title: Antigenic differences associated with genetically distinct Pneumocystis carinii from rats.
abstract: Pneumocystis carinii is a family of organisms found in a wide variety of mammalian lungs. In immunocompromised hosts, the organisms are able to produce an oftentimes fatal pneumonia. The existence of distinct types of Pneumocystis populations is strongly supported by antigenic and genetic evidence. In the present study, we assessed the antigenic profiles of two genetically distinct Pneumocystis carinii populations, P. carinii f. sp. carinii and P. carinii f. sp. ratti, as well as two types of P. carinii f. sp. carinii defined by electrophoretic karyotyping (forms 1 and 2). The separated and blotted proteins of the organism preparations were probed with four monoclonal antibodies (MAbs) generated to the major surface glycoproteins of rat-derived P. carinii, one anti-human P. carinii MAb, and two polyclonal antisera made with rat-derived P. carinii as the immunogen. Differences in reactivities between the P. carinii f. sp. carinii and P. carinii f. sp. ratti preparations were detected with two of the MAbs, and both of the rat P. carinii polyclonal antisera in the 45- to 55-kDa molecular mass range, but not with the human P. carinii MAb. The reactivities of the 16 P. carinii f. sp. carinii preparations were the same with two exceptions. Two preparations of form 1 showed strong reactivity with the anti-MSG MAb RA-C11. The ratios of cyst forms to trophic forms evaluated by microscopy were not associated with any of the differences observed in the antigenic profiles. The antigenic differences between P. carinii f. sp. carinii and P. carinii f. sp. ratti are consistent with the distinction of these two populations made by molecular genetic techniques, while the two differences detected among the P. carinii f. sp. carinii preparations suggest the organism may be able to modulate antigenic epitopes. The use of immunoblotting to differentiate infecting organism populations and assess antigenic modulation holds promise for future epidemiologic studies.
authors.affiliation: Department of Internal Medicine, James Quillen College of Medicine, Johnson City, Tennessee 37614-0622, USA.
authors.forename: J
authors.initials: J
authors.lastname: Vasquez
authors.forename: A G
authors.initials: AG
authors.lastname: Smulian
authors.forename: M J
authors.initials: MJ
authors.lastname: Linke
authors.forename: M T
authors.initials: MT
authors.lastname: Cushion
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000382:microbiology; D000818:Animals; D000908:Antibodies, Fungal; D000911:Antibodies, Monoclonal; D000946:Antigens, Fungal / Q000276:immunology*; D015139:Blotting, Southern; D002454:Cell Differentiation; D015169:Colony Count, Microbial; D005656:Fungal Proteins / Q000276:immunology; D006801:Humans; D015151:Immunoblotting; D016867:Immunocompromised Host; D008562:Membrane Glycoproteins / Q000276:immunology; D011010:Pneumocystis / Q000145:classification / Q000235:genetics* / Q000276:immunology*; D051381:Rats; D017207:Rats, Sprague-Dawley / Q000382:microbiology*; D013045:Species Specificity
chemical_list: D000908:Antibodies, Fungal; D000911:Antibodies, Monoclonal; D000946:Antigens, Fungal; D005656:Fungal Proteins; D008562:Membrane Glycoproteins; C077556:GPA protein, Pneumocystis carinii sp.