AJTMH Transactions of the Royal Society of Tropical Medicine and Hygiene
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Am. J. Trop. Med. Hyg., 75(4), 2006, pp. 683-687
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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SCABIES MITE INACTIVATED SERINE PROTEASE PARALOGUES ARE PRESENT BOTH INTERNALLY IN THE MITE GUT AND EXTERNALLY IN FECES

CHARLENE WILLIS, KATJA FISCHER*, SHELLEY F. WALTON, BART J. CURRIE, AND DAVID J. KEMP
Queensland Institute of Medical Research, Brisbane, Queensland, Australia; The University of Queensland, Brisbane, Queensland, Australia; Menzies School of Health Research, Darwin, Northern Territory, Australia; Charles Darwin University, Darwin, Northern Territory, Australia

The scabies mite, Sarcoptes scabiei, is the causative agent of scabies, a disease that is common among disadvantaged populations and facilitates streptococcal infections with serious sequelae. Previously, we encountered large families of genes encoding paralogues of house dust mite protease allergens with their catalytic sites inactivated by mutation (scabies mite inactivated protease paralogues [SMIPPs]). We postulated that SMIPPs have evolved as an adaptation to the parasitic lifestyle of the scabies mite, functioning as competitive inhibitors of proteases involved in the host–parasite interaction. To propose testable hypotheses for their functions, it is essential to know their locations in the mite. Here we show by immunohistochemistry that SMIPPs exist in two compartments: 1) internal to the mite in the gut and 2) external to the mite after excretion from the gut in scybala (fecal pellets). SMIPPs may well function in both of these compartments to evade host proteases.

Received April 19, 2006. Accepted for publication June 18, 2006.

Acknowledgments: We thank Malcolm Jones (Queensland Institute of Medical Research), Wayne Thomas (Telethon Institute, Perth), and Euan Tovey (Woolcock Institute, Sydney) for technical advice and Larry Arlian (Wright State University) for confirming our interpretation of early data.

Financial support: This work was supported by Program Grant 290208 and a fellowship to D.J.K. from the Australian National Health and Medical Research Council. C.W. is supported by a NHMRC Dora Lush scholarship.

* Address correspondence to Katja Fischer, Queensland Institute of Medical Research, 300 Herston Road, Herston, Queensland 4006, Australia. E-mail: Katja.Fischer{at}qimr.edu.au

Authors’ addresses: Charlene Willis, Queensland Institute of Medical Research, 300 Herston Road, Herston, Queensland 4006, Australia, Telephone: 61-7-3362-0420, Fax: 61-7-3362-0104, E-mail: Charlene.Willis{at}qimr.edu.au. Katja Fischer, Queensland Institute of Medical Research, 300 Herston Road, Herston, Queensland 4006, Australia, Telephone: 61-7-3362-0417, Fax: 61-7-3362-0104, E-mail: Katja.Fischer{at}qimr.edu.au. Shelley F. Walton, Menzies School of Health Research, Rocklands Drive, Darwin Northern Territory 0811, Australia, Telephone: 61-8-8922-8928, Fax: 61-8-8927-5187, E-mail: Shelley.Walton{at}menzies.edu.au. Bart J. Currie, Menzies School of Health Research, Rocklands Drive, Darwin, Northern Territory 0811, Australia, Telephone: 61-8-8922-8056, Fax: 61-8-8927-5187, E-mail: Bart.Currie{at}menzies.edu.au. David J. Kemp, Queensland Institute of Medical Research, 300 Herston Road, Herston, Queensland 4006, Australia, Telephone: 61-7-3362-0402, Fax: 61-7-3362-0104, E-mail: Dave.Kemp{at}qimr.edu.au.




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