Background/Aim: The omentum has an important role as part of peritoneal defense mechanisms. The aim of this study is to show the bactericidal activity of peritoneal fluid and the role of the omentum as a peritoneal defense mechanism in experimental animals with intra-abdominal infections. Methods: 40 male Spraque-Dawley rats weighing between 250 and 300 g were used in this study. The rats were randomly divided into four groups consisting of 10 animals. The operative procedures were done under sterile conditions. In group I sham laparotomy was done. In group II, the distal part of the cecum was ligated, and cecum perforation was performed. In group III, total omentectomy was performed after cecal ligation and perforation. In group IV only omentectomy was performed. Baseline and 2- and 4-hour peritoneal fluid samples were taken using a Pasteur pipette during laparotomy under anesthesia. Total peritoneal cells counts, bactericidal activity of peritoneal fluid, and types of phagocytic cells in the peritoneal fluid were assessed. Results: As compared with baseline values, the total peritoneal cell counts were increased at the 2nd and 4th h in all groups (p < 0.05). A significant increase was observed after 4 h as compared with 2 h in sham laparotomy, cecal ligation+perforation+omentectomy, and omentectomy groups (p < 0.05). A significant increase in the cell counts after 2 h was found in the other groups when compared to the sham laparotomy group (p = 0.0001). After 4 h, there was a significant difference between the groups, but especially prominent in the cecum ligation+perforation+omentectomy group (p = 0.0001). Proliferating colony counts of Escherichiacoli and Pseudomonas aeruginosa decreased after 2 h, and there was no proliferation in the subsequent cultures. It was observed that the macrophage counts significantly increased after 2 and 4 h as compared with baseline in intragroup assessments (p = 0.0001). In the intergroup assessment, an increase was observed in the macrophage counts at baseline and after 2 and 4 h, and this was significant in the cecal ligation+perforation+omentectomy group (p = 0.0001). In the omentectomy group, a significant decrease was observed in the macrophage counts between the 2nd and 4th h (p = 0.0001). Conclusion: Removal of the omentum in the presence of intra-abdominal infections causes the peripherally derived macrophages to take over the defensive role of macrophages of peritoneal origin as a compensatory mechanism, thus the peritoneal bactericidal activity against E. coli, the major pathogen in intra-abdominal infections, does not change after omentectomy.
Single nucleotide polymorphisms (SNPs) in the human angiotensinogen (hAGT) gene may modulate its transcription and affect the regulation of blood pressure via activation of the renin-angiotensin aldosterone system (RAAS). In this regard, we have identified polymorphisms in the 2.5 Kb promoter of the hAGT gene that form two haplotype (Hap) blocks: -6A/G (-1670A/G, -1562C/T, -1561T/C) and -217A/G (-532T/C, -793A/G, -1074T/C & -1178G/A). hAGT gene with Hap -6A/-217A (Hap I) is associated with increased blood pressure whereas, Hap -6G/-217G (Hap II) is associated with normal blood pressure in human subjects. Since RAAS over activity contributes to hypertension in obesity, we have made transgenic mice (TG) containing either Hap I or Hap II of the hAGT gene to understand the role of obesity on its transcriptional regulation. Although, a high-fat diet (60% Kcal from fat, 12 weeks) elevates hAGT and mAGT regardless of haplotype, this effect is significantly (p<0.05) accentuated in Hap I mice, in both adipose and liver tissues. Chromatin Immuno- precipitation (ChIP) assay shows an increased binding of transcription factors including, GR, CEBPβ and STAT3 to the chromatin of the Hap I TG mice after high-fat diet as compared to Hap II TG mice (p<0.05). Differential plasma levels of hAGT in Hap II and I mice, after high-fat diet, further corroborate the variable transcriptional regulation of the hAGT, governed by gene-haplotypes. Taken together, our results show that SNPs in the Hap-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-β and STAT3, which lead to elevated expression of the hAGT gene in hepatic and adipose tissues.
To investigate the effects of pneumoperitoneum on the peritoneal defense mechanism induced by streptozocin infusion during laparoscopic surgery in diabetic rats and to show the importance of regulation of diabetes for peritoneal defense mechanisms. One hundred twenty-six Sprague-Dawley male rats were allocated into six groups each consisting of 21 rats: group 1, nondiabetic sham laparotomy (control); group 2, nondiabetic pneumoperitoneum (control); group 3, uncontrolled diabetes plus sham laparotomy; group 4, controlled diabetes plus sham laparotomy; group 5, uncontrolled diabetes plus pneumoperitoneum; and group 6, controlled diabetes plus pneumoperitoneum. Diabetes was constituted by intraperitoneal infusion of one dose of 60 mg/kg streptozotocin, and diabetes was regulated (in groups 4 and 6) by subcutaneous injection of 10 IU/kg insulin in the morning and evening after the blood glucose measurements since the fourth day. Peritoneal fluid samples were taken at the zero, second, and sixth hours after sham laparotomy for groups 1, 3, and 4 and after pneumoperitoneum for groups 2, 5, and 6 on the seventh day. Total peritoneal cell count, antibacterial activity of the peritoneal fluid, and types of phagocytic cells in the peritoneal fluid were assessed. Peritoneal cell count was found to be lower in uncontrolled diabetes due to high blood glucose levels (>200 mg/dL), which led to slow migration of phagocytic cells into the peritoneum. Pneumoperitoneum had augmented the effect on phagocytic cell migration to the peritoneum compared with the sham laparotomy in controlled diabetic rats. Uncontrolled and controlled diabetes have adverse effects on peritoneal defense mechanism killing functions by interfering with the antimicrobial activity of peritoneal fluid.
Angiotensin II (Ang II) contributes to the pathophysiologies of cardiovascular and renal systems. Angiotensin receptor type 1 (AT1R) mediates these effects, and genetic variations that increase AT1R can increase these pathological outcomes. Physiological variables like age or pathologies like the metabolic syndrome alter the transcriptional milieu of cells and can provide for feedback activation of genes. In this regard, we have identified two haplotype blocks of single nucleotide polymorphisms (SNPs) in the hAT1R gene: haplotype II (Hap II: -810A, -713G, -214C, -153G) and I (Hap I: -810T, -713T, -214A, -153A). In clinical studies, Hap I is linked to human hypertension. We have generated transgenic mice (TG) with haplotypes-II and I of the hAT1R gene to study its regulation during metabolic syndrome (MetS). At baseline, ChIP assay shows increased RNA-Pol II binding (~1.6 fold higher) to the chromatin extracts from renal tissues of adult (4-6 months) male Hap I-TG mice with increased hAT1R expression (~6 fold higher). This was accompanied by higher baseline blood pressure in Hap I-TG mice (Hap I- 126±3 vs. Hap II- 115±4, p<0.05). To induce MetS, these mice were fed Western diet (45% Kcal from fat and carbohydrate each) for 12 wks. Change in body weight is higher (p<0.05) in Hap I (161.5 gm.) vs. Hap II (10.41.2 gm.) mice. MetS phenotype is characterized by increase in blood pressure that is significantly greater in Hap I mice (1362 vs. 1203 in Hap II). Transcription factors, p38/MAPK and STAT3, were induced by MetS to similar extent in both groups. However, MetS-induced up regulation of the hAT1R gene is significantly higher in vascular tissues of Hap I mice (≈6 fold), when compared to Hap II. Complementary experiments show increased inflammatory and redox markers in vascular tissues of Hap I mice, when compared to Hap II, during MetS; including, IL1 (2.2 fold), IL6 (1.8 fold), NOX1 (3.5 fold), VEGF (1.5 fold), and ICAM1 (14 fold). Thus, haplotype-dependent transcriptional regulation of the hAT1R gene causes increased hAT1R expression and blood pressure, in Hap I TG mice. Importantly, MetS exacerbates this differential gene-expression regulation, further increasing hAT1R and promoting a prooxidant/inflammatory milieu in mice with Hap I.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.