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PubMed1995

Auditory brain stem response changes after application of endotoxin to the round window membrane in experimental otitis media.

The effects of endotoxin (purified Escherichia coli lipopolysaccharide 0111:B4) on cochlear function in normal and otitis media animals were evaluated. Two types of experimental otitis media models were developed in guinea pigs: eustachian tube obstruction and intratympanic injection of endotoxin. In normal animals, three different concentrations (0.01, 0.1, or 1.0 mg/ml) of endotoxin were applied onto the round window membrane, and auditory brain stem responses were recorded at 1, 3, 6, and 12 hours and 1, 2, 3, and 14 days after the application of endotoxin. Concentrations of 0.01 and 0.1 mg/ml of endotoxin did not affect the auditory brain stem response thresholds, whereas a concentration of 1.0 mg/ml resulted in elevation of the auditory brain stem response thresholds. Alteration of the auditory brain stem response threshold began at 3 hours, reached a peak at 24 or 48 hours, and returned to a normal level 2 weeks after the application of endotoxin. However, when the same concentration (1.0 mg/ml) of endotoxin was applied to the round window membranes of animals that underwent eustachian tube obstruction or intratympanic injection of endotoxin, the endotoxin did not cause any alteration of the auditory brain stem response threshold compared with normal animals.

Animals↗
PubMed2006

Inflammatory, coagulatory and circulatory responses to logarithmic increases in the endotoxin dose in the anaesthetised pig.

Although porcine intravenous endotoxin shock models are widely employed in experimental sepsis, endotoxin dose-effect studies are scarce. Our primary aim was to establish the dose response to increasing endotoxin doses in inflammatory, coagulatory and haemodynamic effect variables, as well as to determine the optimal time point for assessment in a pig model. A secondary aim was to study pathophysiological covariations between the different responses. Twenty anaesthetised piglets received endotoxin intravenously in doses of 0.063 (n = 3), 0.25 (n = 3), 1.0 (n = 3), 4.0 (n = 3), 8 (n = 3) and 16 microg/kg/h (n = 2). In addition, non-endotoxin piglets constituted a control group (n = 3). Physiological variables were registered and blood samples analysed for TNF-alpha, IL-6, leukocyte, platelet and haemoglobin concentrations hourly for 6 h. Increases in the endotoxin dose induced significant log-log cytokine responses as well as log-linear leukocyte and platelet responses. Significant log-linear responses were observed for circulatory parameters, plasma leakage, hypoperfusion and pulmonary compliance. Significant covariations in the responses were noted. In conclusion, there were log-log or log-linear responses to endotoxin suggesting a greater effect of a given dose at lower pre-existing endotoxin concentrations and lower doses of < or = 1 microg/kg/h may be of advantage in experiments designed to study potential anti-endotoxin effects of experimental drugs or measures.

Anesthesia↗
PubMed1999

Endotoxin-induced inhibition of growth hormone receptor signaling in rat liver in vivo.

The bacterial lipopolysaccharide endotoxin induces a catabolic response characterized by resistance to multiple anabolic hormones. The objective of this study was to determine the effects of endotoxin on the GH signaling pathway in rat liver in vivo. After the iv injection of Escherichia coli endotoxin (1 mg/kg), there was a progressive decrease in liver STAT5 (signal transducer and activator of transcription-5) tyrosine phosphorylation in response to GH (40% decrease 6 h after endotoxin), which occurred in the absence of a change in abundance of the STAT5 protein. Endotoxin resulted in a rapid 40-fold increase in liver Janus family kinase-2 (JAK2) messenger RNA, followed by a 2-fold increase in JAK2 protein abundance. This was associated with a 50% decrease in phosphorylated/total JAK2 after GH stimulation. GH receptor abundance was unchanged, suggesting a postreceptor site of endotoxin-induced GH resistance. Rat complementary DNAs for three members of the suppressor of cytokine signaling gene family were cloned [cytokine-inducible sequence (CIS), suppressor of cytokine signaling-2 (SOCS-2), and SOCS-3] and, using these probes, messenger RNAs for SOCS-3 and CIS were shown to be increased 10- and 4-fold above control values, respectively, 2 h after endotoxin infusion. The finding of endotoxin inhibition of in vivo STAT5 tyrosine phosphorylation in response to a supramaximal dose of GH in the absence of a change in GH receptor abundance or total GH-stimulated JAK2 tyrosine phosphorylation provides the first demonstration of acquired postreceptor GH resistance. We hypothesize that this may occur through a specificity-spillover mechanism involving the induction of SOCS genes by cytokines released in response to endotoxin and subsequent SOCS inhibition of GH signaling.

Animals↗
PubMed1983

Bacillus thuringiensis var israelensis crystal delta-endotoxin: effects on insect and mammalian cells in vitro and in vivo.

Bacillus thuringiensis var israelensis parasporal crystal delta-endotoxin was purified by ultracentrifugation on a discontinuous sucrose gradient. Native delta-endotoxin crystals showed no detectable toxicity in the vitro and in vivo systems that are described. By contrast alkali-solubilized crystal delta-endotoxin caused rapid cytological and cytopathological changes in Aedes albopictus, Choristoneura fumiferana 63 CF1, Spodoptera frugiperda and Trichoplusia ni cell lines as observed by phase-contrast microscopy and vital staining. Mouse fibroblasts, primary pig lymphocytes and three mouse epithelial carcinoma cell types showed a similar response to the alkali-soluble crystal delta-endotoxin. In addition the soluble crystal delta-endotoxin protein caused haemolysis of rat, mouse, sheep, horse and human erythrocytes. Intravenous administration of the alkali-soluble crystal delta-endotoxin to Balb. c mice at a dose rate of 15-30 micrograms of protein per gram body weight resulted in rapid paralysis followed by death within 12h. Subcutaneous inoculation of 15-30 micrograms of protein per gram body weight resulted in death of suckling mice in 2-3 h. The alkali-solubilized crystal delta-endotoxin was not toxic however, when administered per os. A comparison is made with a similar alkali-soluble fraction from the parasporal crystal delta-endotoxin of B. thuringiensis var kurstaki. With the exception of the Lepidopteran cell line, Choristoneura fumiferana 63 CF1, this soluble crystal delta-endotoxin protein showed no in vitro or in vivo toxicity, and no haemolytic activity.

Animals↗
PubMed1995

Depressive effect of a traditional Chinese medicine (sho-saiko-to) on endotoxin-induced nitric oxide formation in activated murine macrophage J774A.1 cells.

The present study investigated whether or not Sho-saiko-to (crude powder extract, TJ-9) can suppress nitric oxide (NO) generation by endotoxin-activated J774A.1 cells in order to study the preventive mechanism of Sho-saiko-to against endotoxemia. In this experiment, we estimated the NO2- in the murine macrophage cell line J774A.1 using the Griess method. Our results clearly demonstrated that J774A.1 cells stimulated with endotoxin (0.01-10 micrograms/ml) can effectively produce NO, and the production was dependent on the dose of endotoxin. On the other hand, we investigated the suppressive effect of TJ-9 (10-100 micrograms/ml) on NO generation by endotoxin (0.1 microgram/ml)-activated J774A.1 cells. The NO level when the cells were incubated with endotoxin and TJ-9 (10-20 micrograms/ml) was slightly lower than that in cells treated with endotoxin alone. In contrast, treatment with TJ-9 (50-100 micrograms/ml) significantly inhibited endotoxin-activated NO generation in J774A.1 cells, whereas the treatment with TJ-9 (10-100 micrograms/ml) alone was ineffective in inducing NO formation and in inhibiting cell viability in the J774A.1 cells. These findings suggest that a Kampo presciption of Sho-saiko-to shows a suppressive effect on NO generation in macrophages stimulated with endotoxin, and that it may be useful in improving endotoxin-shock symptoms.

Animals↗
PubMed2002

Endotoxin contamination of particles produces misleading inflammatory cytokine responses from macrophages in vitro.

Particulate prosthetic materials are often studied by adding them to monocytic cells in vitro and measuring the release of cytokines as an indicator of their inflammatory potential. Endotoxin is known to be a contaminant of particle preparations and also stimulates the release of cytokines. It is usual to use a proprietary endotoxin test to avoid erroneous results. Four different formulations of cement were found to be free from endotoxin using standard, gel-clot tests but stimulated different levels of release of cytokines from macrophages. These differences were explained when a more sensitive, kinetic endotoxin assay showed that release correlated with minor contamination with endotoxin. In a repeat experiment using cement particles with low or undetectable levels of endotoxin by kinetic assay, differences in the ability of the formulations to stimulate the release of cytokines were not seen. Endotoxin is adsorbed on to the surface of particles and it is this combination which stimulates increased release of cytokines. In both the above methods for determination of endotoxin, the water in which the particles had been soaked was examined rather than the particles directly. Further investigations showed that a kinetic assay directly on a particle suspension is the most sensitive method to measure contamination with endotoxin.

Adsorption↗
PubMed1996

Potential transfer of endotoxin across high-flux polysulfone membranes.

It has been postulated that synthetic membranes, such as polysulfone membranes, are rather impermeable for endotoxin or endotoxin fragments and can be used for sterile filtration of dialysate. It has never been investigated, however, whether endotoxin permeability may be different in commercially available polysulfone membranes. In vitro, we found a significantly different permeability for endotoxin in two standard dialyzers and one test dialyzer with high-flux polysulfone membranes. In contrast to the F-60 dialyzer with a very low permeability for endotoxin, a stepwise increasing load of endotoxin concentration in the dialysate compartment of the PN 1913 test dialyzer and Primus 1350 polysulfone dialyzer was followed by a stepwise increase of endotoxin in the blood compartment. A significant transfer across the membranes was found when the endotoxin concentration in the dialysate compartment was > 10 ng/mL in the PN 1913 and > 0.5 ng/mL in the Primus 1350. In the latter, about 0.5% of the endotoxin concentration of the dialysate compartment was found in the blood compartment. The data suggest that manufacturers have to evaluate the performance and other properties of their synthetic membranes in detail.

Biocompatible Materials↗
PubMed1985

Determination of the presence of root-bound endotoxin using the local Shwartzman phenomenon (LSP).

The purpose of these studies was to determine, by attempting to elicit the local Shwartzman phenomenon (LSP), if the material extracted from periodontally involved root surfaces is actually endotoxin or only an endotoxin-like substance. A total of 719 periodontally involved teeth and 201 unerupted third molars yielded pooled samples of root surface grindings which were treated with the endotoxin extraction technique nonpyrogenic saline or pyrogen-free water. In the first study each of the reconstituted extracts was injected into the right palatal gingiva of New Zealand white rabbits which had demonstrated the ability to elicit an LSP. Commercial Salmonella enteritidis endotoxin was injected into the left (control) palatal gingiva. This was followed 18 hours later by a provoking injection of 200 to 300 microgram S enteritidis endotoxin in a marginal ear vein. In the second study, reconstituted extracts were injected into the right side of the abdomen of New Zealand white rabbits. The left (control) side received varying amounts of S enteritidis endotoxin. Twelve hours later each animal received a provoking injection of 400 microgram of S enteritidis endotoxin in a marginal ear vein. In both studies the animals were examined 6 hours later for visual signs of an LSP. After sacrifice, the tissues were prepared and histologic sections evaluated by two examiners who were unaware of how the specimens had been treated. The results indicated that a heat-stable, phenol-water extractable and highly irritating substance could be obtained from periodontally involved root surfaces. However, it is questionable if the substance extracted was actually endotoxin. If a true endotoxin, it was present only in extremely small amounts.

Adolescent↗
PubMed1989

Suppression of fibroblast growth by Bacteroides gingivalis endotoxin is not reduced by serum lipoproteins.

Previous studies indicated that Bacteroides and E. coli endotoxins caused a dose-dependent inhibition of human fibroblast growth. However, these endotoxins were relatively weak inhibitors of growth. Since cells were grown with serum, we questioned whether serum lipoproteins, which lessen endotoxin cytotoxicity in vivo, reduced the growth inhibitory effects of endotoxins in vitro. To determine whether serum lipoproteins reduced the growth inhibitory effects of endotoxins, logarithmically growing human periodontal cells were incubated with endotoxin and high density (HDL) or low density lipoprotein (LDL). Neither HDL nor LDL significantly reduced the initial growth inhibitory effects of B. gingivalis or E. coli endotoxins, as judged by 3H-thymidine incorporation. Even with prolonged exposure of up to 10 days in culture, HDL did not ameliorate growth inhibition by endotoxin, as determined by direct cell counts. We conclude that serum lipoproteins do not provide any significant protective effects against fibroblast growth inhibition by endotoxins in vitro.

Bacteroides↗
PubMed1992

The effects of the Nd:YAG laser on in vitro fibroblast attachment to endotoxin-treated root surfaces.

The purpose of this study was to evaluate the effects of the Nd:YAG laser on in vitro fibroblast attachment to endotoxin-treated root surfaces and to describe any laser-induced cementum surface alterations. Thirty 4 mm x 4 mm cementum segments were obtained from unerupted third molars. The treatment groups were as follows: 1) control, healthy root segment; 2) non-lased, endotoxin treated; and 3) lased, endotoxin treated. The endotoxin treated roots were soaked in E. coli 055:B5 lipopolysaccharide (556 EU/ml) for 72 hours. The lased, endotoxin-treated root segments were treated with a Nd:YAG laser using a 320 microns contact optic fiber handpiece with an energy setting of 80 mJ at 10 pulses per second for one minute. The root segments were subsequently placed in fibroblast culture dishes for 40 hours and then prepared for scanning electron microscopy (SEM) observation. SEM examination revealed two different types of attachment: flat and round. Flat cells represented firmly attached cells due to well-defined points of attachment and numerous lamellapodia. Round cells possessed few attachment processes and were, therefore, considered poorly attached. The lased, endotoxin-treated root segments had significantly decreased numbers of flat fibroblasts versus the control and non-lased, endotoxin-treated root segments. The absence of flat fibroblasts in the laser treated root segments was a consistent finding. The non-lased, endotoxin-treated root segments had significantly increased numbers of round fibroblasts versus the control and lased, endotoxin treated groups. The lased root segments exhibited surface alterations which included charring, crater formation, cementum meltdown, and tracking.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Silicates↗
PubMed1987

Involvement of endogenous opiates in glucose-stimulated hyperinsulinism of canine endotoxin shock. Inhibition by naloxone.

Hyperinsulinism has been associated with infection and endotoxin shock in rodents, dogs, and humans. In dogs with Escherichia coli-induced endotoxin shock, this hyperinsulinism was in response to glucose administration. To determine the role of endogenous opiates in endotoxin-induced glucose-stimulated hyperinsulinism, plasma beta-endorphin, Met-enkephalin, Leu-enkephalin, insulin, and glucose concentrations were measured for 6 h in fasted, anesthetized dogs given LD70 of E. coli endotoxin; endotoxin and glucose; endotoxin, glucose, and naloxone (an opiate antagonist); glucose and naloxone; or glucose alone. Plasma endogenous opiate immunoreactivity was elevated in dogs that received endotoxin, regardless of the presence of glucose or naloxone. The elevation of plasma Met-enkephalin and beta-endorphin preceded the onset of hyperinsulinism, but the elevation of plasma Leu-enkephalin did not. Plasma insulin was elevated 100-fold by 360 min in dogs given endotoxin and glucose. The magnitude of this hyperinsulinism was markedly reduced by naloxone, supporting the hypothesis that endogenous opiates are involved in the development of the glucose-stimulated hyperinsulinism associated with endotoxin shock. Interestingly, naloxone, given in conjunction with glucose, appeared to have a stimulatory effect on insulin secretion.

Animals↗
PubMed1988

Kinetics of endotoxin release by gram-negative bacteria in the intestinal tract of mice during oral administration of bacitracin and during in vitro growth.

The release of endotoxin by gram-negative bacteria was studied during bacitracin-induced intestinal colonization in C3H/Law mice and during in vitro growth. The "free" endotoxin concentration was determined by the Limulus amebocyte lysate test in faecal and in culture supernatants, respectively. After oral administration of bacitracin for 2 days a significant (p less than 0.001) increase of the faecal concentration of gram-negative bacteria of 3-4 logs accompanied a significant (p less than 0.001) increase of the faecal endotoxin concentration from 10(1.8 +/- 0.2) to 10(3.3 +/- 0.2) micrograms endotoxin/g faeces. In vitro, however, an increase of the concentration of gram-negative bacteria of 3-4 logs resulted in a 3-4 log increase of the concentration of endotoxin during the exponential and early stationary growth phase. The faecal endotoxin level after 8 days of bacitracin treatment dropped to a value not significantly different from the initial value, regardless of a high faecal level of gram-negative bacteria. Endotoxin determination by the Limulus amebocyte lysate test appeared to be unaffected by the amount of bacitracin present in faecal preparations after oral administration of this antibiotic. In addition, the in vitro release of endotoxin was not influenced by bacitracin. From these results we conclude, that "free" endotoxin is a product of extensive proliferation of gram-negative bacteria. Therefore, the intestinal endotoxin level does not necessarily correlate with the level of gram-negative bacteria, but corresponds with the proliferative activity of these bacteria.

Animals↗
PubMed1993

Hyperlipidemic response to endotoxin--a part of the host-defence mechanism.

Endotoxin administration into experimental animals leads to an acute hyperlipidemic response. In addition, lipoproteins can inhibit various biological activities of endotoxin both in vitro and in vivo. The endotoxin-binding and endotoxin-inactivating abilities of lipoproteins, as well as the plasma levels of lipoproteins, are thus increased following endotoxin administration. The endotoxin-induced hyperlipoproteinemia may not only represent the consequence of endotoxemia, but may also be a physiological defence mechanism whereby the body attempts to combat the toxic effects of circulating endotoxin. This minireview discusses the interaction between lipoproteins and endotoxin, and the role of this acute hyperlipidemic response to endotoxin in the context of the host-defence mechanism.

Animals↗
PubMed1993

The distribution of 3H-labeled endotoxin in the kidney of liver cirrhotic rats.

Although the etiology and pathogenesis of progressive renal failure is largely unknown, endotoxin is supposed to be one of the contributory factors. However, the distribution of endotoxin in liver cirrhosis has not been clarified. Therefore we studied the distribution of 3H-labeled endotoxin in the kidney in rats with CCl4-induced liver injury. Daily inhalations of CCl4 on rats for 6 and 10 weeks produced liver fibrosis (LF group, N = 5) and cirrhosis (LC group, N = 5), respectively. At 6 or 10 weeks, animals were sacrificed 24 hours after an intravenous injection of endotoxin labeled with 3H at the galactose moiety (12,000 cpm/1 g body weight). In the liver, 3H-labeled endotoxin was taken up mainly by Kupffer cells as determined by autoradiography. Compared to control rats, in rats of the LC or LF group the measured amount of 3H-labeled endotoxin per gram kidney or ml blood increased, while that of the liver was significantly decreased. A positive correlation of the amount of 3H-labeled endotoxin per weight or volume respectively was shown between kidney and blood, but not between lung or spleen and blood. These results suggest that overflow of endotoxin due to decreased inactivation in the liver causes endotoxemia in liver injury and that the resulting endotoxemia may directly affect the kidney. The resulting endotoxin-induced vasoconstriction may be a contributory factor for the progressive renal failure frequently observed in liver cirrhosis.

Animals↗
PubMed1995

Antioxidants attenuate endotoxin-gentamicin induced acute renal failure in rats.

The synergistic mechanism by which endotoxin enhances the nephrotoxic potential of gentamicin is unknown. In this study, we attempted to shed light on this mechanism by injecting rats with endotoxin plus gentamicin. Renal injury was assessed by measuring creatinine, inulin and PAH clearance, NADH levels and electrolyte reabsorption, for 24 hr following this injection. Gentamicin alone (20 mg/100 g) induced no renal injury, while endotoxin without gentamicin (0.075 mg/100 g) induced mild injury. However, endotoxin plus gentamicin resulted in acute renal failure. In an attempt to halt the progressive renal dysfunction, the antioxidants NAO (5 mg/100 g), Vitamin E (0.2 mg/100 g per day) and dimethylthiourea (DMTU-50 mg/100 g) were administered, or early endotoxin tolerance was induced before injecting the rats with endotoxin plus gentamicin. The reduction in renal function was markedly slower in rats administered with antioxidants compared with untreated rats. Similar results were obtained with endotoxin tolerance. These data suggest that NAO, vitamin E, DMTU and endotoxin tolerance are potentially beneficial in arresting progressive renal damage associated with endotoxin plus gentamicin.

Animals↗
PubMed1981

Endotoxin dose-related leukocytosis in milk of guinea pigs.

Objectives were to determine minimum and maximum doses of Escherichia coli endotoxin that would stimulate leukocytosis in the mammary gland of the guinea pig. Endotoxin concentrations of .005, .05, .5, 5.0, and 50.0 microgram/ml in 1 ml were used to stimulate migration of polymorphonuclear leukocytes in milk of guinea pigs at five times (2, 4, 6, 8, and 12 h postinjection with endotoxin). There were three animals in each experimental group per endotoxin concentration. Each animal served as its own control by having sterile saline injected into one mammary gland and endotoxin into the other. A control group of three animals had no saline or endotoxin injected. Guinea pigs were milked with a modified milking apparatus. Leukocyte numbers in the uninjected mammary gland did not differ from those in saline injected glands. The difference in mean leukocyte numbers between saline injected and .005 microgram/ml endotoxin injected glands approached significance at 5%. There was no difference between mean numbers recruited by the 5.0 and 50.0 microgram/ml endotoxin doses at 4, 6, 8, and 12 h. The chemotactic effect and, therefore, the rate of polymorphonuclear leukocyte recruitment was maximal at the 5 microgram/ml endotoxin dose.

Animals↗
PubMed1987

Suppressed in vitro blastogenic responsiveness of rat spleen cells after continuous infusion of endotoxin by an implanted osmotic pump.

Continuous infusion of a gram-negative bacterial endotoxin in relatively small doses into rats by means of an implanted osmotic pump was studied. The model system was designed to examine the effects of endotoxin on the blastogenic response of spleen cells to the endotoxin itself and to a nonspecific T-cell mitogen, concanavalin A (Con A). Rats were implanted with an osmotic pump which delivered saline for the first 42 hr to provide postsurgical recovery before the onset of endotoxin infusion. Previous studies had shown that during the first 1-4 days after administration of endotoxin marked alterations of metabolism and some changes in physiologic parameters such as blood pressure and in vitro myocardial performance occurred. In the present study the blastogenic responsiveness of spleen cells to endotoxin itself as well as to the nonspecific T-cell mitogen Con A was markedly decreased after several days of continuous administration of endotoxin. Control animals receiving only saline for the same period of time showed a similar depression of blastogenic responsiveness to the lipopolysaccharide (LPS), as well as to Con A, however, with a delay of 2-4 days before comparable levels of suppression became evident. These results indicate that marked alterations of immune competence as measured by blastogenesis of spleen cells to Escherichia coli LPS and to a mitogen such as Con A may occur after implantation of an osmotic pump, with or without continuous infusion of endotoxin. Further studies seem warranted to determine the role of the foreign body reaction to the osmotic pump as well as to the endotoxin administered by the pump.

Animals↗
PubMed2004

Regulation of endotoxin-induced proinflammatory activation in human coronary artery cells: expression of functional membrane-bound CD14 by human coronary artery smooth muscle cells.

Low-level endotoxemia has been identified as a powerful risk factor for atherosclerosis. However, little is known about the mechanisms that regulate endotoxin responsiveness in vascular cells. We conducted experiments to compare the relative responses of human coronary artery endothelial cells (HCAEC) and smooth muscle cells (HCASMC) to very low levels of endotoxin, and to elucidate the mechanisms that regulate endotoxin responsiveness in vascular cells. Endotoxin (</=1 ng/ml) caused production of chemotactic cytokines in HCAEC. Endotoxin-induced cytokine production was maximal at LPS-binding protein:soluble CD14 ratios <1, typically observed in individuals with subclinical infection; higher LPS-binding protein:soluble CD14 ratios were inhibitory. Endotoxin potently activated HCASMC, with cytokine release >10-fold higher in magnitude at >10-fold lower threshold concentrations (10-30 pg/ml) compared with HCAEC. This remarkable sensitivity of HCASMC to very low endotoxin concentrations, comparable to that found in circulating monocytes, was not due to differential expression of TLR4, which was detected in HCAEC, HCASMC, and intact coronary arteries. Surprisingly, membrane-bound CD14 was detected in seven different lines of HCASMC, conferring responsiveness to endotoxin and to lipoteichoic acid, a product of Gram-positive bacteria, in these cells. These results suggest that the low levels of endotoxin associated with increased risk for atherosclerosis are sufficient to produce inflammatory responses in coronary artery cells. Because CD14 recognizes a diverse array of inflammatory mediators and functions as a pattern recognition molecule in inflammatory cells, expression of membrane-bound CD14 in HCASMC implies a potentially broader role for these cells in transducing innate immune responses in the vasculature.

Arteries↗