Role of Lymph Nodes in Adjuvant-Induced Arthritis in Rats

Newbould, B. B.

doi:10.1136/ard.23.5.392

Cited by 61 publications

(21 citation statements)

References 5 publications

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“…Early works on adjuvant arthritis suggested the role of draining lymph nodes in the development of joint lesions (4,42). More recently, investigations conducted in the B27-transgenic rat model for spondyloarthritis showed that Th17 cells contribute to both intestinal and joint inflammation; IL-17-producing cells were expanded in mesenteric as well as in popliteal lymph nodes (16).…”

Section: Discussionmentioning

confidence: 99%

Salmonella enterica Induces Joint Inflammation and Expression of Interleukin-17 in Draining Lymph Nodes Early after Onset of Enterocolitis in Mice

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Salmonella enterica Induces Joint Inflammation and Expression of Interleukin-17 in Draining Lymph Nodes Early after Onset of Enterocolitis in Mice

et al. 2012

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“…One day before CAPS treatment, 12 rats were given a single intradermal injection of CFA (0.1 ml) into the subplantar area of the right hind paw [53][54][55][56]. Twelve control rats were given an intradermal injection of an equivalent volume of the vehicle.…”

Section: Adjuvant-induced Arthritismentioning

confidence: 99%

Local Application of Capsaicin into the Draining Lymph Nodes Attenuates Expression of Adjuvant-Induced Arthritis

Lorton

Lubahn

Engan

et al. 2000

Neuroimmunomodulation

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Adjuvant-induced experimental arthritis (AA) was examined in adult male Lewis rats after isolated capsaicin (CAPS)-induced loss of small, nonmyelinated, afferent fibers in lymph nodes draining the site of adjuvant challenge. AA was induced by intradermal injection of Freund’s complete adjuvant (CFA) into the subplantar area of the right hind paw. Controls received similar injections of mineral oil, the vehicle for CFA. One day later, half of the CFA-treated rats and half of the mineral oil-treated rats received injections of CAPS bilaterally into the draining lymph nodes (DLN). The DLN of remaining rats were injected with 50:50 ethanol/sterile physiological saline, the vehicle for CAPS. This paradigm resulted in four groups designated: CFA/CAPS, CFA/vehicle, vehicle/CAPS and vehicle/vehicle. Since substance P (SP) is present in small, nonmyelinated, afferent fibers, the target of the neurotoxin, CAPS, a radioimmunoassay specific for SP was used to verify the loss of these nerve fibers. CAPS injections into the DLN resulted in a loss in SP concentration in the DLN, with no depletion of SP in the spleen or sciatic nerve. These findings support the destruction of SP-containing nerves, which we interpret as verification of the selective loss of small, non-myelinated afferent nerves in the DLN with no significant spread of the neurotoxin to the nearby sciatic nerves which supply small, nonmyelinated, afferent fibers to the hind limb joints. Also, preservation of SP content in spleen indicates CAPS did not circulate via the lymphatic drainage. No chronic inflammation was observed in the fore or hind limbs from rats treated with the vehicle for CFA (vehicle/vehicle, vehicle/CAPS) at any time during the study. In CFA/vehicle-treated rats, bilateral, symmetrical inflammation of the hind limbs was apparent 14 days after challenge with CFA, and became progressively more inflamed through day 20. In contrast, hind limb inflammation in arthritic rats treated with CAPS was not symmetrical. On days 14 and 20 after challenge with CFA, the inflammatory response in the left hind limb, contralateral to the site of CFA injection, was significantly (p < 0.05) attenuated compared with the response seen on the right side of CFA/CAPS-treated rats, and with the response seen in left hind limb of CFA/vehicle-treated animals. In fact, the mean dorsoplantar width of contralateral hind limbs from CFA/CAPS-treated animals was not different from that measured in non-AA control groups. These findings support a role for small, nonmyelinated, sensory nerves that modulate immune responses in DLN in the development and progression of AA in Lewis rats.

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“…Adjuvant disease of rats is an experimental polyarthritis induced by intradermal injection of an oily vehicle containing bacterial components, i.e., complete Freund's adjuvant (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16). Adjuvant arthritis can be passively transferred by lymphoid cells (17)(18)(19), implicating immunologic mechanisms in its pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Autoimmunity to collagen in adjuvant arthritis of rats.

Trentham¹,

McCune²,

Susman³

et al. 1980

J. Clin. Invest.

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A B S T R A C T Arthritis can be induced in rats bv intradermal injection of oil containing bacterial derivatives (adjuvant-induced arthritis) or cartilage collagen (type II collagen-induced arthritis). It was of interest, therefore, to determine whether collagen functions as an autoantigen in rats with adjuvant arthritis. Blood mononuclear cells from the majority of rats with adjuvant arthritis exhibited enhanced thymidine incorporation to homologous types I and II collagens, as well as to purified protein derivative of tuberculin. In contrast, cells from rats remaining nonarthritic after injection of adjuvant did not respond to collagen, although they did react to tuberculin. Similar results were obtained with a radiometric ear assay used to quantifv intradermal delayed-type hypersensitivity in vivo. Using passive hemagglutination, autoantibodies to these collagens and their denatured a-chains were frequently detected in the sera of rats late in the course of adjuvant arthritis. Rats with inflammation of a hindlimb induced by turpentine did not acquire sensitivity to collagen. These data indicate that autoimmunity to collagen is a common feature of adjuvant-and collagen-induced arthritis, both of which are considered to be mediated by immunologic mechanisms.

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Role of Lymph Nodes in Adjuvant-Induced Arthritis in Rats

Cited by 61 publications

References 5 publications

Salmonella enterica Induces Joint Inflammation and Expression of Interleukin-17 in Draining Lymph Nodes Early after Onset of Enterocolitis in Mice

Salmonella enterica Induces Joint Inflammation and Expression of Interleukin-17 in Draining Lymph Nodes Early after Onset of Enterocolitis in Mice

Local Application of Capsaicin into the Draining Lymph Nodes Attenuates Expression of Adjuvant-Induced Arthritis

Autoimmunity to collagen in adjuvant arthritis of rats.

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