Distribution of CD14+ macrophages, CD4+, CD8+ lymphocytes and mRNA expression of inducible nitric oxide synthase in the endometrium of repeat breeding cows

2013 ◽  
Vol 16 (3) ◽  
pp. 443-451 ◽  
Author(s):  
W. Barański ◽  
J. Kaleczyc ◽  
S. Zduńczyk ◽  
W. Podlasz ◽  
E. Długołęcka-Malinowska ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Polymorphonuclear Neutrophils ◽  
Control Group ◽  
Inos Mrna ◽  
Oxide Synthase ◽  
Subclinical Endometritis ◽  
Inducible Nitric Oxide

Abstract The expression of CD14+ macrophages, CD4+, CD8+ lymphocytes and mRNA of inducible nitric oxide synthase (iNOS) was investigated in the endometrium of repeat breeders with subclinical endometritis [experimental group (EXP), n = 10] and healthy [control group (CTRL), n = 10] cows. The cows were selected on the basis of repeat breeding (3 unsuccessful inseminations), clinical and cytological examinations (> 10% polymorphonuclear neutrophils in uterine smears obtained by cytobrush). From all the cows endometrial biopsies were collected and the presence of CD14+, CD4+ and CD8+ cells in the endometrium was evaluated immunohistochemically using semi quantitative counting method. The mRNA expression of iNOS was determined using reverse transcription-PCR. In general, there were no significant differences between EXP and CTRL groups in the expression of CD4+ and CD8 + lymphocytes in all endometrial structures. In contrast, we observed a higher number of CD14+ macrophages in repeat breeding group compared to the control cows, however, this difference was slightly pronounced. CD14+ cells were detectable only in the stratum compactum and stratum spongiosum. The statistically significant (p ≤ 0.05) higher expression of iNOS mRNA was measured in the cows with subclinical endometritis compared to the healthy animals. Our results suggest that the increased expression of CD14+ macrophages and iNOS mRNA may be associated with embryonal mortality in repeat breeding cows with subclinical endometritis.

Prolonged colonic epithelial hyporesponsiveness after colitis: role of inducible nitric oxide synthase

1999 ◽  
Vol 276 (3) ◽  
pp. G703-G710 ◽  
Author(s):  
Samuel Asfaha ◽  
Cameron J. Bell ◽  
John L. Wallace ◽  
Wallace K. MacNaughton
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Mucosal Inflammation ◽  
Inos Mrna ◽  
Trinitrobenzenesulfonic Acid ◽  
Ussing Chambers ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Colonic epithelial secretion is an important host defense mechanism. We examined whether a bout of colitis would produce long-lasting changes in epithelial function that persisted after resolution of mucosal inflammation. Colitis was induced in rats with intracolonic trinitrobenzenesulfonic acid. Six weeks later, colonic damage and inducible nitric oxide synthase (iNOS) mRNA expression and activity were measured. Segments of distal colon were mounted in Ussing chambers for measurement of permeability and responsiveness to secretory stimuli. Basal electrolyte transport parameters and permeability were not different from untreated controls. Despite normal macroscopic and histological appearance, secretory responses to electrical field stimulation (EFS), isobutylmethylxanthine (IBMX), and carbachol were significantly depressed (by 60–70%) relative to controls. iNOS mRNA expression and enzyme activity were significantly elevated. Dexamethasone reversed epithelial hyporesponsiveness and significantly reduced iNOS mRNA expression. A selective iNOS inhibitor normalized the secretory responses to EFS and IBMX but not to carbachol. These data suggest that ongoing synthesis of nitric oxide by iNOS contributes to chronic suppression of epithelial secretory function after episodes of colitis.

Effects of macrophage inducible nitric oxide synthase in murine septic lung injury

2006 ◽  
Vol 290 (6) ◽  
pp. L1164-L1172 ◽  
Author(s):  
K. S. Farley ◽  
L. F. Wang ◽  
H. M. Razavi ◽  
C. Law ◽  
M. Rohan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Lung Injury ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Cecal Ligation ◽  
Intratracheal Instillation ◽  
Inos Mrna ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Inducible nitric oxide synthase (iNOS) contributes importantly to septic pulmonary protein leak in mice with septic acute lung injury (ALI). However, the role of alveolar macrophage (AM) iNOS in septic ALI is not known. Thus we assessed the specific effects of AM iNOS in murine septic ALI through selective AM depletion (via intratracheal instillation of clodronate liposomes) and subsequent AM reconstitution (via intratracheal instillation of donor iNOS+/+ or iNOS−/− AM). Sepsis was induced by cecal ligation and perforation, and ALI was assessed at 4 h: protein leak by the Evans blue (EB) dye method, neutrophil infiltration via myeloperoxidase (MPO) activity, and pulmonary iNOS mRNA expression via RT-PCR. In iNOS+/+ mice, AM depletion attenuated the sepsis-induced increases in pulmonary microvascular protein leak (0.3 ± 0.1 vs. 1.4 ± 0.1 μg EB·g lung−1·min−1; P < 0.05) and MPO activity (37 ± 4 vs. 67 ± 8 U/g lung; P < 0.05) compared with that shown in non-AM-depleted mice. In AM-depleted iNOS+/+ mice, septic pulmonary protein leak was restored by AM reconstitution with iNOS+/+ AM (0.9 ± 0.3 μg EB·g lung−1·min−1) but not with iNOS−/− donor AM. In iNOS−/− mice, sepsis did not induce pulmonary protein leak or iNOS mRNA expression, despite increased pulmonary MPO activity. However, AM depletion in iNOS−/− mice and subsequent reconstitution with iNOS+/+ donor AM resulted in significant sepsis-induced pulmonary protein leak and iNOS expression. Septic pulmonary MPO levels were similar in all AM-reconstituted groups. Thus septic pulmonary protein leak is absolutely dependent on the presence of functional AM and specifically on iNOS in AM. AM iNOS-dependent pulmonary protein leak was not mediated through changes in pulmonary neutrophil influx.

Effects of chronic inhibition of inducible nitric oxide synthase in hyperthyroid rats

2005 ◽  
Vol 288 (6) ◽  
pp. E1252-E1257 ◽  
Author(s):  
Isabel Rodríguez-Gómez ◽  
Rosemary Wangensteen ◽  
Juan Manuel Moreno ◽  
Virginia Chamorro ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Control Group ◽  
Hemodynamic Variable ◽  
Male Wistar Rats ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Inducible Nitric Oxide

We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphological and renal variables in hyperthyroid rats were analyzed. The following four groups ( n = 8 each) of male Wistar rats were used: control group and groups treated with AG (50 mg·kg−1·day−1, via drinking water), thyroxine (T4, 50 μg·rat−1·day−1), or AG + T4. All treatments were maintained for 3 wk. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats and morphological, plasma, and renal variables. T4 administration produced a small BP (125 ± 2, P < 0.05) increase vs. control (115 ± 2) rats. AG administration to normal rats did not modify BP (109 ± 3) or any other hemodynamic variable. However, coadministration of T4 and AG produced a marked increase in BP (140 ± 3, P < 0.01 vs. T4). Pulse pressure and HR were increased in both T4- and T4 + AG -treated groups without differences between them. Plasma NOx (μmol/l) were increased in the T4 group (10.02 ± 0.15, P < 0.05 vs. controls 6.1 ± 0.10), and AG reduced this variable in T4-treated rats (6.81 ± 0.14, P < 0.05 vs. T4) but not in normal rats (5.78 ± 0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T4.

Prostasin attenuates inducible nitric oxide synthase expression in lipopolysaccharide-induced urinary bladder inflammation

2006 ◽  
Vol 291 (3) ◽  
pp. F567-F577 ◽  
Author(s):  
Li-Mei Chen ◽  
Cindy Wang ◽  
Mengqian Chen ◽  
Matthew R. Marcello ◽  
Julie Chao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Cytokine Signaling ◽  
Bladder Inflammation ◽  
Tnf Α ◽  
Cox 2 ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Prostasin is a glycosylphosphatidylinositol-anchored serine protease, with epithelial sodium channel activation and tumor invasion suppression activities. We identified the bladder as an expression site of prostasin. In the mouse, prostasin mRNA expression was detected by reverse transcription and real-time polymerase chain reaction in the bladder, and the prostasin protein was localized by immunohistochemistry in the urothelial cells. In mice injected intraperitoneally with bacterial lipopolysaccharide (LPS), bladder prostasin mRNA expression was downregulated, whereas the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interferon-γ (IFN-γ), TNF-α, IL-1β, and IL-6 was upregulated. Viral promoter-driven expression of the human prostasin homolog in the bladder of transgenic mice attenuated the LPS induction of iNOS but did not abolish the induction. LPS induction of COX-2, TNF-α, IL-1β, and IL-6 expression, however, was not reduced by prostasin transgene expression. Liposome-mediated delivery of prostasin-expressing plasmid into mouse bladder produced similar attenuation effects on LPS-induced iNOS expression, while not affecting COX-2 or cytokine induction. Mice receiving plasmid expressing a catalytic mutant prostasin did not manifest the iNOS induction attenuation phenotype. We propose a proteolytic mechanism for prostasin to intercept cytokine signaling during LPS-induced bladder inflammation.

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