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The paper by Murayama et al 1 contains the unwary statement that their study may have been the first to demonstrate the suppressive effects ofAspergillus products on antifungal host defences by both human alveolar macrophages and PMNs. A search forAspergillus in theeThorax website would have saved both them and your referees from accepting this. In a series of papers published in the 1980s Maura Robertson and I showed this in animal and human cells, demonstrated the paradoxical effect of complement and, perhaps importantly, showed that the substance produced by the spores had similar effects on soil protozoa, thus explaining the biological paradox as to why an organism that gains nothing from colonising animal lungs should have developed such exquisite antiphagocytic properties. Some of this work was summarised in our paper pupblished in theLancet in 1989.2 These effects are discussed in at least one well known textbook of respiratory disease.3
It is to be hoped that the “wheel reinventing” tendency of authors who search the literature back only five years and the short memory or ignorance of referees may be alleviated by use of your new web site.
authors' reply We thank the editors for the opportunity to respond to the concerns raised by Professor Seaton. His group1-1-1-4 and Drs Mullbacher, Eichner et al in Australia1-5 1-6are pioneers in studies of the antiphagocytic activity ofAspergillus derived products and they have done some excellent work. We cited some of their original articles in our previous paper.1-7 Professor Seatonet al have shown that spores and spore diffusates of A fumigatus suppress the production of superoxide anion and hydrogen peroxide by rodent phagocytic cells1-1 and that diffusates ofA fumigatus spores inhibit phagocytosis of antibody coated radiolabelled sheep red blood cells by mouse peritoneal exudate cells.1-2 They have also performed experiments using human cells and have shown that spore diffusates ofA fumigatus reduce the migration of human polymorphonuclear leucocytes and decrease the capacity of mouse peritoneal exudate cells to spread on glass.1-3 They have measured the ability of human pulmonary macrophages to bind and killA fumigatus spores and have examined the effects on killing of heat labile serum components.1-4However, they have not presented data on the suppressive effects ofAspergillus derived products on polymorphonuclear leucocyte mediated damage to A fumigatus.
It has been considered that selective protection againstAspergillus spores by mononuclear phagocytes and against hyphae of Aspergillus by polymorphonuclear phagocytes are critical host defences in humans.1-8 Since Aspergillusspores enter mainly through the respiratory tract and proliferate in mycelial form in human tissues, our study has focused on interactions between Aspergillus spores and human alveolar macrophages, and also betweenAspergillus hyphae and human polymorphonuclear leucocytes. In our study1-9 we showed thatA fumigatus culture filtrate suppressed not only human polymorphonuclear leucocyte mediated A fumigatus hyphal damage but also inhibition of spore germination of A fumigatus by human alveolar macrophages, and suggested that A fumigatusproduces a variety of substances, some of which may suppress antifungal (anti-A fumigatus) activity of human alveolar macrophages and polymorphonuclear leucocytes. To our knowledge, our study is the first to demonstrate the suppressive effects of Aspergillus derived products on human polymorphonuclear leucocyte mediated hyphal damage ofAspergillus and also on inhibition of spore germination of Aspergillus by human alveolar macrophages.
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