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In utero exposure to maternal chronic inflammation transfers a pro-inflammatory profile to generation F2 via sex-specific mechanisms

dc.contributor.authorAdams, Rozanne Charlene McChary
dc.contributor.authorSmith, Carine
dc.date.accessioned2020-03-02T10:04:41Z
dc.date.available2020-03-02T10:04:41Z
dc.date.issued2020
dc.identifier.citationAdams, R. C. M. & Smith, C. 2020. In utero exposure to maternal chronic inflammation transfers a pro-inflammatory profile to generation F2 via sex-specific mechanisms. Frontiers in Immunology, 11:48, doi:10.3389/fimmu.2020.00048
dc.identifier.issn1664-3224 (online)
dc.identifier.otherdoi:10.3389/fimmu.2020.00048
dc.identifier.urihttp://hdl.handle.net/10019.1/107559
dc.descriptionCITATION: Adams, R. C. M. & Smith, C. 2020. In utero exposure to maternal chronic inflammation transfers a pro-inflammatory profile to generation F2 via sex-specific mechanisms. Frontiers in Immunology, 11:48, doi:10.3389/fimmu.2020.00048.
dc.descriptionThe original publication is available at https://www.frontiersin.org
dc.descriptionPublication of this article was funded by the Stellenbosch University Open Access Fund.
dc.description.abstractGenerational transfer of maladaptations in offspring have been reported to persist for multiple generations in conditions of chronic inflammation, metabolic and psychological stress. Thus, the current study aimed to expand our understanding of the nature, potential sex specificity, and transgenerational plasticity of inflammatory maladaptations resulting from maternal chronic inflammation. Briefly, F1 and F2 generations of offspring from C57/BL/6 dams exposed to a modified maternal periconception systemic inflammation (MSPI) protocol were profiled in terms of leukocyte and splenocyte counts and cytokine responses, as well as glucocorticoid sensitivity. Overall, F1 male and female LPS groups presented with glucocorticoid hypersensitivity (with elevated corticosterone and increased leukocyte glucocorticoid receptor levels) along with a pro-inflammatory phenotype, which carried over to the F2 generation. The transfer of inflammatory and glucocorticoid responsiveness from F1 to F2 is evident, with heritability of this phenotype in F2. The findings suggest that maternal (F0) perinatal chronic inflammation resulted in glucocorticoid dysregulation and a resultant pro-inflammatory phenotype, which is transferred in the maternal lineage but seems to affect male offspring to a greater extent. Of further interest, upregulation of IL-1β cytokine responses is reported in female offspring only. The cumulative maladaptation reported in F2 offspring when both F1 parents were affected by maternal LPS exposure is suggestive of immune senescence. Given the potential impact of current results and the lack of sex-specific investigations, more research in this context is urgently required.en_ZA
dc.description.urihttps://www.frontiersin.org/articles/10.3389/fimmu.2020.00048/full
dc.format.extent15 pages
dc.language.isoen_ZAen_ZA
dc.publisherFrontiers Media
dc.subjectMaternal chronic inflammation transfersen_ZA
dc.subjectGlucocorticoidsen_ZA
dc.subjectMaladaptions -- Genetic aspectsen_ZA
dc.subjectSex-spesific transfer of maladaptionsen_ZA
dc.titleIn utero exposure to maternal chronic inflammation transfers a pro-inflammatory profile to generation F2 via sex-specific mechanismsen_ZA
dc.typeArticleen_ZA
dc.description.versionPublisher's version
dc.rights.holderAuthors retain copyright


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