Several strains of Aeromonas salmonicida were toxic to cultured peritoneal macrophages of Atlantic salmon, Salmo salar, in minimum doses of 5 x 10(6) CFU, whereas other strains were not. There was no correlation between cytotoxicity and in vivo virulence of the bacteria, the presence or absence of the two major surface components of A. salmonicida (namely, the A-layer and the O-polysaccharide chain of the LPS) nor, finally, with the ability of the strains to produce the following enzymes in vitro: protease, hemolysin, elastase and lecithinase. Toxicity was only observed with metabolically active bacteria and not with formalin- or heat-killed bacteria. The exact nature of the toxic factor remains unknown but is most likely associated with the surface of the bacteria. It is not extracellular since 24 and 48 h culture supernatants of the cytotoxic strains had no apparent effect on macrophages. The cytotoxic effect was found to be severe and rapid, it is likely a major virulence factor of A. salmonicida, but the exact role of such a potent toxin in the pathology of furunculosis has yet to be clarified.

Aeromonas↗

PubMedDate not supplied

Polyarthritis and the air pouch reaction: dissimilarity of adjuvant and collagen models.

The formation of an air pouch in the subcutaneous tissues of a rat previously inoculated intradermally with Freund's mycobacterial adjuvant for the induction of arthritis, provokes a marked but transient inflammatory reaction in the cavity lining of the pouch. The dependence of this reaction on arthritis development was investigated. It was found that rats inoculated with mycobacterial adjuvant by subcutaneous or intraperitoneal injection failed to produce either a pouch reaction or develop arthritis. Intradermal injections of carrageenan, mycobacteria (M. tuberculosis in saline), Freund's incomplete adjuvant alone or containing Salmonella typhimurium lipopolysaccharide and Bordetella pertussis organisms or mycobacterial adjuvant containing egg albumin were also ineffective. Intradermal injections of type II collagen in Freund's incomplete adjuvant did induce arthritis but no pouch reaction; however, this could be elicited after direct challenge with antigen. Pretreatment of rats intraperitoneally with saline suspensions of mycobacteria or a moderate dose of cyclophosphamide prevented both the pouch reaction and arthritis developing to intradermal mycobacterial adjuvant. Pretreatment of rats with mycobacteria was without effect on type II collagen-induced arthritis. From the results of this study it would appear that the air pouch reaction and arthritis induced by adjuvant are directly associated. The inability of collagen to induce a similar reaction demonstrates a fundamental dissimilarity with mycobacterial adjuvant in its mechanism of production of arthritis.

Animals↗

PubMedDate not supplied

Oral dosing of rats with OM-89 results in the appearance of specific OM-89 antibodies of the IgG2a isotype: possible significance in the treatment of rheumatoid arthritis.

OM-89 is a glycoprotein-rich extract of Escherichia coli shown to be effective in the treatment of rheumatoid arthritis (RA). It has been reported that oral dosing of animals results in the appearance of specific OM-89 antibodies. In the current study we have investigated some of the immunoglobulin isotypes that may be involved. OM-89 antibodies of IgG1, IgG2a and IgM isotypes were measured by ELISA in serum from rats dosed three times a week for 3 weeks at 4 or 40 mg kg(-1). The results showed a small but significant rise in IgM and a greater rise in IgG2a. The possibility that antigens within OM-89 (e.g. hsp65) may have homology with antigens involved in RA raises the possibility that OM-89 antibodies, particularly of the IgG2 class, may block pathogenic antigens from being recognized by T cells.

Administration, Oral↗

PubMedDate not supplied

Homotransplantation of the liver in pigs.

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Animals↗

PubMedDate not supplied

Cartilage contribution to gender differences in joint disease progression. A study with rat articular cartilage.

OBJECTIVE: Rheumatoid arthritis is associated with a worse prognosis in females and is influenced by sex hormone changes. Similar observations in osteoarthritis support the hypothesis that gender differences in cartilage make a hitherto unrecognized contribution to gender differences in arthritis. The aim of the present study was to investigate potential gender differences in articular cartilage biochemistry, metabolism and response to inflammatory mediators. METHODS: Femoral head cartilages from age-matched male and female Wistar rats were analysed for the water, glycosaminoglycan, hydroxyproline and collagen crosslink contents. Proteoglycan loss and synthesis were assessed in vitro, and in the presence and absence of serum and interleukin-1. An in vivo model of inflammation-induced cartilage degradation was employed to investigate gender differences in cartilage susceptibility to erosion caused by granulomatous tissue. RESULTS: Articular cartilage from male Wistar rats presented higher levels of both proteoglycan and collagen and showed a lower spontaneous glycosaminoglycan loss and higher proteoglycan synthesis in vitro than cartilage from females. Proteoglycan synthesis from female, but not male, cartilage was significantly stimulated by foetal calf serum. Female cartilage was more sensitive to IL-1 inhibition of proteoglycan synthesis while the opposite was observed in IL-1-induced proteoglycan loss. Female cartilage was more susceptible to granuloma-induced degradation than male when implanted into female mice, but no differences were observed between male and female cartilage implanted in male mice. CONCLUSION: These results demonstrate important gender differences in cartilage biochemistry, metabolism and susceptibility to inflammatory mediators which may have important consequences for the joint destruction in arthritis and support a role for hormone therapy.

Animals↗