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PubMedDate not supplied

[Molecular mechanism for pathogenicity of Salmonella sp].

Salmonella is a Gram negative bacillus that behaves like a facultative intracellular pathogen. Its environment is the human and animal gastrointestinal tracts, it is never found like a normal microbiota. It is associated with gastrointestinal problems, septicaemic disease and abortion, due to its cellular invasion capacity and its intraphagocytic survival. Nowadays, it is known that Salmonella contains five pathogenicity islands. Several genes involved in the cellular invasion of nonphagocytic cells such as epithelial cells, apoptosis of macrophages, activation of routes of MAP kinases and transcription factors are located in centisome 63, constituting the pathogenicity island 1 (SPI-1). The SPI-2 and SPI-3 islands control the intracellular survival and replication. The SPI-4 island encodes a putative type I secretion system and its believed that it participates in the intracellular survival. Finally, the SPI-5 island encodes for factors involved in the fluid secretion and inflammatory reaction in the intestinal mucosa. Due to a coordinated and precise regulation of the Salmonella genes, it allows for adaptation to environmental changes that occur during an inflammatory process.

Animals↗
PubMed1987

Influence of sodium deoxycholate on morphology, net fluid transport and motility in the small intestine of the rat.

Intestinal fluid secretion and motility were induced by luminal perfusion of rat small intestine with sodium deoxycholate, a dihydroxy bile salt for 1-3 h. Changes in intestinal morphology were studied simultaneously with the changes in fluid transport and motility. The results suggest that the bile salt causes epithelial lesions which may lead to a reduced fluid absorption in the villi, thereby explaining part of the total change in net fluid transport caused by the bile salt. Pyrilamine and indomethacin did not influence the bile salt-induced secretion. Based on earlier studies, it is proposed that the major part of the bile salt-evoked secretion is mediated via activation of intramural nervous reflex(es), which also stimulate the intestinal smooth muscle cells.

Animals↗
PubMed2000

Vibrio cholerae ACE stimulates Ca(2+)-dependent Cl(-)/HCO(3)(-) secretion in T84 cells in vitro.

ACE, accessory cholera enterotoxin, the third enterotoxin in Vibrio cholerae, has been reported to increase short-circuit current (I(sc)) in rabbit ileum and to cause fluid secretion in ligated rabbit ileal loops. We studied the ACE-induced change in I(sc) and potential difference (PD) in T84 monolayers mounted in modified Ussing chambers, an in vitro model of a Cl(-) secretory cell. ACE added to the apical surface alone stimulated a rapid increase in I(sc) and PD that was concentration dependent and immediately reversed when the toxin was removed. Ion replacement studies established that the current was dependent on Cl(-) and HCO(3)(-). ACE acted synergistically with the Ca(2+)-dependent acetylcholine analog, carbachol, to stimulate secretion in T84 monolayers. In contrast, the secretory response to cAMP or cGMP agonists was not enhanced by ACE. The ACE-stimulated secretion was dependent on extracellular and intracellular Ca(2+) but was not associated with an increase in intracellular cyclic nucleotides. We conclude that the mechanism of secretion by ACE involves Ca(2+) as a second messenger and that this toxin stimulates a novel Ca(2+)-dependent synergy.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1984

Source of the fluid component of secretions from tracheal submucosal glands in cats.

The idea that the fluid component of cat tracheal submucosal gland secretions is produced by Na-linked secretion of Cl was tested. Gland secretion was stimulated with phenylephrine; gland fluid flow, net salt movement, and output of 35SO4-labeled macromolecules were measured. With CI, I, NO3, or Br as the major anion, phenylephrine caused equal increases in gland flow and output of 35S-labeled macromolecules while increasing net transepithelial 22Na movement from 0 to about 10 mu eq X cm-2 X h-1. With the impermeant gluconate as a major anion, phenylephrine caused the same increase in output of 35S label, a smaller increase in gland flow, and had no effect on net 22Na movement. Short circuiting in the presence of Cl, or high concentrations of the loop diuretics, furosemide or bumetanide, did not alter the actions of phenylephrine. Ouabain or replacement of Na by choline or Li abolished all secretory effects of phenylephrine. We conclude that active Cl secretion is not responsible for the transepithelial flows of salt and water induced by phenylephrine. Instead, these flows may be secondary to the release of osmotically active components of the secretory granules.

Animals↗
PubMed1988

Effects of secretin and caerulein on luminal feedback regulation of pancreatic enzyme secretion in rats.

The stimulatory pancreatic response to exclusion of pancreatic proteases from the intestine was compared with the response to stepwise increasing doses of secretin and caerulein in conscious rats. Secretin stimulated pancreatic fluid secretion in a dose-related manner with or without intraduodenal return of pancreatic juice, while it could not significantly affect enzyme secretion. The dose response curve for enzyme secretion to caerulein was smooth during return of the juice. However, the already increased enzyme secretion by pancreatic juice diversion was only stimulated with the smallest dose of caerulein. The maximal dose of caerulein for enzyme secretion during return had been supramaximal dose during diversion. Intraduodenal trypsin inhibitor failed to stimulate enzyme secretion during diversion but induced the same stimulatory effect as the submaximal dose of caerulein during return. Different doses of intraduodenal trypsin caused an almost dose-related inhibition. It is concluded that a submaximal level of endogenous CCK might participate in the feedback regulation of pancreatic enzyme secretion in rats.

Animals↗
PubMed1994

Long-term uncoupling of chloride secretion from intracellular calcium levels by Ins(3,4,5,6)P4.

Osmoregulation, inhibitory neurotransmission and pH balance depend on chloride ion (Cl-) flux. In intestinal epithelial cells, apical Cl- channels control salt and fluid secretion and are, in turn, regulated by agonists acting through cyclic nucleotides and internal calcium ion concentration ([Ca2+]i). Recently, we found that muscarinic pretreatment prevents [Ca2+]i increases from eliciting Cl- secretion in T84 colonic epithelial cells. By studying concomitant inositol phosphate metabolism, we have now identified D-myo-inositol 3,4,5,6-tetrakisphosphate (Ins(3,4,5,6)P4), as the inositol phosphate most likely to mediate this uncoupling. A novel, membrane-permeant ester prepared by total synthesis delivers Ins(3,4,5,6)P4 intracellularly and confirms that this emerging messenger does inhibit Cl- flux resulting from thapsigargin- or histamine-induced [Ca2+]i elevations.

Atropine↗
PubMed1982

Taurine transport by isolated flounder renal tubules.

Previous in vivo clearance studies (Schrock et al., '82) have revealed that taurine is secreted by marine fish kidneys. In the present study taurine secretion by the flounder (Pseudopleuronectes americanus) renal tubule was investigated by assaying the transport of 14C-taurine in vitro. Collections from isolated fluid-secreting flounder tubules confirmed the presence of a tubular mechanism for taurine secretion. The flounder renal tubule concentrated taurine in the lumen at a lumen/bath ratio of 25, with the movement across the peritubular membrane identified as the concentrating step of taurine transport. Studies with teased flounder renal tubules identified transport as Na+ and C1- dependent. Taurine transport was inhibited by beta alanine, gamma-aminobutyric acid, and hypotaurine. In a study of the hormonal control of taurine transport, only the adrenal steroid dexamethasone stimulated taurine uptake by the flounder renal tubules. Transport was not affected by the second messengers adenosine 3'5'-cyclic monophosphate, guanosine 3'5'-cyclic monophosphate, adenosine, or Ca++ ionophore (A12384).

Animals↗
PubMed1983

Toxin A of Clostridium difficile: production, purification and effect in mouse intestine.

Clostridium difficile produces one diarrhoeogenic toxin designed A, and one cytopathogenic toxin designed B. Toxin A was purified in a four-step-fractionation procedure. In the last purification step the toxin was separated by elution with galactose from an agarose gel. The purified toxin A induced a clear and watery hypersecretion in intestinal loops of mouse, while mixtures of toxin A and B induced a haemorrhagic secretion. At an ED50 value for the purified toxin A of 0.5 microgram there was a brief, optimal hypersecretion after four hours. Like the fluid secretion induced by cholera toxin, that induced by toxin A could be inhibited by chlorpromazine or by depletion of intestinal bile. In contrast to cholera toxin, however, toxin A did not activate intestinal adenylate cyclase--at least not permanently. Antisera which neutralized cholera toxin did not neutralize toxin A, and vice versa.

Adenylyl Cyclases↗
PubMed1987

Neuropeptides and secretion.

In the rat parotid gland, an atropine-resistant parasympathetic-nerve-evoked secretion was demonstrated in vivo. In the absence of atropine, the non-adrenergic, non-cholinergic transmitter release seemed to contribute to the fluid secretion and to be largely responsible for the secretion of amylase and acinar secretory granules. The gland was reached by nerve fibers containing substance P (SP), vasoactive intestinal peptide (VIP), and, to some extent, calcitonin-gene-related peptide (CGRP) via the parasympathetic auriculo-temporal nerve. Upon electrical stimulation of the nerve, these peptides were released. SP and substance K (SK), a novel tachykinin, induced a profuse watery secretion when injected i.v., while VIP caused a sparse but amylase-rich secretion. CGRP caused no secretion on its own. The tachykinin-evoked secretory response was enhanced by VIP and CGRP. A SP-analogue almost abolished the SP-evoked response, while the atropine-resistant parasympathetic response was only halved. None of the peptides under study can on its own account for the atropine-resistant parasympathetic secretion. The neuropeptides may play complementary roles in the regulation of the exocrine functions of the gland.

Amylases↗
PubMed1982

Hormonal control of renal functions in insects.

Insect Malpighian tubules secrete an isosmotic, KCl-rich primary urine containing low concentrations of most other blood solutes. Neuropeptide diuretic hormones (DH), possibly related to vasopressin, stimulate tubular fluid secretion by 2- to 200-fold in response to water loading, e.g., feeding. DH acts on tubules through cyclic AMP (cAMP) to stimulate salt transport without measurable change in osmotic permeability. Changes in composition of tubular secretion after stimulation and the possible control of DH release are discussed. Most of the water, ions, and metabolites in tubular secretion are normally reabsorbed by active mechanisms in the rectum, where the urine may finally become either hyposmotic or strongly hyperosmotic to the blood. A newly discovered neuropeptide, chloride transport-stimulating hormone, controls (via cAMP) reabsorption of the principal salt by stimulating K-dependent, electrogenic transport of Cl- across the apical cell border. Passive net absorption of K+ is thereby enhanced. Diuretic and antidiuretic factors may control osmotic permeability of the rectal wall and thereby influence the osmotic concentrations of the rectal absorbate and final urine. The increased recycling of a KCl-rich fluid through the Malpighian tubule-rectal system after feeding probably serves to clear the body of unwanted substances ingested with, and produced by, metabolism of the meal.

Animals↗
PubMed1994

Protein phosphatase 1 and 2A in tick salivary glands as assessed by responses to okadaic acid.

Crude protein phosphatase activity was inhibited 80% by nanomolar okadaic acid (OA) in salivary glands of unfed ticks but only 40% in salivary glands of feeding ticks. An additional 40% of protein phosphatase was inhibited by micromolar OA in the salivary glands of feeding ticks but only 10% in salivary glands of unfed ticks. Cyclic AMP and OA alone or together increased the phosphorylation of multiple proteins in a plasma membrane-enriched 900 g supernatant fraction of tick salivary glands. Exogenous cyclic AMP stimulated increased incorporation of phosphate into proteins with approximate molecular weights of 109, 70, 64, 51, 48, 42 and 18.5 kDa. Micromolar OA in the absence of exogenous cyclic AMP stimulated increased incorporation of phosphate into proteins with apparent molecular weights of 109, 93, 74.5, 70, 51, 48, 42 and 18.5 kDa. Cyclic AMP and OA (10(-6) and 10(-9) M) stimulated significantly greater phosphorylation of an 18.5 kDa mol. wt protein above that observed in response to stimulation by OA (10(-6) and 10(-9) M) or exogenous cyclic AMP alone. Micromolar okadaic acid inhibited the amount and number of proteins but not volume of saliva secreted by whole ticks in response to stimulation by DA and theophylline. However, micromolar and nanomolar okadaic acid inhibited the ability of dopamine to stimulate fluid secretion by isolated salivary glands. Overall, the data support the existence of type 1 and 2A protein phosphatases in tick salivary glands and a role for protein phosphatases in modulating tick salivary secretion.

Animals↗
PubMed2000

Choroid plexus in the central nervous system: biology and physiopathology.

Choroid plexuses (CPs) are localized in the ventricular system of the brain and form one of the interfaces between the blood and the central nervous system (CNS). They are composed of a tight epithelium responsible for cerebrospinal fluid secretion, which encloses a loose connective core containing permeable capillaries and cells of the lymphoid lineage. In accordance with its peculiar localization between 2 circulating fluid compartments, the CP epithelium is involved in numerous exchange processes that either supply the brain with nutrients and hormones, or clear deleterious compounds and metabolites from the brain. Choroid plexuses also participate in neurohumoral brain modulation and neuroimmune interactions, thereby contributing greatly in maintaining brain homeostasis. Besides these physiological functions, the implication of choroid plexuses in pathological processes is increasingly documented. In this review, we focus on some of the novel aspects of CP functions in relation to brain development, transfer of neuro-humoral information, brain/immune system interactions, brain aging, and cerebral pharmaco-toxicology.

Choroid Diseases↗
PubMed1997

Endogenous plasma atrial natriuretic peptide and the control of salt gland function in the Pekin duck.

Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were used to investigate the role of endogenous plasma ANP in the control of salt gland function of conscious, saltwater-adapted Pekin ducks. Salt gland secretion was initiated and maintained either by a hypervolemic (290 mosmol/kg NaCl i.v. at 2 ml/min) or hyperosmotic (1,000 mosmol/kg NaCl i.v. at 0.4 ml/min) stimulus. Both experimental conditions caused significant elevations in endogenous plasma ANP concentrations. At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. The activity of salt glands driven by hyperosmolality was not changed by anti-ANP. The results show that the high circulating concentrations of endogenous ANP associated with conditions of sustained volume expansion promote salt gland secretion.

Acclimatization↗
PubMed1983

Effect of atropine on rat basal pancreatic secretion during return or diversion of bile-pancreatic juice.

The effect of atropine on basal pancreatic exocrine secretion in conscious rats was determined with and without return of bile-pancreatic juice (BPJ) to the intestine. Rats were prepared with cannulas draining bile and pancreatic juice separately and with duodenal cannulas for return of secretions. Experiments were begun 3 days postoperatively. During continuous return of bile-pancreatic secretions, intravenous atropine (100 micrograms/kg-hr) caused a sustained 80-90% inhibition of pancreatic protein secretion, with a much smaller suppressive effect on pancreatic juice volume. Diversion of bile-pancreatic juice from the intestine markedly increased pancreatic protein and fluid secretion in control and atropine-infused rats, but the response was significantly inhibited by atropine (volume 31% inhibition, protein output 41% inhibition). The results indicate that basal pancreatic protein secretion during return of BPJ is largely maintained by cholinergic influence, possibly due to an enteropancreatic reflex, and that the inhibition of the pancreatic response to acute diversion of BPJ by atropine is probably secondary to inhibition of gastric secretion.

Animals↗
PubMed1984

Magnesium sulfate-induced water secretion in hamster small intestine.

We studied possible mechanisms of magnesium sulfate (MgSO4)-induced diarrhea. In vivo perfusion of hamster small intestine with an isotonic electrolyte solution containing 50 mM MgSO4 produced nearly three times as much fluid secretion as did a solution containing an equiosmotic amount of mannitol. We found that magnesium was absorbed at a faster rate than mannitol under these conditions, suggesting that differences in solute permeability do not explain the differences in secretory rates. Magnesium ion rather than sulfate appeared largely responsible for the effect as replacement of sulfate with chloride did not diminish the response. MgSO4 perfusion of a proximal intestinal segment did not affect water transport in an isolated distal segment suggesting that release of cholecystokinin or alterations in serum levels of other hormones were not responsible. Intestinal permeability, morphology, and cyclic nucleotide levels were normal after MgSO4 perfusion. Thus, MgSO4-induced diarrhea cannot be explained by the usual mechanisms, and additional processes responsible for intestinal secretion must exist.

Animals↗
PubMed2006

Ambroxol-induced modification of ion transport in human airway Calu-3 epithelia.

Ambroxol is often used as a mucolytic agent in various lung diseases. However, it is unclear how ambroxol acts on bronchial epithelial cells. To clarify the action of ambroxol, we studied the effects of ambroxol on the ion transport in human Calu-3 cells, a human submucosal serous cell line, measuring the transepithelial short-circuit current and conductance across monolayers of Calu-3 cells. Ambroxol of 100 microM diminished the terbutaline (a beta2-adrenergic agonist)-stimulated Cl-/HCO3(-)-dependent secretion without any decreases in the conductance of cystic fibrosis transmembrane conductance regulator (CFTR) channel locating on the apical membrane. On the other hand, under the basal (unstimulated) condition ambroxol increased the Cl(-)-dependent secretion with no significant change in the apical CFTR channel conductance and decreased the HCO3- secretion associated with a decrease in the apical CFTR channel conductance. Ambroxol had no major action on the epithelial Na+ channel (ENaC) or the ENaC-mediated Na+ absorption. These results indicate that in Calu-3 cells: (1) under the basal (unstimulated) condition ambroxol increases Cl- secretion by stimulating the entry step of Cl- and decreases HCO3- secretion by diminishing the activity of the CFTR channel and/or the Na+/HCO3(-)-dependent cotransporter, (2) under the adrenergic agonist-stimulated condition, ambroxol decreases Cl- secretion by acting on the Cl-/HCO3- exchanger, and (3) ambroxol has a more powerful action than the adrenergic agonist on the Cl-/HCO3- exchanger, leading fluid secretion to a moderately stimulated level from a hyper-stimulated level.

Ambroxol↗
PubMed1980

Parasympathetic and sympathetic regulation of secretion from submucosal glands in airways.

We developed methods to study secretions from airway submucosal glands in vivo: micropipettes with tips specially designed to seal around individual gland duct openings allowed us to collect all of the fluid secreted from individual glands. We visualized the secretions from large numbers of glands simultaneously by coating the airway surface with powdered tantalum; secreted mucus formed "hillocks" over each gland duct opening. Measurement of hillock size provided an estimate of secretion rate. We modified the "hillocks" method to study tracheal glands in vitro. To study regulation of mucin secretion in vitro, we measured the radioactivity from 35S bound to mucins secreted from the luminal surface of pieces of trachea mounted in Using-type chambers. Using these techniques, we demonstrated both cholinergic and alpha-adrenergic regulation of the glands.

Animals↗