Hemoglobin protects from streptococcal cell wall–induced arthritis
NL McCartney‐Francis, XY Song… - … : Official Journal of …, 1999 - Wiley Online Library
NL McCartney‐Francis, XY Song, DE Mizel, CL Wahl, SM Wahl
Arthritis & Rheumatism: Official Journal of the American College …, 1999•Wiley Online LibraryObjective To investigate the ability of hemoglobin (Hgb), a nitric oxide (NO) scavenger, to
deplete excess NO and reduce inflammation and injury in synovial tissue from joints with
inflammatory arthritis. Methods The severity of streptococcal cell wall–induced arthritis was
monitored following administration of Hgb. Plasma nitrite and nitrate levels were measured,
and inducible NO synthase (iNOS) and cytokine messenger RNA (mRNA) expression in
peripheral blood mononuclear cells (PBMC) and joint tissue were evaluated. Results …
deplete excess NO and reduce inflammation and injury in synovial tissue from joints with
inflammatory arthritis. Methods The severity of streptococcal cell wall–induced arthritis was
monitored following administration of Hgb. Plasma nitrite and nitrate levels were measured,
and inducible NO synthase (iNOS) and cytokine messenger RNA (mRNA) expression in
peripheral blood mononuclear cells (PBMC) and joint tissue were evaluated. Results …
Objective
To investigate the ability of hemoglobin (Hgb), a nitric oxide (NO) scavenger, to deplete excess NO and reduce inflammation and injury in synovial tissue from joints with inflammatory arthritis.
Methods
The severity of streptococcal cell wall– induced arthritis was monitored following administration of Hgb. Plasma nitrite and nitrate levels were measured, and inducible NO synthase (iNOS) and cytokine messenger RNA (mRNA) expression in peripheral blood mononuclear cells (PBMC) and joint tissue were evaluated.
Results
Following systemic administration of Hgb to arthritic rats, plasma levels of nitrite and nitrate as well as iNOS mRNA expression in the joints and PBMC were significantly reduced. Moreover, inflammatory cell accumulation and disease pathology in the joint tissue were dramatically attenuated without obvious side effects. Consistent with this reduction in the inflammatory response, cytokine gene expression was decreased in the synovium of Hgb‐treated rats.
Conclusion
Modulation of NO levels through the use of a NO scavenger, Hgb, influences the development and severity of arthritis. These findings suggest that depletion of excess NO by NO scavengers provides a prototype for further exploration of potential treatments for chronic arthritis.
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