scholarly journals Phosphocholine-Modified Lipooligosaccharides of Haemophilus influenzae Inhibit ATP-Induced IL-1β Release by Pulmonary Epithelial Cells

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1979 ◽  
Author(s):  
Katrin Richter ◽  
Christian Koch ◽  
Alexander Perniss ◽  
Philipp Wolf ◽  
Elke Schweda ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Haemophilus Influenzae ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Opportunistic Pathogen ◽  
Mammalian Host ◽  
Nicotinic Acetylcholine ◽  
Pulmonary Epithelial Cells ◽  
Airway Infections ◽  
Human Lung Carcinoma

Phosphocholine-modified bacterial cell wall components are virulence factors enabling immune evasion and permanent colonization of the mammalian host, by mechanisms that are poorly understood. Recently, we demonstrated that free phosphocholine (PC) and PC-modified lipooligosaccharides (PC-LOS) from Haemophilus influenzae, an opportunistic pathogen of the upper and lower airways, function as unconventional nicotinic agonists and efficiently inhibit the ATP-induced release of monocytic IL-1β. We hypothesize that H. influenzae PC-LOS exert similar effects on pulmonary epithelial cells and on the complex lung tissue. The human lung carcinoma-derived epithelial cell lines A549 and Calu-3 were primed with lipopolysaccharide from Escherichia coli followed by stimulation with ATP in the presence or absence of PC or PC-LOS or LOS devoid of PC. The involvement of nicotinic acetylcholine receptors was tested using specific antagonists. We demonstrate that PC and PC-LOS efficiently inhibit ATP-mediated IL-1β release by A549 and Calu-3 cells via nicotinic acetylcholine receptors containing subunits α7, α9, and/or α10. Primed precision-cut lung slices behaved similarly. We conclude that H. influenzae hijacked an endogenous anti-inflammatory cholinergic control mechanism of the lung to evade innate immune responses of the host. These findings may pave the way towards a host-centered antibiotic treatment of chronic airway infections with H. influenzae.

Human and Rodent Bronchial Epithelial Cells Express Functional Nicotinic Acetylcholine Receptors

1998 ◽  
Vol 54 (5) ◽  
pp. 779-788 ◽  
Author(s):  
Arno D. J. Maus ◽  
Edna F. R. Pereira ◽  
Peter I. Karachunski ◽  
Robert M. Horton ◽  
Duraiswamy Navaneetham ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Bronchial Epithelial Cells ◽  
Nicotinic Acetylcholine ◽  
Bronchial Epithelial

scholarly journals Terminally Differentiated Epithelial Cells of the Thymic Medulla and Skin Express Nicotinic Acetylcholine Receptor Subunitα3

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Aichurek Soultanova ◽  
Alexandra R. Panneck ◽  
Amir Rafiq ◽  
Wolfgang Kummer
Keyword(s):  
Epithelial Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Biological Activities ◽  
Egfp Expression ◽  
Epidermal Keratinocytes ◽  
Basal Cells ◽  
Stratum Granulosum ◽  
Nicotinic Acetylcholine ◽  
Thymic Medulla

In the thymus, T cell maturation is influenced by cholinergic signaling, and the predominantly expressed receptor is theα3-subunit of nicotinic acetylcholine receptors, encoded by thechrna3gene. We here determined its cellular distribution utilizing an appropriate eGFP-expressing reporter mouse strain. Neither T cells (CD4, CD8) nor mesenchymal cells (desmin-positive) expressed eGFP. In the thymic medulla, eGFP-positive cells either were scattered or, more frequently, formed small clusters resembling Hassall’s corpuscles. Immunolabeling revealed that these cells were indeed terminally differentiated epithelial cells expressing keratin 10 (K10) but neither typical cortical (K8, K18) nor medullary keratins (K5, K14). These labeling patterns reflected those in the epidermis of the skin, where overlap of K10 and eGFP expression was seen in the stratum granulosum, whereas underlying basal cells displayed K5-immunoreactivity. A substantial portion of thymic eGFP-positive cells was also immunoreactive to chromogranin A, a peptide previously reported in epidermal keratinocytes in the stratum granulosum. Its fragment catestatin has multiple biological activities, including suppression of proinflammatory cytokine release from macrophages and inhibition ofα3β4 nAChR. The present findings suggest that its thymic production and/or release are under cholinergic control involving nAChR containing theα3-subunit.

scholarly journals Expression of functional nicotinic acetylcholine receptors in rat urinary bladder epithelial cells

2006 ◽  
Vol 290 (1) ◽  
pp. F103-F110 ◽  
Author(s):  
Jonathan M. Beckel ◽  
Anthony Kanai ◽  
Sun-Ju Lee ◽  
William C. de Groat ◽  
Lori A. Birder
Keyword(s):  
Epithelial Cells ◽  
Urinary Bladder ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotinic Receptors ◽  
Urothelial Cells ◽  
Intravesical Administration ◽  
Nicotinic Acetylcholine ◽  
Rat Urinary Bladder ◽  
Stimulation Of

Although nicotinic acetylcholine receptors in both the central and peripheral nervous systems play a prominent role in the control of urinary bladder function, little is known regarding expression or function of nicotinic receptors in the bladder epithelium, or urothelium. Nicotinic receptors have been described in epithelial cells lining the upper gastrointestinal tract, respiratory tract, and the skin. Thus the present study examined the expression and functionality of nicotinic receptors in the urothelium, as well as the effects of stimulation of nicotinic receptors on the micturition reflex. mRNA for the α3, α5, α7, β3, and β4 nicotinic subunits was identified in rat urothelial cells using RT-PCR. Western blotting also confirmed urothelial expression of the α3- and α7-subunits. Application of nicotine (50 nM) to cultured rat urothelial cells elicited an increase in intracellular Ca2+ concentration, indicating that at least some of the subunits form functional channels. These effects were blocked by the application of the nicotinic antagonist hexamethonium. During in vivo bladder cystometrograms in urethane-anesthetized rats, intravesical administration of nicotine, choline, or the antagonists methyllycaconitine citrate and hexamethonium elicited changes in voiding parameters. Intravesical nicotine (50 nM, 1 μM) increased the intercontraction interval. Intravesical choline (1–100 μM) also affected bladder reflexes similarly, suggesting that α7 nicotinic receptors mediate this effect. Intravesical administration of hexamethonium (1–100 μM) potentiated the nicotine-induced changes in bladder reflexes. Methyllycaconitine citrate, a specific α7-receptor antagonist, prevented nicotine-, choline-, and hexamethonium-induced bladder inhibition. These results are the first indication that stimulation of nonneuronal nicotinic receptors in the bladder can affect micturition.

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