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Biomedical subjects

J Ekström

Publications and source records attributed to J Ekström.

At least 37 records · Page 2Linked to original sources
PubMed2000

Heme oxygenase-1, heme oxygenase-2 and biliverdin reductase in peripheral ganglia from rat, expression and plasticity.

The expression of inducible and constitutive heme oxygenase and biliverdin reductase was studied in normal and cultured peripheral ganglia from adult rats, using immunocytochemistry and in situ hybridization. Dramatic changes were induced by one to two days' culturing of dorsal root ganglia, nodose ganglia, otic ganglia, sphenopalatine ganglia and superior cervical ganglia. An up-regulation of inducible heme oxygenase was found in satellite cells of the cultured nodose ganglia, dorsal root ganglia, sphenopalatine ganglia and otic ganglia, whereas only a few satellite cells in the superior cervical ganglia responded with an increase in inducible heme oxygenase immunoreactivity. In the superior cervical ganglia inducible heme oxygenase also appeared in a subpopulation of macrophages. During culturing, expression of inducible heme oxygenase immunoreactivity also increased in axons and in nerve cell bodies. In situ hybridization corroborated the immunocytochemical findings, revealing a strong up-regulation of inducible heme oxygenase messenger RNA in satellite cells, and less pronounced up-regulation in nerve cell bodies. Constitutive heme oxygenase immunoreactivity was found in most neurons in all of the ganglia studied. No significant changes in constitutive heme oxygenase immunoreactivity could be observed in cultured ganglia. Biliverdin reductase immunoreactivity was barely detectable in any of the normal ganglia; however, after culturing it appeared in axons, single nerve cell bodies and nerve cell nuclei. The results show that inducible heme oxygenase is up-regulated in peripheral ganglia after axonal injury, and suggest a role for carbon monoxide in cellular signaling and a requirement for the antioxidant (bilirubin) during the regeneration process.

Animals↗
PubMed2000

Parasympathetic non-adrenergic, non-cholinergic-induced protein synthesis and mitogenic activity in rat parotid glands.

Electrical stimulation of the parasympathetic auriculo-temporal nerve (40 Hz, 30 min), in the anaesthetized rat under - and -adrenoceptor blockade, increased [3H]thymidine and [3H]leucine uptake into the parotid glands by 80 and 263 %, respectively. The increase in response to parasympathetic stimulation was almost the same ([3H]thymidine 82 % and [3H]leucine 283 %) when atropine (2 mg kg-1 I.P. or I.V.) was included in the pretreatment. Neither intravenous infusion of vasoactive intestinal peptide (0.5-20 mg kg-1 min-1, 30 min) nor of bethanechol (10 mg kg-1 min-1, 30 min), under adrenoceptor blockade, increased the uptake of [3H]thymidine into the glands. However, these drugs increased [3H]leucine uptake, and in combination they interacted positively. Whereas vasoactive intestinal peptide is likely to be involved in the parasympathetic nerve-evoked protein synthesis, the nature of the non-adrenergic, non-cholinergic component(s) involved in the mitogenic response is presently unknown.

Adrenergic Antagonists↗
PubMed1999

Iscom and iscom-matrix enhance by intranasal route the IgA responses to OVA and rCTB in local and remote mucosal secretions.

Iscoms, with rCTB incorporated via the GM1 receptor, enhanced in mice the mucosal immunogenicity of rCTB as antigen after intranasal (i.n.) administration both by inducing IgA response in the remote intestinal tract mucosa and by a 100-fold increase of the specific IgA locally in the lungs. Iscom-matrix as a separate entity mixed with rCTB enhanced the rCTB-IgA response similarly. While OVA in iscoms induced high mucosal IgA responses, iscom-matrix co-administered with OVA induced low or no mucosal IgA response to OVA. A synergism between iscoms and rCTB could only be seen as an adjuvant targeting effect enhancing the IgA response to OVA in the remote genital tract mucosa. In serum, the immunomodulatory effect of iscoms after i.n. administration was seen as an enhanced serum IgG2a response.

Adjuvants, Immunologic↗
PubMed1999

High-resolution electrophoretic analysis of rat parotid salivary proteins.

Silver staining and high-resolution electrophoretic methods have been used to compare the protein composition of rat parotid saliva evoked in response to (i) parasympathetic stimulation (including the nonadrenergic, noncholinergic, atropine-associated secretion), (ii) sympathetic stimulation, or (iii) the infusion of neuropeptides with secretagogue activity (substance P, calcitonin gene-related peptide, neuropeptide Y, or vasoactive intestinal peptide). The different stimuli influenced the protein concentration and flow rate of the evoked secretion but had little effect upon the protein composition of the saliva. In contrast to earlier studies using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Coomassie blue staining, the combination of silver staining and two-dimensional electrophoresis (2-DE) revealed many newly detected proteins. The results indicate that the protein composition of rat parotid saliva is more complex than previously reported but is unaffected by the mode of stimulation.

Animals↗
PubMed1999

The protein composition of ferret parotid saliva as revealed by high-resolution electrophoretic methods.

Ferret parotid saliva has been analysed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and two-dimensional electrophoresis (2-DE) to determine, for the first time, its protein composition. SDS-PAGE, in combination with Coomassie Brilliant Blue (CBB) staining, revealed up to 20 bands and the patterns were characterised by major protein constituents of Mr 105000, 51000, 47000, 33000, 22000 and 16 400 common to all samples from all animals. Sequential samples collected from the same animal during prolonged stimulation of the parasympathetic nerve (40 min at 40 Hz) showed subtle but reproducible protein changes. Saliva collected from different animals varied widely in the amount of a protein Mr 66000. 2-DE, in combination with silver staining, revealed up to 300 spots and the patterns were characterised by major protein constituents of Mr 105000 (pI 6.3-7.2), Mr 66000 (pI 4.7-5.3), Mr 51000 (pI 5.0-5.7), Mr 47000 (pI 6.0-7.5), and Mr 33000 (pI 4.7-6.0). Many of the polypeptide spot clusters consisted of one or more horizontal strings of spots suggesting extensive microheterogeneity. Both SDS-PAGE and 2-DE indicated that the protein patterns of ferret parotid saliva evoked by electrical stimulation of the parasympathetic nerve in the absence or presence of atropine are similar, i.e., the protein composition of the atropine-resistant nonadrenergic, noncholinergic (NANC) secretion is similar to that of saliva evoked in the absence of muscarinic receptor blockade.

Animals↗
PubMed1999

Induction of antibody responses in the common mucosal immune system by respiratory syncytical virus immunostimulating complexes.

Immunostimulating complexes (ISCOMs) containing envelope proteins of respiratory syncytial virus (RSV) were explored as a mucosal delivery system for the capacity of inducing a common mucosal antibody response. Two intranasal (i.n.) administrations of BALB/c mice with ISCOMs induced potent serum IgG, and strong IgA responses to RSV locally in the lungs and the upper respiratory, and remotely in the genital and the intestinal tracts. Virtually no measurable IgA response was found in these mucosal organs after two subcutaneous (s.c.) immunizations. Virus neutralizing (VN) antibodies were detected in serum and in all of the mucosal organ extracts after both s.c. and i.n. immunizations indicating that the neutralizing epitopes were preserved after both mucosal and parenteral modes of administration. While the mucosal IgA response appears to be of mucosal origin, the IgG antibodies to RSV detected in the mucosal organs were likely of serum origin. However, the mucosal VN antibodies correlated with the IgG rather than the IgA levels. An enhanced IgA response to gp120 in various mucosal organs was recorded after i.n. immunization with gp120 incorporated in RSV ISCOMs, indicating a role of RSV envelope proteins in enhancing and targeting mucosal responses to passenger antigens.

Animals↗
PubMed1998

Vascular protein leakage in the rat parotid gland elicited by reflex stimulation, parasympathetic nerve stimulation and administration of neuropeptides.

Evans blue accumulated in parotid glands of conscious rats in response to feeding (over 60 min), in the absence of atropine and adrenoceptor antagonists and in their presence, and after pretreatment with the sensory neurotoxin capsaicin. Stimulation of the auriculo-temporal nerve (40 Hz, 10 or 20 min), without and with the blockers, caused Evans blue to accumulate. A periglandular oedema also contained the dye. Administration (i.v.) of neurokinin A accumulated Evans blue, while substance P, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating peptide (PACAP), calcitonin gene-related peptide (CGRP) and pilocarpine lacked effect. Pilocarpine enhanced the action of neurokinin A and, furthermore, substance P combined with either VIP, PACAP or CGRP resulted in accumulation of Evans blue. In the sublingual + submandibular glands, Evans blue increased in response to neurokinin A and pilocarpine; furthermore, substance P and VIP, and substance P and CGRP, interacted positively. Bradykinin lacked effect in the glands. Comparisons were made with the urinary bladder. Accumulation of Evans blue reflects plasma protein extravasation. In salivary glands, the phenomenon occurred during feeding and was independent on intact sensory innervation; instead, the parasympathetic innervation containing the neuropeptides was in focus. In the clinic, the present findings may have implications for the aetiology of gland swelling and pain.

Animals↗
PubMed1998

Non-adrenergic, non-cholinergic reflex secretion of parotid saliva in rats elicited by mastication and acid applied on the tongue.

Chewing and acid on the tongue evoked a flow of saliva from the duct-cannulated parotid gland of the conscious rat despite pretreatment with atropine and adrenoceptor antagonists. This non-adrenergic, non-cholinergic (NANC) response depended on an intact parasympathetic innervation and was abolished by a tachykinin antagonist. The present findings are consistent with a physiological role for the secretory NANC mechanisms of the salivary glands.

Adrenergic Antagonists↗
PubMed1998

Depletion of acinar secretory granules in the ferret parotid gland: effects of substance P and vasoactive intestinal peptide.

The acinar cells of the ferret parotid gland are supplied with parasympathetic nerve fibres containing vasoactive intestinal peptide (VIP) and substance P. In this study intracarotid infusions of the two peptides (0.5-1.0 microgram kg-1 min-1 of each for 40 min) in the pentobarbitone-anaesthetized ferret, treated with atropine and adrenoceptor antagonists, induced a loss of acinar secretory granules from this gland, by 32 % in response to VIP and by 46 % in response to substance P. Stimulation of the parasympathetic auriculo-temporal nerve (40 Hz, in the presence of adrenoceptor antagonists) caused a larger loss of acinar granules from the gland than stimulation of the sympathetic superior cervical ganglion (intermittently, 50 Hz for 1 s every 10th second, in the presence of atropine) over 40 min (52 % versus 10 %). A 27 % granular loss in response to parasympathetic stimulation followed upon atropinization. The parasympathetic response was not further diminished by the tachykinin antagonist Spantide ((d-Arg1, d-Pro2, d-Trp7,9, Leu)-substance P). Thus, despite the large exocytotic response to the infusion of substance P, the parasympathetic non-adrenergic, non-cholinergic secretion of storage granules seemed, under the present experimental conditions, to occur independently of the action of substance P.

Animals↗
PubMed1998

Parasympathetic non-adrenergic, non-cholinergic mechanisms in salivary glands and their role in reflex secretion.

Parasympathetic atropine-resistant vasodilatation is a well-known phenomenon in salivary glands. Less well known is the fact that there also exists an atropine-resistant secretory response to parasympathetic stimulation: some glands secrete saliva, albeit at a reduced rate, whereas others just release protein and acinar secretory granules. A number of peptides, including vasoactive intestinal peptide (VIP) and substance P, are likely to be involved in the so called non-adrenergic, non-cholinergic (NANC) transmission of the parasympathetic secretory impulses. We here report a series of experiments where we have found these NANC-mechanisms to be mobilized during reflex secretion. Loss of acinar granules, morphometrically assessed, and reduction in glandular amylase activity indicated secretory activity in the parotid gland of the conscious rat, in the presence of atropine and adrenoceptor antagonists, in response to food intake. As judged by these indices, the NANC mechanisms were potentially responsible for the whole parasympathetic response and, thus, for the major part of the marked response in the absence of the antagonists. Furthermore, the reflex mobilization of the NANC mechanisms depended on mastication rather than on taste, and involved the release of VIP and substance P. The results presented give weight to a physiological role for these mechanisms, and support the idea that, under normal conditions, the NANC mechanisms act in concert with cholinergic and adrenergic mechanisms to generate the most purposeful secretory reflex response to the afferent stimulation.

Animals↗
PubMed1997

Nitric oxide synthase immunoreactive nerves in rat and ferret salivary glands, and effects of denervation.

Nitric oxide has been implicated in mechanisms mediating nerve-evoked vasodilatory and secretory responses in salivary glands. In the present study, the occurrence and distribution of nitric oxide synthase (NOS)-immunoreactive nerves in ferret and rat salivary glands were investigated using immunocytochemistry with rabbit and sheep NOS antisera, and using NADPH-diaphorase enzyme histochemistry. In the parotid, submandibular and sublingual glands of the rat and the ferret, NOS-immunoreactive varicose terminals encircled acini and arteries of various sizes. In the ferret, collecting ducts were also supplied with NOS-immunoreactive fibres. In the rat, only the granular ducts of the submandibular gland were supplied with such fibres. The NOS-immunoreactive innervation of acinar cells was more abundant in the rat than in the ferret, whereas the opposite was true for the innervation of blood vessels. No NOS immunoreactivity was observed in the vascular endothelium. In both species, NOS-positive ganglionic cell bodies were found in the hilar regions of the submandibular and sublingual glands, whereas none could be detected in the parotid glands. NADPH-diaphorase reactivity had the same neuronal distribution as NOS immunoreactivity and, in addition, NADPH-diaphorase reactivity was expressed in ductal epithelium. Neither sympathetic denervation (by removal of the superior cervical ganglion) nor treatment with the sensory neurotoxin capsaicin reduced the NOS-immunoreactive innervation of the parotid gland. However, parasympathetic denervation (by cutting the auriculo-temporal nerve) caused an almost total disappearance of the NOS-immunoreactive innervation. The present findings provide a morphological background to the suggested role of nitric oxide in parasympathetic secretory and vascular responses of salivary glands.

Animals↗
PubMed1997

Pituitary adenylate cyclase activating peptide (PACAP) in salivary glands of the rat: origin, and secretory and vascular effects.

Pituitary adenylate cyclase activating peptide (PACAP)-38, injected i.v. to the anaesthetized rat, evoked secretion of saliva from the three major salivary glands, the submandibular glands responding with the greatest and the sublingual glands with the smallest volumes. The parotid saliva was rich in amylase and protein. In vitro, pieces of parotid and submandibular gland tissues released K+ and protein in response to PACAP-38, with atropine and adrenoceptor antagonists present. The blood flow in the submandibular gland increased in response to PACAP-38, despite a marked fall in mean aortic blood pressure. PACAP is a vasoactive intestinal peptide (VIP)-like neuropeptide. A comparison between the two peptides showed PACAP-38 to be more effective than VIP with respect to vascular responses and less or equi-effective with VIP with respect to the secretory responses, thus suggesting the involvement of PACAP type I and type II receptors, respectively PACAP-38 and -27 were present in the parotid gland as judged by radioimmunoassay, the concentration of the former being about twice that of the latter. Parasympathetic denervation, by cutting the auriculo-temporal nerve, reduced the total parotid gland contents of PACAP-38 and -27 by 23 and 44%, respectively (compared with a previously demonstrated 95% reduction of VIP). Sympathetic denervation, section of the facial nerve or treatment with the sensory neurotoxin capsaicin did not affect the content of PACAP. The difference in efficacy between PACAP and VIP in the vascular and secretory responses as well as the difference in localization suggest that the two peptides play different physiological roles in the salivary glands.

Animals↗
PubMed1997

Nitric oxide in the control of submandibular gland function in the anaesthetized ferret.

Stimulation of parasympathetic innervation of the submandibular gland (2 or 20 Hz continuously or 20 Hz for 1 s at 10 s intervals), in the ferret, produced secretion of fluid and protein and a fall in vascular resistance. The responses following the administration of N omega-nitro-L-arginine methyl ester (L-NAME; 2 mmol kg-1 i.a.) to block the synthesis of nitric oxide (NO) were reduced, and the persisting responses were abolished (at 2 Hz continuously and 20 Hz intermittently) or further reduced (at 20 Hz continuously) by the additional administration of atropine. The output of vasoactive intestinal peptide (VIP) from the gland was not affected. Neither the secretory nor the vascular response to intra-arterial infusions of acetylcholine (1.25 nmol kg-1) was affected by L-NAME, whereas the vascular responses to both VIP (10 pmol kg-1) and pituitary adenylate cyclase-activating peptide (1-38) (PACAP) (0.5 pmol kg-1) were reduced thereby. Neither peptide evoked a fluid secretion per se. However, when infused during parasympathetic stimulation of saliva secretion, VIP increased both flow rate and the output of protein. These effects of VIP were abolished by L-NAME. The experiments were performed in the presence of sodium nitroprusside at doses (4-8 nmol min-1 kg-1 i.v.) aimed to counterbalance the systemic effects of L-NAME. The results show that, in the ferret, parasympathetic nerve activity increases submandibular blood flow, and elicits the flow of saliva and output of protein by mechanisms that involve in situ generation of NO, upon which the effects of VIP and PACAP but not acetylcholine are largely dependent.

Animals↗
PubMed1996

Loss of the adrenoceptor-mediated secretory drive on the rat parotid gland during eating and the effect on parasympathetic substance P and VIP.

Phentolamine and propranolol (2 mg/kg i.p. of each) were administered to rats to be fed hard chow over a period of 80 min and to their fasting controls. The pharmacological elimination of the adrenoceptor mediated secretory drive on the parotid gland cells during feeding did not affect the gland content of the peptides substance P and vasoactive intestinal peptide localized to parasympathetic nerve fibres of the gland and thought to transmit secretory impulses. This is in contrast to the previously demonstrated effect of elimination of the parasympathetic acetylcholine-evoked secretion following administration of atropine, which resulted in reduced gland contents of these peptides.

Animals↗
PubMed1996

Neuropeptide Y in salivary glands of the rat: origin, release and secretory effects.

In the parotid gland, double immunostaining showed the perivascular and most of the periductal neuropeptide Y (NPY)-immunoreactive nerve fibres to contain dopamine beta-hydroxylase, while the majority of periacinar NPY-fibres contained vasoactive intestinal peptide. Sympathectomy caused a marked depletion of perivascular and periductal NPY-fibres, leaving periacinar NPY-fibres less affected. Following combined sympathectomy and parasympathectomy, only a few NPY-fibres persisted. The parasympathetic auriculotemporal nerve contributed most (75%) and the cervical sympathetic nerve least (15%) to the parotid gland content of NPY as judged by radioimmunoassay. The sensory neurotoxin capsaicin was without effect on the occurrence and gland content of NPY. Upon long-lasting electrical stimulation of the auriculo-temporal nerve at a high frequency, the gland content of NPY was reduced (by 55%), a depletion thought to indicate release of the peptide from parasympathetic nerve terminals. In vitro, tissues of parotid, submandibular and sublingual glands released concentration-dependently protein (and as to the parotid gland amylase also) in response to NPY; the protein response was largest from sublingual tissue (per unit weight). A concentration-dependent in vitro release of potassium from tissues of parotid and submandibular glands in response to NPY occurred and here, submandibular gland tissue was the most sensitive. Comparisons between the action of some secretagogues (at 10(-6) M) showed NPY to be less effective than vasoactive intestinal peptide and adrenaline, but as effective as bethanechol and substance P, in releasing protein (and amylase) in parotid and submandibular gland tissues; in sublingual gland tissue NPY was less effective than vasoactive intestinal peptide, in the range of adrenaline and more effective than bethanechol and substance P. As to potassium release (at agonist concentration of 10(-6) M) from tissues of parotid and submandibular glands NPY was less effective than substance P and vasoactive intestinal peptide. The fluid response to NPY upon i.v. administration was scanty from parotid and submandibular glands. NPY is likely to play a complementary role in mediating parasympathetic secretory responses in salivary glands of the rat. It seems preferentially involved in the control of protein secretion.

Amylases↗
PubMed1996

Equine herpesvirus type 2 (EHV-2) as a predisposing factor for Rhodococcus equi pneumonia in foals: prevention of the bifactorial disease with EHV-2 immunostimulating complexes.

Equine herpesvirus type 2 (EHV-2), a member of the Gammaherpesvirinae subfamily, was studied in a two-phase respiratory disease complex of young foals as a predisposing factor for the secondary bacterial invasion of lungs with Rhodococcus equi (R. equi). Foals were immunized against EHV-2 on a farm where R. equi pneumonia regularly occurred during the last years. The immunizations were performed by using a subunit vaccine which selectively presents envelope glycoproteins of EHV-2 in a multimeric form of immunostimulating complexes (iscoms). The etiological role of EHV-2 was estimated by observing the occurrence of the respiratory disease complex in groups of foals immunized against the virus, in comparison to non-immunized controls. The immunization trials of young animals revealed that the iscom subunit vaccine formulation is able to overcome the interference of maternal antibodies. Active immunization of foals with a single dose of the iscoms provided a certain degree of protection, while two injections of iscoms yielded complete protection against the disease complex in the majority of the treated animals, by preventing the manifestation of R. equi pneumonia. The present findings strongly support the hypothesis that EHV-2 is a predisposing factor for the R. equi invasion of the respiratory tract. The EHV-2 iscom formulation provides highly specific and effective means to prevent the disease complex.

Actinomycetales Infections↗
PubMed1996

Electrophoretic analysis of rat parotid salivary protein composition: investigation of the parasympathetic atropine-resistant secretion.

Rats pretreated with atropine and adrenoceptor antagonists show secretion of saliva upon electrical stimulation of the parasympathetic nerve of the parotid gland. The protein composition of this secretion has been analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and compared with the protein profiles obtained with secretions evoked by parasympathetic stimulation (in the absence of atropine) or infusion of bethanechol with or without vasoactive intestinal peptide (VIP, a probable transmitter conveying parasympathetic secretory impulses). The SDS-PAGE patterns were highly reproducible for an individual rat although minor differences were detected between different rats. The method requires only microlitre volumes of unconcentrated rat saliva and thus is ideal for monitoring sequential aliquots collected from the same rat. The SDS-PAGE patterns indicated (i) little change in the protein profile during prolonged stimulation, (ii) a similar profile with parasympathetic stimulation or infusion of bethanechol, and (iii) a quantitative, rather than qualitative, response to administration of atropine (during parasympathetic stimulation) or VIP (during bethanechol infusion). Thus, the salivary protein composition associated with non-adrenergic, non-cholinergic (NANC) secretion appears similar to that evoked in response to parasympathetic nerve stimulation in the absence of muscarinic receptor blockade.

Animals↗