Nitric oxide up‐regulates the release of inflammatory mediators by mouse macrophages

Marcinkiewicz, Janusz; Grabowska, Agnieszka; Chain, Benjamin M.

doi:10.1002/eji.1830250414

Cited by 133 publications

(80 citation statements)

References 20 publications

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“…Further, we suggest that NO is likely to play a key role in the amplification of the inflammatory response through stimulation of TNF-α release. Although the effects of inflammatory cytokines on regulating NO production have been extensively studied (38)(39)(40), the reverse relationship pertaining to the effect of NO on cytokines remains controversial (41)(42)(43)(44). A recent study demonstrated that suppression of NO could inhibit LPS-induced TNF-α and IL-1 release and pinpointed such modulation to the pretranslational level (45).…”

Section: Discussionmentioning

confidence: 99%

HIF-1α expression regulates the bactericidal capacity of phagocytes

Peyssonnaux¹,

Datta²,

Cramer³

et al. 2005

J. Clin. Invest.

636

695

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Hypoxia is a characteristic feature of the tissue microenvironment during bacterial infection. Here we report on our use of conditional gene targeting to examine the contribution of hypoxia-inducible factor 1, α subunit (HIF-1α) to myeloid cell innate immune function. HIF-1α was induced by bacterial infection, even under normoxia, and regulated the production of key immune effector molecules, including granule proteases, antimicrobial peptides, nitric oxide, and TNF-α. Mice lacking HIF-1α in their myeloid cell lineage showed decreased bactericidal activity and failed to restrict systemic spread of infection from an initial tissue focus. Conversely, activation of the HIF-1α pathway through deletion of von Hippel-Lindau tumor-suppressor protein or pharmacologic inducers supported myeloid cell production of defense factors and improved bactericidal capacity. HIF-1α control of myeloid cell activity in infected tissues could represent a novel therapeutic target for enhancing host defense.

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Section: Discussionmentioning

confidence: 99%

HIF-1α expression regulates the bactericidal capacity of phagocytes

Peyssonnaux¹,

Datta²,

Cramer³

et al. 2005

J. Clin. Invest.

636

695

View full text Add to dashboard Cite

show abstract

“…Beirith et al (2002) demonstrated that nociception induced by glutamate is greatly mediated by the release of NO. NO increases the synthesis/release of pro-inflammatory mediators such as cytokines and reactive oxygen species (ROS) (Lyons, 1995;Marcinkiewicz et al, 1995) and prostanoids (Sautebin et al, 1995), resulting in promotion of inflammatory reaction. In view of this, we evaluated also the participation of the L-arginine/NO pathway in the antinociceptive action of BMD in the glutamate test.…”

Section: Discussionmentioning

confidence: 99%

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Donato

Pavin

Goes

et al. 2014

Pharmaceutical Biology

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(2015) Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action, Pharmaceutical Biology, 53:3, 395-403, DOI: 10.3109/13880209.2014 -nitro-L-arginine ( L-NOARG), but the effect of BMD was not abolished by naloxone. Mechanical hyperalgesia induced by Cg and CFA was attenuated by BMD, 70 ± 4% and 65 ± 4%, respectively. Furthermore, a single oral dose of BMD did not change plasma aspartate (AST) and alanine aminotransferase (ALT) activities or urea and creatinine levels. Conclusion: BMD demonstrated as a promising compound because of the antinociceptive and anti-hyperalgesic properties in mice.

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“…In addition, NO is also able to enhance the production of a variety of mediators, such as TNF-␣ and IL-1␤, which participate in the macrophage-dependent inflammatory response (Marcinkiewicz et al, 1995).…”

mentioning

confidence: 99%

Modulatory Effect of Bolinaquinone, a Marine Sesquiterpenoid, on Acute and Chronic Inflammatory Processes

Lucas¹,

Giannini²,

D’Auria³

et al. 2002

J Pharmacol Exp Ther

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The marine metabolite bolinaquinone is a novel inhibitor of secretory phospholipase A 2 (sPLA 2 ), with a potency on the human synovial enzyme (group II) higher than that of manoalide. This activity on the sPLA 2 was confirmed in vivo in the 8-h zymosan rat air pouch on the secretory enzyme accumulation in the pouch exudate. Additionally, bolinaquinone decreased potently the synthesis and release of leukotriene B 4 (LTB 4 ) in calcimycin (A23187)-stimulated human neutrophils as a consequence of the inhibition of 5-lipoxygenase activity, as well as PGE 2 and NO production on zymosan-stimulated mouse peritoneal macrophages. This compound exerted anti-inflammatory effects by topical and oral routes on the mouse ear edema induced by 12-O-tetradecanoylphorbolacetate, with ID 50 values of 76.7 g/ear and 5.6 mg/kg, respectively, with a significant decrease in PGE 2 , LTB 4 , and tumor necrosis factor-␣ (TNF-␣) levels being more effective than indomethacin. This effect was confirmed in the mouse paw carrageenan edema after oral administration. Moreover, bolinaquinone was able to reduce the inflammatory response of adjuvant arthritis by inhibiting PGE 2 , NO, and TNF-␣ production in paw homogenates without affecting PGE 2 levels in the stomach. Additionally, bolinaquinone inhibited inducible nitric oxide synthase expression and reduced the degree of bone resorption, soft tissue swelling, and osteophyte formation.

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Nitric oxide up‐regulates the release of inflammatory mediators by mouse macrophages

Cited by 133 publications

References 20 publications

HIF-1α expression regulates the bactericidal capacity of phagocytes

HIF-1α expression regulates the bactericidal capacity of phagocytes

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Modulatory Effect of Bolinaquinone, a Marine Sesquiterpenoid, on Acute and Chronic Inflammatory Processes

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