Tachykinin-mediated modulation of the primary antibody response in rats: evidence for mediation by an NK-2 receptor

Eglezos, Anthony; Andrews, Paul V.; Boyd, Richard; Helme, Robert D.

doi:10.1016/0165-5728(91)90066-g

Cited by 26 publications

(8 citation statements)

References 33 publications

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“…Unlike SP, NKA significantly stimulated the PFC response in capsaicin-treated rats at concentrations as low as 10 nmol/L, suggesting mediation of this response by NK-2 receptors. Mediation by NK-2 reeeptors was further validated by examination of the potency ratio of the D-and L-Pro analogues of [Glp^, Pro'']-SP6-ii (7), which was 1:1 (19). This result is in accordance with the in vitro results of Casini el al.…”

Section: In Vitrosupporting

confidence: 86%

“…data). A similar immunostimulatory effect was also observed following infusion of NKA (19). NKA was 10 times more potent than SP, increasing the response to over 100% ofthe normal response at 10 vmol/L.…”

Section: In Vitrosupporting

confidence: 59%

“…Indirect evidence has shown the existence of NK-1 type receptors on human lymphocytes (16) and guinea-pig macrophages (17). NK-2 receptors have been implicated in mediation ofthe modulatory effects ofthe TK on in vitro and in vivo lymphocyte function (18,19).…”

Section: Tachykinin Receptorsmentioning

confidence: 99%

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Modulation of the immune response by tachykinins

Eglezos

Andrews²,

Boyd

et al. 1991

Immunology & Cell Biology

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Summary Neuro‐immunology is becoming an increasingly important discipline of immunology. This review has examined the immunomodulatory function of one group of neuropeptides, the TK, particularly SP and NKA. These peptides are localized in primary afferent nerves which have been shown to innervate several immune organs. In addition, binding sites for the TK have been demonstrated in thymus, spleen and lymph node. Several immune cell types also express neurokinin receptors including human circulating lymphocytes with binding to the Th/i class predominating, murine T and B cells, a human T lymphoblastoid cell line, human monocytes, rabbit polymorphonuclear leucocytes and guinea‐pig macrophages. The apposition of nerves with immune cells and receptors for neuropeptides thus produces an environment for interaction between the nervous and immune systems. Studies in vitro and, more recently, in vivo have examined how the TK regulate immune cell responses. The TK stimulate proliferation of T cells, enhance mitogen‐induced release of cytokines including IFN‐γ, TNF‐α, IL‐1 and IL‐6 from mononuclear cells and macrophages, enhance immunoglobulin secretion and affect cellular chemotaxis and phagocytosis. Studies in vivo have shown a role for TK in lymphocyte recirculation of sheep lymph nodes, reversal of stress‐induced thymic involution and Ig production in both rat and mouse. Many of these effects appear to be mediated via NK‐2 type receptors. To date, most of the work has involved studies in vitro, but the results from these are now being validated by studies in vivo where both the immune system and neuropeptides are able to interact at many anatomical sites. The complexities of the immune and the nervous systems mean that only a small number of potential interactions has been examined. Future studies can be expected to amplify these observations, especially with respect to the understanding of inflammatory and immune diseases in humans.

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Section: In Vitrosupporting

confidence: 86%

Section: In Vitrosupporting

confidence: 59%

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Modulation of the immune response by tachykinins

Eglezos

Andrews²,

Boyd

et al. 1991

Immunology & Cell Biology

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“…Both and d opioid receptors have been located on primary afferent sensory nerves [24,25] and these receptors could be mediating the inhibitory effect of hemorphin-7. It is unlikely that opioid receptors on immunocytes are involved in the action of hemorphin-7 in our experiments, as migration of these cells to the site of tissue injury does not occur until the late phase of acute inflammation (about 5-6 h after blister induction) [26,27].…”

Section: Discussionmentioning

confidence: 95%

Modulation of peripheral inflammation by locally administered hemorphin-7

1998

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The results of this study suggest that hemorphins might play a role in inhibiting the inflammatory response in acute, but not in recurrent or chronic injury conditions. Evidence is also provided that the modulatory inhibitory effect of hemorphin-7 is mediated via activation of opioid receptor(s). The significance of this study in conjunction with our previous work, is that it raises the possibility that different endogenous inhibitory mechanisms may operate under different injury conditions - endogenous hemorphins and opioids may modulate acute and chronic inflammation, respectively.

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“…In other model systems, however, b-funaltrexamine, an irreversible m-selective antagonist, have fully reversed the actions of endomorphins [9] suggesting the involvement of m-receptors. It is unlikely that opioid receptors on immunocytes are involved in the action of EM-1 in our experiment, as migration of these cells to the site of tissue injury does not occur until the late phase of acute inflammation (about 5-6 h after blister induction) [28,29].…”

Section: Discussionmentioning

confidence: 98%

Modulation of peripheral inflammation by locally administered endomorphin-1

Khalil¹,

Sanderson

Modig

et al. 1999

Inflammation Research

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The current results demonstrate a greater inhibitory effect of EM-1 on the inflammatory response to electrical nerve stimulation (58% inhibition) compared to SP (34% inhibition) suggesting the involvement of both pre- and post-terminal mechanisms in the inhibitory modulatory actions of EM-1. Evidence is provided for the involvement of opioid receptors in this inhibitory effect. The results also suggest that EM-1 is equipotent in inhibiting the inflammatory response under different injury conditions.

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Tachykinin-mediated modulation of the primary antibody response in rats: evidence for mediation by an NK-2 receptor

Cited by 26 publications

References 33 publications

Modulation of the immune response by tachykinins

Modulation of the immune response by tachykinins

Modulation of peripheral inflammation by locally administered hemorphin-7

Modulation of peripheral inflammation by locally administered endomorphin-1

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