Epidermal keratinocytes initiate wound healing and pro-inflammatory immune responses following percutaneous schistosome infection.
Bottom Line: Keratinocytes constitute the majority of cells in the skin's epidermis, the first line of defence against percutaneous pathogens.Here we address the hypothesis that cercariae activate epidermal keratinocytes to promote the development of a pro-inflammatory immune response in the skin.Together, these observations indicate that S.mansoni cercariae and their excretory/secretory products act directly upon epidermal keratinocytes, which respond by initiating barrier repair and pro-inflammatory mechanisms similar to those observed in epidermal wound healing.
Affiliation: Centre for Immunology and Infection, University of York, York YO10 5DD, United Kingdom. Electronic address: email@example.com.Show MeSH
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Mentions: Given the recently identified diversity within basal keratinocyte populations (Hsu et al., 2011; Jensen et al., 2008; Nagao et al., 2012), the numbers and proportions of keratinocyte sub-types was investigated following infection with S. mansoni cercariae. Within the non-haematopoietic (CD45âˆ’) epidermal keratinocytes, two populations of cells were identified according to expression of the interfollicular keratinocyte marker CD326+ (EpCAM) or hair follicle keratinocyte precursor marker CD34+ (Fig. 2A) (Jensen et al., 2008; Hsu et al., 2011; Nagao et al., 2012). Following percutaneous exposure to S. mansoni cercariae, CD326+ keratinocytes in infected epidermis did not differ significantly from naÃ¯ve samples in either percentage or cell number at any time point (Fig. 2Ba; ANOVA F: 0.426, PÂ =Â 0.736 and Fig. 2Bb; ANOVA F: 1.457, PÂ =Â 0.249). In contrast, there was a progressive increase in the percentage of CD34+ cells with time p.i. (Fig. 2Ba; ANOVA F: 3.601, PÂ =Â 0.027), although the increase was not statistically significant until 96Â h p.i. The number of CD45âˆ’ CD326âˆ’ CD34+ hair follicle-associated keratinocytes also significantly increased 24Â h after infection and this expansion was sustained at 96Â h p.i. (Fig. 2Bb; ANOVA F: 23.98, PÂ <Â 0.001).
Affiliation: Centre for Immunology and Infection, University of York, York YO10 5DD, United Kingdom. Electronic address: firstname.lastname@example.org.