Receptors In Trachea Research Articles

Qualitative and quantitative analyses of influenza virus receptors in trachea and lung tissues of humans, mice, chickens and ducks

To accurately determine the expression and distribution patterns of two influenza virus receptors (SAα2,3-gal and SAα2,6-gal) in trachea and lung tissues of humans, mice, chickens and ducks, we analyzed lectin immunofluorescence stainings of various tissue sections qualitatively and quantitatively. Results from the qualitative analysis showed that both influenza virus receptors were expressed in lung tissues of humans, mice, chickens and ducks as well as trachea tissues of mice and ducks. However, SAα2,6-gal receptor was expressed only in the human trachea tissue and SAα2,3-gal receptor was expressed only in the chicken trachea tissue. Results from the quantitative analysis demonstrated that both receptors were expressed in trachea tissues of human and mouse, as well as in lung tissues of humans, chickens and ducks. Meanwhile, our results also showed that the expression and distribution of influenza virus receptors in the same tissue were not always uniform, indicating that their distribution and expression in various tissues are not simply the distinction between the presence or absence of receptors, but rather the difference in the amount of expressed receptors.

Qualitative and quantitative analyses of influenza virus receptors in trachea and lung tissues of human, mouse, chicken and duck

To determine precisely the expression and distribution patterns of two influenza virus receptors(SAα2,3-gal and SAα2,6-gal) in trachea and lung tissues of human,mouse,chicken and duck,we analyzed lectin immunofluorescence stainings of various tissue sections qualitatively and quantitatively.Results from the qualitative analysis showed that both influenza virus receptors were expressed in lung tissues of human,mouse,chicken and duck as well as trachea tissues of mouse and duck;however,SAα2,6-gal receptor was expressed only in the human trachea tissue and SAα2,3-gal receptor was expressed only in the chicken trachea tissue.Results from the quantitative analysis demonstrated that both receptors were expressed in trachea tissues of human and mouse,as well as in lung tissues of human,chicken and duck.Meanwhile,our results also showed that the expression and distribution of influenza virus receptors in the same tissue were not always uniform,indicating that their distribution and expression in various tissues are not simply the distinction between the presence or absence of receptors,but rather the difference in the amount of expressed receptors.

Avian and human influenza A virus receptors in trachea and lung of animals

Influenza A viruses are capable of crossing the specific barrier between human beings and animals resulting in interspecies transmission. The important factor of potential infectivity of influenza A viruses is the suitability of the receptor binding site of the host and viruses. The affinities of avian and human influenza virus to bind with the receptors and the distributions of receptors in animals are different. This study aims to investigate the anatomical distribution of avian and human influenza virus receptors using the double staining lectin histochemistry method. Double staining of lectin histochemistry was performed to identify both SA alpha2,3 Gal and SA alpha2,6 Gal receptors in trachea and lung tissue of dogs, cats, tigers, ferret, pigs, ducks and chickens. We have demonstrated that avian and human influenza virus receptors were abundantly present in trachea, bronchus and bronchiole, but in alveoli of dogs, cats and tigers showed SA alpha2,6 Gal only. Furthermore, endothelial cells in lung tissues showed presence of SA alpha2,3 Gal. The positive sites of both receptors in respiratory tract, especially in the trachea, suggest that all mammalian species studied can be infected with avian influenza virus. These findings suggested that dogs and cats in close contact with humans should be of greater concern as an intermediate host for avian influenza A in which there is the potential for viral adaptation and reassortment.

CAMP immunocytochemistry provides evidence for functional VIP receptors in trachea

Vasoactive intestinal peptide (VIP), first isolated from porcine intestine (S. I. Said and V. Mutt, Science Wash. DC 169: 1217-1218, 1970), has been identified in postganglionic autonomic axons of many tissues. VIP has potent regulatory effects on the function of various cell types within these tissues, ranging from relaxation of smooth muscle to ion transport. Recently, VIP has been implicated in the regulation of mucus secretion in the respiratory tract, a process involving release of macromolecules from exocrine cells and transport of ions and water across the airway mucosa. However, because airway glands and mucosa both consist of mixed cell populations, it was unclear which specific cells contained VIP receptors and contributed to VIP-evoked responses. We identified these specific cells by using immunocytochemical techniques to monitor concentration changes in adenosine 3',5'-cyclic monophosphate (cAMP), the intracellular compound known to mediate VIP responses. Serous and mucous cells of ferret tracheal submucosal glands and ciliated and basal cells of dog tracheal mucosa all increased cAMP in response to VIP stimulation. We conclude that these cell types possess VIP receptors and thus participate in VIP-stimulated responses. In contrast, ferret tracheal epithelium and dog epithelial goblet cells showed little or no reactivity after VIP, and thus we believe that these cells lack VIP receptors.

Purine receptors in trachea: Studies with adenosine deaminase and dipyridamole

ATP, adenosine, adenine and inosine exhibited similar potency in relaxing transverse strips of guinea-pig trachea. Dipyridamole potentiated responses to ATP and adenosine equally but antagonized responses to inosine and failed to affect responses to adenine. In dipyridamole-treated preparations, adenosine deaminase markedly reduced responses to ATP and adenosine; responses to adenine and inosine were unaffected. The results suggest that ATP acts via its adenosine metabolite and that inhibitory ATP receptors are absent.

Mapping of adrenergic receptors in the trachea by autoradiography.

We investigated the distribution of adrenergic receptors in ferret trachea using autoradiography. [3H]Dihydroalprenolol, used to identify beta-adrenoceptors, revealed a high density of specific binding sites over surface epithelium and submucosal glands, with less labelling of smooth muscle. [3H]prazosin labelling showed that alpha 1-receptors were numerous in glands and epithelium, but sparse in smooth muscle. Comparison of adrenergic receptor densities in tracheal sections from the same animals showed a rank order for submucosal glands of alpha 1 greater than beta, for epithelium beta greater than alpha 1 and for smooth muscle beta greater than alpha 1. Within the submucosal glands, alpha 1- and beta-adrenergic receptors were differentially distributed, with alpha 1-receptors being significantly more numerous over serous than mucous cells and beta receptors being significantly more numerous over mucous than serous cells. This technique provides insight into adrenergic regulation of airway function and should be useful in investigations of how relative receptor densities may be altered in disease.

Relaxant beta-receptors in the trachea, but not prejunctional alpha 2-receptors in the tracheal cholinergic neurones, are subjected to homologous desensitization.

Guinea-pigs were pretreated with either isoprenaline, terbutaline or the alpha 2 agonist B-HT 920 in order to asses the hypothesis that beta-and alpha 2 receptors in trachea are subjected to homologous desensitization. In these experiments the beta receptor activity was investigated on tracheal ring preparations contracted with carbacholine. Both in the isoprenaline and the terbutaline pretreated group the relaxant responses to beta agonists were diminished. Pretreatment with B-HT 920 did not affect the sensitivity of the trachea to beta stimulation. In order to asses the responsiveness of alpha 2 receptors the trachea was contracted by electrical field stimulation in the presence of propranolol. During these conditions contractions were mediated by activation of cholinergic neurones and inhibitory effects of alpha stimulation were due to inhibition of the cholinergic neurotransmission by stimulation of prejunctional alpha 2 receptors. In these tests neither isoprenaline, terbutaline nor B-HT 920 pretreatment affected the responsiveness of alpha stimulation to inhibit the electrically induced contractions.

Location of stretch receptors in the trachea and bronchi of the dog.

1. Using single fibre vagal afferent recording techniques, we have investigated the longitudinal and circumferential location of slowly adapting stretch receptors in a functionally isolated, in situ segment of the trachea in dogs. 2. We have also studied the depth of these receptors within the airway wall and their response to reflex and drug induced contraction of the airway smooth muscle. 3. Thirty-four per cent of the receptors studied were in the extrathoracic trachea; calculations indicate that about 17-1% of all airway stretch receptors lie outside the thorax. 4. All the receptors were located in the membranous posterior wall of the trachea, and those tested responded more to transverse than to longitudinal stretching of the wall. 5. Receptors in the extrathoracic trachea continued to function after the regional mucosa had been widely resected; subsequent removal of histolocially proven smooth muscle tissue caused the abrupt cessation of receptor discharge. 6. Contraction of airway smooth muscle brought about an increase in receptor discharge frequency. 7. Similar results were found for a smaller number of stretch receptors located in the mainstem and lobar bronchi. 8. These findings procided evidence that stretch receptors are anatomically located within the smooth muscle layer of the airways and are functionally aranged in series with the muscle fibres.

Evidence for existence of alpha-adrenergic receptors in the mammalian trachea.

Evidence for existence of alpha-adrenergic receptors in the mammalian trachea.