithelial layer. Understanding tissue interactions during infections is therefore critical in determining the effects of pathogens on human tissues.

microbiology↗