Macrophage activation in rat models of inflammation and arthritis: Systemic activation precedes arthritis induction and progression

Johnson, W. J.; Muirhead, Katharine A.; Meunier, Paul C.; Votta, Bart; Schmitt, Thomas; DiMartino, Michael J.; Hanna, Nabil

doi:10.1002/art.1780290910

Cited by 54 publications

(24 citation statements)

References 20 publications

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“…AIA develops in susceptible rat strains after the injection of FCA (1)(2)(3)(4)(5)(6)(7)(8)(9). The first step in the development of AIA is the production of an immune response to FCA.…”

Section: Discussionmentioning

confidence: 99%

“…Although these 2 models have many clinical similarities, fundamental differences in their pathophysiology and genetic control are clearly evident. AIA is a particularly informative model because it predominantly involves T cell-mediated mechanisms (1)(2)(3)(4)(5)(6)(7)(8), in contrast to CIA, which requires both humoral (14)(15)(16)(17)(18)(19)(20) and cellular immunity (21).…”

mentioning

confidence: 99%

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Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Cannon

Openshaw

Hibbs

et al. 1996

Arthritis & Rheumatism

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Objective. To investigate the role of nitric oxide (NO) production and NO synthase (NOS) induction during adjuvant-induced arthritis (AIA) and collageninduced arthritis (CIA) in Dark Agouti rats.Methods. Urinary nitrate excretion and immune NOS (iNOS) messenger RNA (mRNA) expression were measured in the joint, lymph node, spleen, and liver tissues following the induction of either AIA or CIA.Results. Urinary nitrate excretion and iNOS mRNA expression increased substantially during joint inflammation in both models of arthritis. However, the increases in urinary nitrate excretion and iNOS mRNA expression observed in the joint, liver, and spleen tissues during AIA were greater than those observed during CIA, although iNOS induction in the lymph nodes was similar for both models. A prior injection with Mycobacterium bovis heat-shock protein resulted in suppression of arthritis and NO production in AIA, but not in CIA.Conclusion. Differences in NO production during AIA versus CIA are a reflection of the fundamental pathophysiologic differences between these 2 models of arthritis. Thus, NO production in these 2 models could not be merely a nonspecific reaction to the adjuvant injection, nor simply a byproduct of local inflammation in the joint.Adjuvant-induced arthritis (AIA) and collageninduced arthritis (CIA) are different models of experi-..Supported by the VA Medical Research Program, the NIH (grants HL-40665 and HL-37615), the Nora Eccles Treadwell Foundation, and a University of Utah Research Grant.Grant W. Cannon, MD, Scott J. Openshaw, BS, John B. Hibbs, Jr., MD, John R. Hoidal, MD, Thomas P. Huecksteadt, Marie M. Griffiths, PhD: VA Medical Center, and the University of Utah, Salt Lake City.Address correspondence to Grant W. Cannon, MD, VAMC (llE), 500 Foothill Drive, Salt Lake City, UT 84148.Submitted for publication September 11, 1995; accepted in revised form May 1, 1996. mental arthritis that are induced by the injection of Freund's complete adjuvant (FCA) (1-12) or type I1 collagen (CII) (13-21), respectively. Although these 2 models have many clinical similarities, fundamental differences in their pathophysiology and genetic control are clearly evident. AIA is a particularly informative model because it predominantly involves T cell-mediated mechanisms (1-8), in contrast to CIA, which requires both humoral (14-20) and cellular immunity (21).Nitric oxide (NO), an unstable radical produced by the action of the enzyme NO synthase (NOS) on 1.-arginine, is a mediator of multiple physiologic functions and may also mediate local inflammation and tissue destruction (22-25). After its production and local action, NO is eventually oxidized to nitrate, which is inactive and excreted in the urine. Urinary nitrate can be reduced to nitrite, which, when measured by the Griess reaction, serves as an indirect measure of NO production (22). The induction of immunehflammatory NOS (iNOS) messenger RNA (mRNA) can be detected by polymerase chain reaction (PCR).Recent evaluations of NO synthesis in streptococcal cell wall...

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“…AIA develops in susceptible rat strains after the injection of FCA (1)(2)(3)(4)(5)(6)(7)(8)(9). The first step in the development of AIA is the production of an immune response to FCA.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Cannon

Openshaw

Hibbs

et al. 1996

Arthritis & Rheumatism

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“…The acute phase response is thought to be regulated by various pro-inflammatory cytokines. We and others have shown that elevated splenic IL-1 levels in AA rats [3,4] can be reduced by dosing animals with various types of antirheumatic compounds such as immunosuppressives [5,6], glucocorticoids [7,8] and the gold DMARD's [9. 10].…”

Section: Introductionmentioning

confidence: 99%

“…In a preclinical model of arthritis, plasma iron levels in AA rats are also depressed [1]. The depression in AA rat plasma iron is accompanied 4 To whom correspondence should be addressed.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of anti-arthritic agents on subnormal plasma iron levels in adjuvant arthritic rats

Connolly

Stecher²,

Speight

et al. 1989

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Nonsteroidal anti-inflammatory drugs (NSAID's) and other antirheumatic compounds such as disease modifying antirheumatic drugs (DMARD's), immunosuppressives and glucocorticoids were tested to determine if daily medication for two weeks could elevate subnormal levels of plasma iron in adjuvant-arthritic (AA) rats. Aspirin, indomethacin, ibuprofen and phenylbutazone were chosen as representative carboxylic acids and pyrazole NSAID's. Although NSAID's at all doses significantly reduced noninjected paw swelling, no NSAID significantly enhanced subnormal plasma iron levels in AA rats. In contrast, the standard DMARD's auranofin and gold sodium thiomalate, as well as the glucocorticoid, dexamethasone and the immunosuppressives, methotrexate and cyclosporin-A all significantly restored plasma iron levels 28 to 100 percent. Plasma iron depression, a parameter of the acute phase response probably under regulation by pro-inflammatory cytokines, is not reversed by NSAID treatment. This appears to be a useful method for distinguishing NSAID's from other anti-arthritic compounds.

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“…Moreover, it can inhibit IL1 production by monocytes (9) and ILl action on T cells (10). Interestingly, it may have a stimulatory effect on IL2 production (7).…”

Section: E C H a N I S M Smentioning

confidence: 99%

Therapeutic Progress–review Xxxvii: Methotrexate–an Immunomodulator With Expanding Indications

Horton

1990

J Clin Pharm Ther

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Macrophage activation in rat models of inflammation and arthritis: Systemic activation precedes arthritis induction and progression

Cited by 54 publications

References 20 publications

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Nitric oxide production during adjuvant‐induced and collagen‐induced arthritis

Differential effects of anti-arthritic agents on subnormal plasma iron levels in adjuvant arthritic rats

Therapeutic Progress–review Xxxvii: Methotrexate–an Immunomodulator With Expanding Indications

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