Delayed tail loss during the invasion of mouse skin by cercariae of Schistosoma japonicum

Parasitology ◽  
2011 ◽  
Vol 139 (2) ◽  
pp. 244-247 ◽  
Author(s):  
TING WANG ◽  
ZHENG-MING FANG ◽  
JIA-HUI LEI ◽  
FEI GUAN ◽  
WEN-QI LIU ◽  
...  
Keyword(s):  
Schistosoma Mansoni ◽  
Schistosoma Japonicum ◽  
Human Skin ◽  
Mouse Skin ◽  
Density Range ◽  
Experimental Conditions ◽  
Density Dependent ◽  
Tail Loss ◽  
Traditional Assumption

SUMMARYA traditional assumption is that schistosome cercariae lose their tails at the onset of penetration. It has, however, recently been demonstrated that, for Schistosoma mansoni, cercarial tails were not invariably being shed as penetration took place and a high proportion of tails entered human skin under experimental conditions. This phenomenon was termed delayed tail loss (DTL). In this paper, we report that DTL also happens with S. japonicum cercariae during penetration of mouse skin. It occurred at all cercarial densities tested, from as few as 10 cercariae/2·25 cm2 of mouse skin up to 200 cercariae. Furthermore, it was demonstrated that there was a density-dependent increase in DTL as cercarial densities increased. No such density-dependent enhancement was shown for percentage attachment over the same cercarial density range.

Schistosoma mansoni: tail loss in relation to permeability changes during cercaria–schistosomulum transformation

Parasitology ◽  
1975 ◽  
Vol 71 (1) ◽  
pp. 9-18 ◽  
Author(s):  
R. E. Howells ◽  
S. E. Gerken ◽  
F. J. Pinto-Ramalho ◽  
U. Kawazoe ◽  
G. Gazzinelli ◽  
...  
Keyword(s):  
Amino Acids ◽  
Methylene Blue ◽  
Schistosoma Mansoni ◽  
Body Region ◽  
Experimental Conditions ◽  
General Body ◽  
Tail Loss ◽  
Permeability Changes ◽  
Extensive Lesion ◽  
Scanning Electron

The hind-body region of Schistosoma mansoni cercariae observed in the scanning electron microscope demonstrates various stages of contraction which may be compared with those of living larvae which are secreting the acetabular gland contents.No evidence for an extensive lesion was found in cercarial bodies which had shed their tails under experimental conditions. Experiments on the permeability of the larvae to sodium fluoride, methylene blue and amino acids demonstrated that tail loss significantly affects the permeability of the bodies although the effect is greater immediately after decaudation than at later times. Subsequent increases in permeability may be correlated with a change in the general body surface.

Penetration of mouse and human skin by cercariae of Schistosoma mansoni; immunological and histological observations

1980 ◽  
Vol 79 (1-3) ◽  
pp. 173-182
Author(s):  
H. V. Smith ◽  
A. McQueen ◽  
J. R. Kusel
Keyword(s):  
Schistosoma Mansoni ◽  
Human Skin ◽  
Bullous Pemphigoid ◽  
Skin Diseases ◽  
Mouse Skin ◽  
Pemphigus Vulgaris ◽  
Intercellular Substance ◽  
Human Cadaver Skin ◽  
Cadaver Skin

SynopsisSera from patients suffering from the autoimmune skin diseases pemphigus vulgaris and bullous pemphigoid were used to demonstrate the presence of intercellular substance (ICS) or bullous pemphigoid antigen (BPA) on the surface of the schistosomula of Schistosoma mansoni which had penetrated mouse and human cadaver skin, and mouse skin percutaneously. Both ICS and BPA were absent from mechanically transformed schistosomula or those formed in the peritoneal cavity of mice. Schistosomula which penetrated slowly through mouse or human skin in vitro, acquired more ICS or BPA than those which penetrated rapidly.During percutaneous infections of mice, schistosomula recovered from skin after 2h and 24h had acquired large quantities of these materials whereas those which were recovered from skin after 10min had no detectable ICS or BPA. These materials must be shed during subsequent migration since schistosomula from lungs and liver, and 7-week old adults do not possess them.Histological examination of both mouse and human skin revealed that the schistosomula remained in the epidermis for varying lengths of time. Schistosomula which remained there for more than 2h became vacuolated, whereas schistosomula which were present in the dermis at 2h appeared undamaged.On cercarial penetration of human skin, the granular layer of the epidermis became disrupted or condensed. The implications of these findings are discussed.

scholarly journals IL-23 induced in keratinocytes by endogenous TLR4 ligands polarizes dendritic cells to drive IL-22 responses to skin immunization

2016 ◽  
Vol 213 (10) ◽  
pp. 2147-2166 ◽  
Author(s):  
Juhan Yoon ◽  
Juan Manuel Leyva-Castillo ◽  
Guoxing Wang ◽  
Claire Galand ◽  
Michiko K. Oyoshi ◽  
...  
Keyword(s):  
T Cells ◽  
Human Skin ◽  
Cd4 T Cells ◽  
Mouse Skin ◽  
Skin Inflammation ◽  
Serum Levels ◽  
Skin Lesions ◽  
Tape Stripping ◽  
Keratinocyte Proliferation ◽  
Th22 Cells

Atopic dermatitis (AD) is a Th2-dominated inflammatory skin disease characterized by epidermal thickening. Serum levels of IL-22, a cytokine known to induce keratinocyte proliferation, are elevated in AD, and Th22 cells infiltrate AD skin lesions. We show that application of antigen to mouse skin subjected to tape stripping, a surrogate for scratching, induces an IL-22 response that drives epidermal hyperplasia and keratinocyte proliferation in a mouse model of skin inflammation that shares many features of AD. DC-derived IL-23 is known to act on CD4+ T cells to induce IL-22 production. However, the mechanisms that drive IL-23 production by skin DCs in response to cutaneous sensitization are not well understood. We demonstrate that IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4+ T cells that mediates epidermal thickening. We also show that IL-23 is released in human skin after scratching and polarizes human skin DCs to drive an IL-22 response, supporting the utility of IL-23 and IL-22 blockade in AD.

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