Adjuvant arthritis (AA) in rats is susceptible to cell-mediated passive transfer. Collagen-induced arthritis (CIA) in rats is susceptible to passive transfer with antibody to type II collagen. We report here the development of strikingly severe arthritis in Lewis rats as the result of synergy between passively transferred antibody to type II collagen from rats with CIA and concanavalin A (Con A)-stimulated lymph node or spleen cells from syngeneic rats with AA. Similar synergy was seen in rats with AA given anticollagen antibody, in rats with CIA given Con A-stimulated adjuvant spleen cells, and in rats actively immunized with CII and complete Freund's adjuvant. The synergistic process caused a very severe polyarthritis, characterized by marked swelling and erythema in all the joints of the distal extremities, with histologic and radiographic evidence of early, extensive erosion of articular cartilage. Synergy was apparent if the lymphoid cells from AA rats were given up to 1 mo after a single injection of anticollagen antibody. No synergy was seen when normal rat immunoglobulin or anti-ovalbumin antibody was substituted for anticollagen antibody, when Con A-stimulated lymphoid cells from normal rats or donors with CIA were used, or when Con A-stimulated AA lymphoid cells were irradiated before transfer. Synergy between separate immune effector mechanisms may represent a general phenomenon in the pathogenesis of inflammatory joint disease.
A particle concentration fluorescence immunoassay has been modified into a bacterial concentration fluorescence immunoassay (BCFIA) to rapidly detect periodontopathic bacteria in human plaque samples. The BCFIA utilizes fluorescently tagged monoclonal antibodies (MAbs) directed against the lipopolysaccharide of selected gram-negative plaque bacteria. Microorganisms closely associated with periodontal disease that can be identified in plaque with the BCFIA include Porphyromonas gingivalis, Bacteroides intermedius, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, and Eikenella corrodens. Briefly, the procedure involved mixing a patient's plaque sample or other bacterial preparation with a species-specific fluorescein isothiocyanate-labeled MAb in a specialized microtiter plate. This mixture was incubated to allow binding of the MAb to its homologous bacteria. The bound and unbound fluorescent tagged MAbs were separated by filtration in the modified microtiter plate, and the total bacterial bound fluorescence was determined with a fluorimeter. The number of a specific bacterial species in a given plaque sample or other bacterial suspension was estimated by reference to a primary standard carried through the BCFIA. The lower detection limit of the BCFIA was 103 to i4 bacterial cells from single cultures of bacteria or i04 bacterial cells in mixed cultures. The coefficient * Corresponding author.
The arthritides induced in rats by complete Freund's adjuvant or native type I1 collagen are extensively studied models of inflammatory joint disease (1,2). Rats of the inbred Lewis (LEW) strain have commonly been found to be 100% susceptible to adjuvant arthritis (3), and have been reported to be 40-100% susceptible to type I1 collagen-induced arthritis (71 Animals. Specific pathogen-free, 4-week-old monis infection was found to be enzootic in our animal colony, and upon further investigation we found that both models of rat arthritis were significantly altered by this common rat pathogen. MATERIALS AND METHODS \LI *LEW rats, like rats of most other strains, are susceptible to infection with Mycoplasma pulmonis (4). Respiratory infections with M pulmonis, often clinically silent, are very common in conventional (i.e., non-barrier-maintained) rat colonies (4). We have recently observed unexpected variability in a series of experiments with both adjuvant and collageninduced arthritis; our results led us to suspect that an environmental factor might be intermittently affecting the incidence and severity of these diseases. M pul- Infection of rats with Mycoplasma pulmonis. Upon arrival, rats were bled from the retroorbital plexus and then divided randomly into 3 treatment groups: 1) uninfected, 2) infected with 3.6 x lo3 viable M pulmonis organisms intranasally, or 3) inoculated intranasally with 3.6 x lo3 heat-killed M pulmonis organisms (sham infected). The M pulmonis used was originally isolated from a rat housed in our conventional animal facility; it was identified as Mpulmonis by its reactivity with reference antiserum (supplied by Dr. J. Felle of the NIH). Organisms were grown in Friis broth (5). Stock cultures for inoculation were stored at -70°C until use. Organisms were enumerated by standard plate counts. At necropsy, the trachea was washed with 9.5 ml of broth and the aspirated material inoculated into both Friis agar and broth. Broth cultures were incubated at 35°C and agar cultures in 5% C 0 2 at 35°C. Induction of arthritis. Adjuvant arthritis was induced by a single intradermal tail injection of heatkilled Mycobacterium butyricum in 0.1 ml mineral oil, prepared as previously described (6). Native bovine type I1 collagen (7) was dissolved in 0.1M acetic acid
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