Experimental polyarthritis in rats produced by Mycoplasma arthritidis

Hill, Auriol C.; Dagnall, G.J.R.

doi:10.1016/0021-9975(75)90083-3

Cited by 22 publications

(9 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, mycoplasmal antigens, many of which are enzymes, can affect cells even after bacteria are dead and lysed, and their presence is difficult to detect by certain conventional methods [49]. Mycoplasma species are also well known to cause arthritis in certain animal species, including chickens [1-7]. Experimental infections of chickens with M. synoviae WVU 1853 resulted in thinning of the articular cartilage 25 days post infection [55].…”

Section: Discussionmentioning

confidence: 99%

“…The condition is presented as an acute joint swelling accompanied by increased volume of synovial fluid, infiltration with macrophages, B and T cells, lining cell hyperplasia and fibroblastic proliferation. In the acute phase of infection, live M. synoviae have been detected in synovial fluids of infected birds, suggesting that M. synoviae can come into direct contact with chondrocytes as is the case with M. pulmonis [6] and M. artritidis [7]. M. synoviae has been reported capable of invasion into non-phagocytic chicken cells including chondrocytes in vitro [8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mycoplasma synoviae induces upregulation of apoptotic genes, secretion of nitric oxide and appearance of an apoptotic phenotype in infected chicken chondrocytes

Dušanić

Benčina

Oven

et al. 2012

Vet Res

View full text Add to dashboard Cite

The role of chondrocytes in the development of infectious arthritis is not well understood. Several examples of mycoplasma-induced arthritis in animals indicate that chondrocytes come into direct contact with bacteria. The objective of this study was to analyze the interaction of an arthrogenic Mycoplasma synoviae strain WVU 1853 with chicken chondrocytes. We found that M. synoviae significantly reduces chondrocyte respiration. This was accompanied by alterations in chondrocyte morphology, namely cell shrinkage and cytoplasm condensation, as well as nuclear condensation and formation of plasma membrane invaginations containing nuclear material, which appeared to cleave off the cell surface. In concordance with these apoptosis-like events in chondrocytes, transcription was increased in several pro-apoptotic genes. Twenty-four hours after infection, strong upregulation was assayed in NOS2, Mapk11, CASP8 and Casp3 genes. Twenty-four and 72 h incubation of chondrocytes with M. synoviae induced upregulation of AIFM1, NFκB1, htrA3 and BCL2. Casp3 and NOS2 remained upregulated, but upregulation ceased for Mapk11 and CASP8 genes. Increased production of nitric oxide was also confirmed in cell supernates. The data suggests that chicken chondrocytes infected with M. synoviae die by apoptosis involving production of nitric oxide, caspase 3 activation and mitochondrial inactivation. The results of this study show for the first time that mycoplasmas could cause chondrocyte apoptosis. This could contribute to tissue destruction and influence the development of arthritic conditions. Hence, the study gives new insights into the role of mycoplasma infection on chondrocyte biology and development of infectious arthritis in chickens and potentially in humans.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mycoplasma synoviae induces upregulation of apoptotic genes, secretion of nitric oxide and appearance of an apoptotic phenotype in infected chicken chondrocytes

Dušanić

Benčina

Oven

et al. 2012

Vet Res

View full text Add to dashboard Cite

show abstract

“…Likewise, the denatured constituent a-chains of type II do not cause disease. Various infections such as M. arthritidis (17) or Salmonella (18) can cause arthritis in rats. However, an infectious agent or product contaminating our preparations is unlikely to explain our results for several reasons: cultures for microorganisms were negative; the identically prepared collagen failed to induce arthritis when injected in the absence of adjuvant; multiple preparations of type II collagen from human, chick or rat sources induced arthritis; collagens prepared and injected in two geographically separate laboratories caused arthritis at all times of the year; the latent period after injection was longer than that usually observed after inoculation with an infectious agent (17); further, the arthritis had a lengthy course with no spontaneous exacerbations; and finally, the synovial infiltration was mononuclear rather than neutrophilic, even initially.…”

Section: Discussionmentioning

confidence: 99%

Autoimmunity to type II collagen an experimental model of arthritis.

Trentham

Townes

Kang

1977

The Journal of Experimental Medicine

1,463

823

View full text Add to dashboard Cite

Immunologic hypersensitivity to collagen, the major structural component of connective tissue, could explain both the systemic nature and chronicity of the inflammation occurring in rheumatoid arthritis. Recent demonstrations of antibodies to collagen in sera from patients with rheumatoid arthritis support this premise (1-8). Also consistent with this hypothesis is the distribution of collagen in structurally distinct types in various tissues. For example, types I and HI collagens are found in the skin and parenchyma of several organs, whereas type II exists in cartilage (9). Thus, an immune response to the cartilage type of collagen (type II) could explain the predilection of rheumatoid arthritis to involve diarthrodial joints.Native collagens consist of three polypeptide chains linked in triple helices. Terminal peptides (telopeptides) do not have a helical structure and are more variable in amino acid content (10). Type I collagen combines two al-type I chains with one a2-chain and is depicted as [al(I)]2a2. Types II and III collagens are comprised of three al-type II chains and three al-type HI chains, respectively. Thus, type II is depicted as [al(II)]3 and type III as [al(III)]3.Injection of heterologous type I and II collagen in complete Freund's adjuvant has been reported to elicit type-specific antibody responses in rats (11) and mice (12). This paper reports that approximately 40% of rats injected intradermally with native type H collagen, derived from human, chick, or rat cartilage, in either complete or incomplete Freund's adjuvant, develop an inflammatory arthritis. In contrast, type I and III collagen are not arthritogenic. This new animal model suggests that immune responses to type II collagen could play a role in inciting or perpetuating joint inflammation in other arthritides. Materials and MethodsRats. Outbred female Wistar, Sprague-Dawley and inbred Wistar-Lewis rats were obtained from Microbiological Associates (Bethesda, Md.), Harlan (Indianapolis, Ind.) or Charles River Breeding Laboratory (Wilmington, Mass.). These rats were housed in metal cages and given water

show abstract

“…74(8): 1083-1086, 2012 Mycoplasma infection causes severe problems in laboratory rodent colonies [1]. The Mycoplasma species isolated from mice and rats, M. pulmonis [13], M. arthritidis [6], M. neurolyticum [7], M. muris [12], and M. collis [5], have been associated with several disease manifestations. M. pulmonis is an especially common pathogen in mice and rats and the etiological agent of murine respiratory mycoplasmosis [11].…”

mentioning

confidence: 99%