The effect of enkephalins and prostaglandins on O2− release by neutrophils

Simpkins, Cuthbert O.; Alailima, S.; Tate, E.; Johnson, Mark E.

doi:10.1016/0022-4804(86)90090-9

Cited by 25 publications

(12 citation statements)

References 22 publications

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“…PMN-positive control samples were prepared by collection of peripheral blood from a healthy donor into a 15-mL heparinized tube. PMNs were harvested and purified from the whole blood sample by mearLs of a lymphocyte-separating medium (Organon Teknika Corp., Durham, NC), as described by Simpkins et al (1986). PMN-negative control samples were obtained from rat brain-stem tissue.…”

Section: Methodsmentioning

confidence: 99%

Immunocytochemical Distribution of Human PMN Elastase and Cathepsin-G in Dental Pulp

1993

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Components of primary (azurophilic) granules of polymorphonuclear leukocytes (PMNs) have been implicated as important mediators in pulpal inflammation. This anatomical study used ultracryoimmunocytochemical techniques and characterized and contrasted the subcellular distributions of human PMN elastase (PMN-E), PMN cathepsin-G (PMN-CG), and alpha-2 macroglobulin (alpha-2M) in healthy and inflamed dental pulps. Inflamed pulpal tissue sections revealed an intense distribution of PMN-E in the extracellular domain throughout the collagen matrix. PMN-E was also localized in the perinuclear cytoplasm of PMNs and distributed in a random fashion. PMN-CG was localized intensely in the intracellular granules of PMNs and observed moderately within the extracellular matrix. Healthy pulpal tissues exposed to PMN-E and PMN-CG antibodies revealed no evidence of PMN infiltration and no specific labeling. alpha-2M, a natural serum inhibitor of PMN-E and PMN-CG, was distributed in an intense fashion within the intravascular compartments of both inflamed and healthy pulpal samples. Immunogold-labeling for alpha-2M was observed in moderate amounts within the extravascular domain of inflamed pulpal samples but only in mild amounts within the same area of healthy tissues. These results suggest that PMN-E and PMN-CG are released to the extracellular matrix of irreversibly inflamed teeth, enabling them to facilitate pulpal connective tissue destruction. Conversely, moderate extravascular labeling for alpha-2M within inflamed samples suggests a physiological attempt at inhibiting the pulpal connective tissue destruction mediated by human PMN-E and PMN-CG.

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Section: Methodsmentioning

confidence: 99%

Immunocytochemical Distribution of Human PMN Elastase and Cathepsin-G in Dental Pulp

1993

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“…Several groups studying morphine's effect on infection examined superoxide release as a mechanism of bacterial killing, noticed that morphine inhibits superoxide production in neutrophils and macrophages (Sharp et al, 1985; Simpkins et al, 1986; Welters et al, 2000). In addition to exogenous opioids, endogenous opioids had similar inhibitory effects where pretreatment with endogenous opioid peptides leucine or methionine enkephalins reduced neutrophil's ability to generate superoxide production in response to the Escherichia coli product, N-formyl methionyl leucyl phenylalanine (FMLP) (Sharp et al, 1985; Simpkins et al, 1986). Morphine mediated suppression of superoxide production was reproduced in human peripheral mononuclear cells in studies done by Peterson et al, which examined respiratory burst activity in response to phorbol myristate acetate (PMA) (Peterson et al, 1987; Peterson et al, 1989).…”

Section: Opioid Modulation Of Immune Cell Functionmentioning

confidence: 99%

Role of the mu-opioid receptor in opioid modulation of immune function

2011

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SUMMARY Endogenous opioids are synthesized in vivo in order to modulate pain mechanisms and inflammatory pathways. Endogenous and exogenous opioids mediate analgesia in response to painful stimuli by binding to opioid receptors on neuronal cells. However, wide distribution of opioid receptors on tissues and organ systems outside the CNS, such as the cells of the immune system, indicate that opioids are capable of exerting additional effects in the periphery, such as immunomodulation. The increased prevalence of infections in opioid abusers based epidemiological studies further highlights the immunosuppressive effects of opioids. In spite of their many debilitating side effects, prescription opioids remain a gold standard for treatment of chronic pain. Therefore, given the prevalence of opioid use and abuse, opioid mediated immune suppression presents a serious concern in our society today. It is imperative to understand the mechanisms by which exogenous opioids modulate immune processes. In this review we will discuss the role of opioid receptors and their ligands in mediating immune suppressive functions. We will summarize recent studies on direct and indirect opioid modulation of the cells of the immune system as well as the role of opioids in exacerbation of certain disease states.

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“…Yet a third possibility is that alcohol induced the formation of oxygen radicals which in turn caused the injury to the basal lamina, and PGE, either prevented their formation or adequately scavenged them so that they were no longer deleterious. Evidence does exist suggesting that ethanol injury to the gastric mucosa may involve oxygen radicals (Pihan et al, 19871, and prostaglandins have been shown to inhibit radical formation (Simpkins et al, 1986). Whether such a mechanism was responsible for our findings will require further study.…”

Section: Discussionmentioning

confidence: 97%

Colloidal gold localization of type IV collagen in the extracellular matrix of rat gastric mucosa: Influence of alcohol and prostaglandin

Rightor¹,

Mitchell²,

Miller

et al. 1991

Anat. Rec.

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The effect of acute alcohol exposure on the gastric mucosal basal lamina, and its major structural protein type IV collagen, was assessed by transmission electron microscopy (TEM) and immunogold (IG) labeling of this collagenous material. Fasted rats orally received either 50% or 100% ethanol. Five or 60 minutes later animals were sacrificed and mucosal samples were obtained from the glandular epithelium for TEM or IG localization of type IV collagen. For IG studies, the number of gold particles/area lamina densa was quantified in interfoveolar, pit, and gland regions as an index of the molecular integrity of type IV collagen. Both ethanol concentrations induced epithelial exfoliation with pleating of the denuded lamina densa. Absolute ethanol, and to a lesser extent 50% ethanol, caused frequent rupture of a thickened, precipitated lamina densa. Immunolabeling of type IV collagen varied with the experimental protocol. In control tissues exposed to oral saline, binding was greatest in the interfoveolar zone. Low binding occurred with 100% ethanol in all regions when compared with controls, but 50% ethanol evoked significantly higher binding in interfoveolar regions, in a similar fashion to controls. In additional studies in which 16,16 dimethyl prostaglandin E2 (PGE2) (10 micrograms/kg) was injected subcutaneously prior to oral ethanol exposure, PGE2 pretreatment prevented the large decrease in IG binding induced by absolute ethanol, but the level still remained significantly less than with corresponding controls. In contrast, pretreatment with PGE2 prior to 50% ethanol exposure restored type IV collagen immunolabeling to control levels. These results indicate that ethanol induces a concentration-dependent lowering of IG binding to type IV collagen which also effects its reversibility by PGE2.

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The effect of enkephalins and prostaglandins on O2− release by neutrophils

Cited by 25 publications

References 22 publications

Immunocytochemical Distribution of Human PMN Elastase and Cathepsin-G in Dental Pulp

Immunocytochemical Distribution of Human PMN Elastase and Cathepsin-G in Dental Pulp

Role of the mu-opioid receptor in opioid modulation of immune function

Colloidal gold localization of type IV collagen in the extracellular matrix of rat gastric mucosa: Influence of alcohol and prostaglandin

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