A monoclonal antibody against the CD18 leukocyte adhesion molecule prevents indomethacin-induced gastric damage in the rabbit

Wallace, John L.; Arfors, Karl-E.; McKnight, G. Webb

doi:10.1016/0016-5085(91)90259-n

Cited by 267 publications

(114 citation statements)

References 16 publications

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“…Unsaturated lipids are particularly sensitive to free-radical attack (9). Which free radicals induced cell damage in the intestinal mucosa is not clear, but many studies suggest that neutrophils may play an important role in the production of active radicals (28,(37)(38)(39). Gram-negative rods like Helicobacter pylori contain lipopolysaccharides which can activate neutrophils (13, 23).…”

Section: Discussionmentioning

confidence: 99%

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

Kinouchi

Kataoka

Bing

et al. 1998

Microbiology and Immunology

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A nonsteroidal antiinflammatory drug, 5-bromo-2-(4-fluoropheny1)-3-(4-methylsulfonylphenyl) thiophene (BFMeT), induced ileal ulcers in rats after oral administration, while no ulcers were observed after subcutaneous injection. The ileal ulcer formation in BFMeT-treated rats was examined to correlate the administration of cultures of Lactobacillus acidophilus or Bifidobacterium adolescentis with intestinal bacteria in the ileal contents and lipid peroxidation of the small intestinal mucosa. Ileal ulcers were observed in more than 85% of the rats treated with BFMeT at a dose of 1,000 mg/kg when they were given tap water as drinking water. The incidence of ulcer formation was repressed by giving culture supernatants of L. acidophilus or B. adolescentis as drinking water, but not by giving the cell suspension as drinking water. Gram staining of the ileal contents of normal rats revealed that 97 % of the stained bacteria were Gram-positive rods and only 1.5% were Gram-negative rods. The percentage of Gram-negative rods 72 hr after BFMeT administration was 49.8% and increased over 30-fold in BFMeT-treated rats. However, the percentage of Gram-negative rods was 9.7% or 16%, respectively, in rats taking culture supernatants of L. acidophilus or B. adolescentis. In addition, thiobarbituric acid-reactive substances in the ileal mucosa increased significantly in the rats given tap water for 72 hr after BFMeT treatment, but not in rats given the culture supernatants of L. acidophilus or B. adolescentis. Since BFMeT induced an unbalanced intestinal microflora, the effect of antibiotic treatment on ulcer formation in rats was examined. The magnitude of the ulcer formation in the antibiotic-treated rats was, in decreasing order, metronidazole > none > kanamycin > a mixture (bacitracin, neomycin and streptomycin). These results suggest that the intestinal microflora plays an important role in ulcer formation and that a metabolite(s) of L. acidophilus and B. ado-, lescentis inhibits ileal ulcer formation by repressing changes in the intestinal microflora and lipid peroxidation in BFMeT-treated rats.

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Section: Discussionmentioning

confidence: 99%

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

Kinouchi

Kataoka

Bing

et al. 1998

Microbiology and Immunology

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“…As incubating PMN in Ca 2+ -free medium in the presence of EGTA prevented NSAID-induced Mac-1 upregulation, we investigated whether the effect of indomethacin on Mac-1 expression was mirrored by agents that cause Ca 2+ mobilization. Figure 2 (upper panel) demonstrates that FMLP, LTB 4 , ionomycin and thapsigargin were all able to upregulate MAC-1 expression. Again the effect was signi®cantly reduced by preincubating the cells in a Ca 2+ -free medium in the presence of Ca 2+ -chelating agents (Figure 2, lower panel).…”

Section: Effect Of Indomethacin On Mac-1 Expression On Human Pmnmentioning

confidence: 99%

“…10±12 Two different classes of receptors have been described: (i) the G protein-linked seven-transmembrane-domain receptors, such as those for formylated peptide (FMLP), LTB 4 , interleukin 8 (IL-8), lipopolysaccaride (LPS) and complement component 5a; and (ii) the single transmembrane-domain receptors for growth-regulating cytokines such as tumour necrosis factor-a (TNFa) and granulocyte-macrophage colony-stimulating factor (GM-CSF), and Fc and integrin receptors. 13,14 Activation of cell-surface receptors triggers either intracellular calcium (Ca 2+ ) mobilization or protein tyrosine phosphorylation.…”

Section: Introductionmentioning

confidence: 99%

NSAIDs upregulate β₂‐integrin expression on human neutrophils through a calcium‐dependent pathway

Fiorucci

Santucci

Gerli

et al. 1997

Aliment Pharmacol Ther

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Background: Margination of circulating neutrophils (PMN) into the gastric microcirculation is an early and critical event in the pathogenesis of non‐steroidal antinflammatory drug (NSAID)‐induced gastropathy. This effect is mediated through the upregulation of β2 integrins on the PMN surface. Aims: To investigate whether indomethacin modulates: (1) Mac‐1 expression; (2) Ca2+ mobilization ([Ca2+]i), protein kinase C and nitric oxide accumulation; and (3) mitogen‐associated protein kinase phosphorylation in human PMN. Methods: Human PMN were isolated by centrifugation through a double Ficoll gradient. [Ca2+]i was measured in PMN loaded with fura‐2 and Mac‐1 expression by flow cytometry. Results: Indomethacin caused a concentration‐ and time‐dependent upregulation of CD11b and CD18 expression and PMN adhesion to endothelial cells. Maximal upregulation of Mac‐1 expression (40–50%) occurred after a 30‐min incubation with 0.1 mM indomethacin. The effect was prevented by removing the Ca2+. Ionomycin and thapsigargin caused a 7–10‐fold increase in [Ca2+]i and a 2–4‐fold increase in Mac‐1 expression. Indomethacin induced a concentration‐dependent phosphorylation of a 41‐kDa mitogen‐associated protein kinase. Tyrosine kinase inhibitors prevented the effect of indomethacin on Mac‐1 expression and Ca2+ mobilization. Indomethacin and ionomycin increased superoxide generation, myeloperoxidase secretion and PMN adherence to endothelial cells and stimulated nitric oxide production. Indomethacin‐induced Mac‐1 upregulation was prevented by a nitric oxide synthase inhibitor. Conclusions: Indomethacin‐induced upregulation of Mac‐1 is mediated by changes in [Ca2+]i and nitric oxide. Phosphorylation of the 41‐kDa mitogen‐associated protein isoform is a previously unreported target of NSAID action. These effects might help to explain the ability of indomethacin to cause gastric neutrophil margination.

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“…Naturally, it is as a result of imbalance between the aggressive damaging effects of gastric acid, pepsin, lipid peroxidation, refluxed bile, abnormal motility etc. and the defense mechanisms, which protect the gastric and duodenal mucosa [1] [2]. The exogenous aggressive factors like Helicobacter pylori, indiscriminate use of non-steroidal anti-inflammatory drugs (NSAIDs), alcohol abuse and smoking have also long been identified as major contributor in the pathogenesis of peptic ulcer disease [3].…”

Section: Introductionmentioning

confidence: 99%

Folic Acid Supplementation Ameliorates Inflammation and Apoptosis in Ethanol-Induced Gastric Ulceration in Rats

Ajeigbe¹,

Jaja²,

Onifade³

et al. 2017

JBM

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Although the gastroprotective potential of folic acid has been reported, little is known about the role of inflammation and apoptosis in the said activity. This study, therefore, assessed lipid peroxidation (LPO), Neutrophil-lymphocyte ratio (NLR), C-reactive protein (CRP) as markers of inflammation and, p53 and BCl-2 as markers of apoptosis in ethanol-induced gastric ulcer pretreated with Folic acid (FA) for twenty-one (21) days. Adult male Wistar rats were arranged into experimental groups (n = 5) viz: 1) Control; 2) Ulcer control; 3) 2FA (2 mg/kg folic acid + Ulcer); 4) 3FA (3 mg/kg folic acid + Ulcer); 5) OMEP (20 mg/kg omeprazole + Ulcer); 6) 2FA + OMEP + Ulcer; and 7) 3FA + OMEP + Ulcer. Ulcer score, LPO, NLR, serum CRP were all determined one hour post ulcer induction. Paraffin gastric sections were stained first with H & E, then immunostained for p53 and BCl-2. Ethanol caused gastric lesion with an index of 3.0 ± 0.2. Ulcer severity and LPO was significantly decreased in the 2FA, 3FA, OMEP, 2FA + OMEP and 3FA + OMEP groups. NLR reduced significantly in the 2FA, 3FA, OMEP and OMEP + 3FA group. Qualitatively, there was absence of C-reactive protein in the 2FA group while quantitatively, presence of CRP appeared sustained in the 3FA and OMEP treated groups. Unlike p53, the expression and labeling index of BCl-2 were significantly enhanced more in the FA and OMEP combination than OMEP alone. Folic acid ameliorates the development of gastric ulcer in rats via its anti-inflammatory and anti-apoptotic activities.

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A monoclonal antibody against the CD18 leukocyte adhesion molecule prevents indomethacin-induced gastric damage in the rabbit

Cited by 267 publications

References 16 publications

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

NSAIDs upregulate β₂‐integrin expression on human neutrophils through a calcium‐dependent pathway

Folic Acid Supplementation Ameliorates Inflammation and Apoptosis in Ethanol-Induced Gastric Ulceration in Rats

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A monoclonal antibody against the CD18 leukocyte adhesion molecule prevents indomethacin-induced gastric damage in the rabbit

Cited by 267 publications

References 16 publications

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

Culture Supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis Repress Ileal Ulcer Formation in Rats Treated with a Nonsteroidal Antiinflammatory Drug by Suppressing Unbalanced Growth of Aerobic Bacteria and Lipid Peroxidation

NSAIDs upregulate β2‐integrin expression on human neutrophils through a calcium‐dependent pathway

Folic Acid Supplementation Ameliorates Inflammation and Apoptosis in Ethanol-Induced Gastric Ulceration in Rats

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NSAIDs upregulate β₂‐integrin expression on human neutrophils through a calcium‐dependent pathway