Effect of capsaicin on carrageenan-induced inflammation in rat pleurisy and exudate substance P level

Raychaudhuri, A.; Colombo, Carmelo; Pastor, Gary; Wong, M.; Jeng, Arco Y.

doi:10.1007/bf01993295

Cited by 19 publications

(16 citation statements)

References 8 publications

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“…The complement factors play a minor role (28,29,32), but the involvement of neutrophils (32) and the kinin system (28, 33) has been demonstrated. In addition, there is evidence for a tachykinin neurogenic component (34)(35)(36). Our results demonstrated a small but significant decrease in edema formation in knockout compared with wild-type mice, but a substantial and highly significant decrease in neutrophil accumulation.…”

Section: Discussionsupporting

confidence: 49%

Neurokinin-1 Receptor Agonists Are Involved in Mediating Neutrophil Accumulation in the Inflamed, But Not Normal, Cutaneous Microvasculature: An In Vivo Study Using Neurokinin-1 Receptor Knockout Mice

Cao¹,

Pintér²,

Al-Rashed³

et al. 2000

The Journal of Immunology

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We have used tachykinin neurokinin-1 receptor (NK1 receptor) knockout mice to learn of the link between NK1 receptors and neutrophil accumulation in normal naive skin, as compared with inflamed skin. Intradermal substance P (300 pmol) induced edema formation in wild-type mice, but not in NK1 knockout mice, as expected. However, in contrast to IL-1β (0.3 pmol), substance P did not induce neutrophil accumulation in wild-type mice. IL-1β-induced neutrophil accumulation was similar in wild-type and knockout mice, but a significant (p < 0.05) contributory effect of added NK1 agonists, which by themselves have no effect on neutrophil accumulation in normal skin, was observed. The results support the concept that NK1 agonists such as substance P cannot act on their own to mediate neutrophil accumulation in naive skin and provide direct evidence that in inflamed skin, under certain circumstances, the NK1 receptor can play a pivotal role in modulating neutrophil accumulation during the ongoing inflammatory process. We investigated responses to two inflammatory stimuli (carrageenin and zymosan). Neutrophil accumulation was significantly attenuated (p < 0.001) in carrageenin- but not zymosan-induced inflammation in NK1 knockout mice. The carrageenin (500 μg)-induced response was inhibited (p < 0.05) by a NK1 receptor antagonist, SR140333 (480 nmol/kg i.v. at −5 min), in the wild-type group. The bradykinin B1 and B2 receptor antagonists (desArg9[Leu8]bradykinin and HOE 140) each reduced neutrophil accumulation to carrageenin in wild-type animals (p < 0.05), but did not cause further reduction of the suppressed response of knockout mice. The results provide evidence that kinin receptors participate in NK1 receptor-dependent neutrophil accumulation in inflamed mouse skin.

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Section: Discussionsupporting

confidence: 49%

Neurokinin-1 Receptor Agonists Are Involved in Mediating Neutrophil Accumulation in the Inflamed, But Not Normal, Cutaneous Microvasculature: An In Vivo Study Using Neurokinin-1 Receptor Knockout Mice

Cao¹,

Pintér²,

Al-Rashed³

et al. 2000

The Journal of Immunology

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“…Calcium ionophore A 23187 was purchased from Calbiochem, La Jolla, CA. Pleurisy was induced as described earlier [7]. Calcium ionophore A 23187 (100 nmol) solubilized in DMSO and phosphatebuffered saline (PBS) (1 : 1) was injected intrapleurally in a volume of 0.2 ml.…”

Section: Methodsmentioning

confidence: 99%

Effect of 5-lipoxygenase inhibitors onin situ LTB4 biosynthesis following calcium ionophore stimulation in the rat pleural cavity

Raychaudhuri¹,

Chertock²,

Peppard³

et al. 1993

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The intrapleural injection of carrageenan in the rat induces exudate formation, cellular influx and leukotriene generation in the pleural cavity. We have demonstrated that the inflammatory response (exudate volume, and LTB4 levels) is increased in situ by the intrapleural administration of calcium ionophore A 23187 (100 nmol/rat) at 4, 16, 24, 48, and 72 h after the injection of carrageenan and that the A 23187-induced increase is dose-dependent. The oral administration of A-64077 and MK-886, two 5-lipoxygenase inhibitors (5-LOIs), at 10 mg/kg causes marked decreases in LTB4 release at the above-mentioned time intervals. However, A 23187-induced augmented exudate formation is not affected by the treatment with 5-LOIs. The results suggest that the use of 5-LOIs to inhibit LTB4 biosynthesis may be beneficial in various LTB4-dependent pathological conditions.

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“…Besides, a lot of studies have shown that, in other systems, allergic and inflammatory responses have a neurogenic component which is capsaicin-sensitive [27][28][29][30][31],…”

Section: Discussionmentioning

confidence: 99%

Involvement of Capsaicin-Sensitive Afferent Nerves in the Intestinal Motor Alterations Induced by Intestinal Anaphylaxis in Rats

Fargeas¹,

Fioramonti²,

Buéno³

1993

Int Arch Allergy Immunol

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Alteration of intestinal myoelectrical activity is a characteristic feature of food protein-induced intestinal anaphylaxis in the conscious rat. The motility changes induced by antigen challenge were appraised in egg-albumin-sensitized rats, chronically implanted with NiCr electrodes in the duodenojejunal wall. Intraduodenal infusion of egg albumin given to fasted sensitized rats triggered a disruption of the cyclic pattern of small intestinal motility lasting 79.1 ± 23.3 min. The duration of the challenge effect on intestinal myoelectrical activity was significantly reduced by systemic capsaicin pretreatment (125 mg/kg) but to a lesser extent by perivagal capsaicin. Substance P (SP) antagonists (SP 4-11 and CP 96.345) and atropine were also able to shorten the duration of the antigen-challenge-induced alteration of intestinal motility. It is concluded that SP and capsaicin-sensitive afferent nerve endings play an important role in the intestinal anaphylaxis-induced disturbances of intestinal motility.

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Effect of capsaicin on carrageenan-induced inflammation in rat pleurisy and exudate substance P level

Cited by 19 publications

References 8 publications

Neurokinin-1 Receptor Agonists Are Involved in Mediating Neutrophil Accumulation in the Inflamed, But Not Normal, Cutaneous Microvasculature: An In Vivo Study Using Neurokinin-1 Receptor Knockout Mice

Neurokinin-1 Receptor Agonists Are Involved in Mediating Neutrophil Accumulation in the Inflamed, But Not Normal, Cutaneous Microvasculature: An In Vivo Study Using Neurokinin-1 Receptor Knockout Mice

Effect of 5-lipoxygenase inhibitors onin situ LTB4 biosynthesis following calcium ionophore stimulation in the rat pleural cavity

Involvement of Capsaicin-Sensitive Afferent Nerves in the Intestinal Motor Alterations Induced by Intestinal Anaphylaxis in Rats

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