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Epidermal keratinocytes initiate wound healing and pro-inflammatory immune responses following percutaneous schistosome infection.

Bourke CD, Prendergast CT, Sanin DE, Oulton TE, Hall RJ, Mountford AP - Int. J. Parasitol. (2015)

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.

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Affiliation: Centre for Immunology and Infection, University of York, York YO10 5DD, United Kingdom. Electronic address: c.bourke@qmul.ac.uk.

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Murine CD34+ epidermal keratinocytes expand and differentiate with time post-Schistosoma mansoni infection. (A) Flow cytometry gating strategy to identify CD45− keratinocytes with a CD326+ interfollicular and CD34+ hair follicle bulge-associated phenotype in epidermal cell suspensions. Surface expression of the pluripotency marker α6integrin is shown within the CD34+ population (representative flow cytometry plots from four independent experiments). (B) Proportions (a) and cell numbers (b) of keratinocyte sub-populations within the non-haematopoietic CD45− gate. (C) Proportions (a) and cell numbers (b) of α6integrin+ and α6integrin− cells within the CD34+ gate (n = 4 independent experiments, three mice per group for each experiment; box plots indicate median ± 95% confidence interval). Unpaired t-tests were performed where ANOVA was significant; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
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f0010: Murine CD34+ epidermal keratinocytes expand and differentiate with time post-Schistosoma mansoni infection. (A) Flow cytometry gating strategy to identify CD45− keratinocytes with a CD326+ interfollicular and CD34+ hair follicle bulge-associated phenotype in epidermal cell suspensions. Surface expression of the pluripotency marker α6integrin is shown within the CD34+ population (representative flow cytometry plots from four independent experiments). (B) Proportions (a) and cell numbers (b) of keratinocyte sub-populations within the non-haematopoietic CD45− gate. (C) Proportions (a) and cell numbers (b) of α6integrin+ and α6integrin− cells within the CD34+ gate (n = 4 independent experiments, three mice per group for each experiment; box plots indicate median ± 95% confidence interval). Unpaired t-tests were performed where ANOVA was significant; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

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 (CD45−) 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 naïve samples in either percentage or cell number at any time point (Fig. 2Ba; ANOVA F: 0.426, P = 0.736 and Fig. 2Bb; ANOVA F: 1.457, P = 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, P = 0.027), although the increase was not statistically significant until 96 h p.i. The number of CD45− CD326− CD34+ hair follicle-associated keratinocytes also significantly increased 24 h after infection and this expansion was sustained at 96 h p.i. (Fig. 2Bb; ANOVA F: 23.98, P < 0.001).


Epidermal keratinocytes initiate wound healing and pro-inflammatory immune responses following percutaneous schistosome infection.

Bourke CD, Prendergast CT, Sanin DE, Oulton TE, Hall RJ, Mountford AP - Int. J. Parasitol. (2015)

Murine CD34+ epidermal keratinocytes expand and differentiate with time post-Schistosoma mansoni infection. (A) Flow cytometry gating strategy to identify CD45− keratinocytes with a CD326+ interfollicular and CD34+ hair follicle bulge-associated phenotype in epidermal cell suspensions. Surface expression of the pluripotency marker α6integrin is shown within the CD34+ population (representative flow cytometry plots from four independent experiments). (B) Proportions (a) and cell numbers (b) of keratinocyte sub-populations within the non-haematopoietic CD45− gate. (C) Proportions (a) and cell numbers (b) of α6integrin+ and α6integrin− cells within the CD34+ gate (n = 4 independent experiments, three mice per group for each experiment; box plots indicate median ± 95% confidence interval). Unpaired t-tests were performed where ANOVA was significant; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
© Copyright Policy - CC BY
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4365920&req=5

f0010: Murine CD34+ epidermal keratinocytes expand and differentiate with time post-Schistosoma mansoni infection. (A) Flow cytometry gating strategy to identify CD45− keratinocytes with a CD326+ interfollicular and CD34+ hair follicle bulge-associated phenotype in epidermal cell suspensions. Surface expression of the pluripotency marker α6integrin is shown within the CD34+ population (representative flow cytometry plots from four independent experiments). (B) Proportions (a) and cell numbers (b) of keratinocyte sub-populations within the non-haematopoietic CD45− gate. (C) Proportions (a) and cell numbers (b) of α6integrin+ and α6integrin− cells within the CD34+ gate (n = 4 independent experiments, three mice per group for each experiment; box plots indicate median ± 95% confidence interval). Unpaired t-tests were performed where ANOVA was significant; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.
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 (CD45−) 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 naïve samples in either percentage or cell number at any time point (Fig. 2Ba; ANOVA F: 0.426, P = 0.736 and Fig. 2Bb; ANOVA F: 1.457, P = 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, P = 0.027), although the increase was not statistically significant until 96 h p.i. The number of CD45− CD326− CD34+ hair follicle-associated keratinocytes also significantly increased 24 h after infection and this expansion was sustained at 96 h p.i. (Fig. 2Bb; ANOVA F: 23.98, P < 0.001).

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.

View Article: PubMed Central - PubMed

Affiliation: Centre for Immunology and Infection, University of York, York YO10 5DD, United Kingdom. Electronic address: c.bourke@qmul.ac.uk.

Show MeSH
Related in: MedlinePlus