Chemotaxis and degranulation of polymorphonuclear leukocytes in the presence of sulfide

Persson, Sven‐Åke; Claesson, Rolf; Carlsson, Jan

doi:10.1111/j.1399-302x.1993.tb00542.x

Cited by 18 publications

(5 citation statements)

References 20 publications

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“…Purified leukotoxin (final concentration 200 µg /ml) was mixed with 10 µg/ml elastase or cathepsin G (Sigma‐Aldrich) or with supernatant of PMNL (2.5×10 7 cells/ml) that had been stimulated to degranulate by incubation with 10 µM cytochalasin B (Sigma‐Aldrich) and 2.5 µM formyl methionine leucine phenylalanine (FMLP; Sigma‐Aldrich) for 5 min at 37°C. The concentration of elastase or cathepsin G released from the stimulated PMNL was about 10 µg enzyme per ml supernatant, which is in accordance with what has been reported previously (13). The mixtures of leuktoxin and PMNL enzymes were incubated for up to 60 min and aspirated samples were added to an equal volume of sample buffer (50 mM Tris‐buffer, pH 7.4, containing 2% SDS, 0.03% bromphenol blue and 20% sucrose) and heated (100°C, 5 min).…”

Section: Methodssupporting

confidence: 92%

Protease inhibitors, the responsible components for the serum‐dependent enhancement of Actinobacillus actinomycetemcomitans leukotoxicity

Johansson

Claesson

Belibasakis

et al. 2001

European J Oral Sciences

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Serum enhances the leukotoxic activity of Actinobacillus actinomycetemcomitans against human polymorphonuclear leukocytes (PMNL) by a mechanism that still is unknown. Early attempts to identify the serum components responsible for this enhancement gave no conclusive results, but indicated that the lipoprotein-containing fraction of the serum was involved in the interaction. This study aimed to clarify the role of serum lipoproteins in the leukotoxin interaction, and to identify other serum components involved. The main hypothesis examined was that the leukotoxicity enhancement might depend on serum protease inhibitors that block proteolytic cleavage of leukotoxin by enzymes released from the leukocytes. PMNL were isolated from human peripheral blood and incubated with purified leukotoxin in the presence of serum or purified serum components or lipoprotein-deficient serum. Leukotoxin was also incubated with purified elastase and cathepsin G or with enzyme mixtures from degranulated PMNL. The leukotoxic activity in these mixtures was determined as the extracellular release of lactate dehydrogenase from PMNL. Cleavage of the toxin was showed by gel electrophoresis and Western blot. Morphological changes in PMNL from the above mixtures were examined by electron microscopy. Enzymes from degranulated PMNL cleaved leukotoxin to non-cytotoxic fragments. Elastase and cathepsin G were mainly responsible for the cleavage. Inhibition of leukotoxin degradation was found in the presence of whole serum or of the serum protease inhibitors alpha2-macroglobulin and alpha1-proteinase inhibitor. Under these conditions enhanced PMNL lysis was also observed. A similar enhancement of PMNL lysis was found when PMNL degranulation was blocked by EDTA. On the other hand, lipoprotein-deficient serum had no influence on the leukotoxic activity. The results indicate that the increased leukotoxicity of A. actinomycetemcomitans observed in the presence of human serum is caused by the serum protease inhibitors that counteract proteolytic degradation of leukotoxin. The degradation is caused by enzymes from degranulated PMNL triggered by leukotoxin.

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Section: Methodssupporting

confidence: 92%

Protease inhibitors, the responsible components for the serum‐dependent enhancement of Actinobacillus actinomycetemcomitans leukotoxicity

Johansson

Claesson

Belibasakis

et al. 2001

European J Oral Sciences

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“…In our study NaHS exerted a negative chemotactic effect on spermatozoa in vitro. A similar phenomenon was observed when polymorphonuclear leukocytes (PMN) were incubated in a 1-2 mmol/l H 2 S solution (PERSSON et al 1993). Analogically, in the experiment of Fang and colleagues, H 2 S decreased human lung fibroblast (MRC5) migration stimulated by fetal bovine serum (FBS) and basic fibroblast growth factor (bFGF) and their proliferation.…”

Section: Tablesupporting

confidence: 54%

Sodium Hydrosulfide Exerts a Transitional Attenuating Effect on Spermatozoa Migration <I>in Vitro</I>

Wiliński¹,

Wiliński²,

Gajda³

et al. 2015

folia biol (krakow)

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Hydrogen sulfide (H S) has been shown to have a prominent role in the regulation of reproductive system function and fertility. The aim of the study was to assess the effect of a H S donor, sodium hydrosulfide (NaHS), on mouse sperm migration in vitro. Special plates with 4 corner wells filled with balanced salt solution (control) and various NaHS solutions in concentrations of 2.5 mmol/l, 5 mmol/l or 10 mmol/l were applied. Spermatozoa from each male mouse were injected (the experiment was repeated with ten BALB/c 5-month old males) into the central pocket, connected with the wells with ducts. After 1 h, 2 h and 4 h of incubation, the number of spermatozoa in each well was determined using Bürkers counting chambers. The number of spermatozoa in all corner wells were summed and the number of the cells in each well was treated as the percentage share of all the migrated spermatozoa. At the time points of 1 hour and 4 hours, no differences regarding chemotactic features of spermatozoa to the utilized solutions were observed. After two hours of incubation the attenuating effect of NaHS medium and high level solutions on spermatozoa migration was observed, but not for the low concentration mixture: H(3, N = 40) = 9.65, P = 0.022; control group vs 5 mmol/l NaHS solution: 36.0% vs 18.5%, P = 0.023; control group vs 10 mmol/l NaHS solution group: 36.0% vs 17.0%, P = 0.011. In conclusion, NaHS has a transitional attenuating effect on spermatozoa migration in vitro.

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“…This was found to be the case in healthy mucosa but remains untested in the inflamed mucosa. Immune cells are tolerant of high levels (>1.5 mM) of hydrogen sulphide31 and may have considerable TMT activity. Apart from such a drawback, the methodology of the assay was carefully applied 28…”

Section: Discussionmentioning

confidence: 99%

Thiol methyltransferase activity in inflammatory bowel disease

Roediger

2000

Gut

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Background-Luminal anionic sulphide may contribute to epithelial damage in ulcerative colitis. Thiol methyltransferase (TMT) governs sulphide detoxification by the colonic mucosa and circulating erythrocytes. Aims-To measure levels of TMT activity in erythrocytes of surgically treated cases of colitis or in rectal biopsies of defined groups of colitis. Patients-Venepuncture blood was obtained from 37 blood donors and 27 subjects who had previously undergone a proctocolectomy for colitis: 18 for ulcerative colitis and nine for Crohn's colitis. Rectal biopsies from 122 cases were obtained: 47 without mucosal disease, 33 post-colon resection for cancer, 14 with moderate to severe ulcerative colitis, 15 with quiescent ulcerative colitis, seven with acute Crohn's colitis, and six with radiation proctitis. Methods-TMT activity was measured by high performance liquid chromatography with radioactive detection to measure 14 C methylmercaptoethanol formation, the reaction product of cell extracts incubated with mercaptoethanol and 14 C S-adenosylmethionine. Results-Erythrocyte TMT activity of surgically treated cases of colitis was significantly elevated (p<0.001) compared with control cases. TMT activity of rectal biopsies was significantly decreased (p<0.02) in acute but not quiescent ulcerative colitis, Crohn's colitis, or radiation colitis. Conclusions-Erythrocyte TMT activity was persistently elevated after proctocolectomy for Crohn's disease and ulcerative colitis. No primary defect of TMT activity was found in any case of unoperated colitis but mucosal activity was diminished with disease progression of ulcerative colitis. Studies of genetic control of TMT activity of erythrocytes in inflammatory bowel disease appear worthwhile.

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Chemotaxis and degranulation of polymorphonuclear leukocytes in the presence of sulfide

Cited by 18 publications

References 20 publications

Protease inhibitors, the responsible components for the serum‐dependent enhancement of Actinobacillus actinomycetemcomitans leukotoxicity

Protease inhibitors, the responsible components for the serum‐dependent enhancement of Actinobacillus actinomycetemcomitans leukotoxicity

Sodium Hydrosulfide Exerts a Transitional Attenuating Effect on Spermatozoa Migration <I>in Vitro</I>

Thiol methyltransferase activity in inflammatory bowel disease

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