Keywords
Foodborne disease
Puerperium
Intestine
How to Cite
Abstract
This study was aimed to analyse the intestinal mucosal response to a foodborne disease by Salmonella Enteritidis (SE) during the early puerperium. BALB/c mice were treated with streptomycin at day 2 postpartum. 24 hs later mice were inoculated with 103 CFU of SE intragastrically. At day 3 post infection (pi), bacterial loads, tight junctions and inflammatory cytokines expression were analysed by qPCR. Results showed that SE ingestion evoked 86% host fatality in puerperal females at 5 days pi. In contrast mortality rate in infected virgin mice was 20%. This adverse maternal outcome is correlated with a disruption of the intestinal barrier, massive bacterial organs colonization and bacteremia. The expression of claudin-4 and zonule occludens-1 was significantly lower in infected mothers compared to the controls (p <0.05). In contrast, claudin-2 and claudin-15 levels were significantly increased in infected parturients respect to controls (p <0.05). Also, levels of TNF-α, IFN-γ, IL-17 and IL-6 in gut of infected puerperal females were significantly higher than control mice (p <0.01). Taken together, SE enterocolitis during early stages of puerperium causes an intensified intestinal inflammatory response that disrupts the maternal intestinal barrier inducing systemic dissemination.
Capaldo CT, Powell DN, Kalman D. Layered defense: how mucus and tight junctions seal the intestinal barrier. J Mol Med. 2017;95:927-934.
Noto-Llana M, Sarnacki SH, Castañeda MD, et al. Salmonella enterica serovar Enteritidis enterocolitis during late stages of gestation induces an adverse pregnancy outcome in the murine model. PLoS One. 2014;9(11):e111282.
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