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Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 721 records · Page 40Linked to original sources
PubMed1998

Biologically active oligodeoxyribonucleotides. Part 11: The least phosphate-modification of quadruplex-forming hexadeoxyribonucleotide TGGGAG, bearing 3-and 5-end-modification, with anti-HIV-1 activity.

We have found that a hexadeoxyribonucleotide (5'TGGGAG3', R-95288), Koizumi, M. et al. Bioorganic & Medicinal Chemistry, 1997, 5, 2235, bearing a 3,4-dibenzyloxybenzyl (3,4-DBB) group at the 5'-end and a 2-hydroxyethylphosphate at the 3'-end, has high anti-HIV-1 activity and the least cytotoxicity in vitro and in vivo. In order to synthesize more potent hexadeoxyribonucleotides, we substituted phosphodiester (P-O) bonds in the 6-mer with the least phosphorothioate (P-S), phosphoramidate (P-N), or methylphosphonate (P-Me) bonds. When more than two P-N or P-Me bonds were introduced into a 6-mer, the phosphate-modified 6-mers had weak or no anti-HIV- activity, in spite of quadruplex structure formation. However, when P-S bonds were substituted for P-O bonds, anti-HIV-1 activity of their 6-mers did not dramatically decrease, compared with compounds substituted with P-N or P-Me bonds. The results suggest that the formation of a quadruplex structure is not always sufficient for anti-HIV-1 activity of the 6-mer, and that net negative charges derived from P-O or P-S bonds in the quadruplex are important for anti-HIV-1 activity. Moreover, among various phosphate-modified ODNs, we found that the anti-HIV-1 activity of ODN PS7 with only one P-S bond was the same as that of R-95288, both having a high stability in human plasma.

Anti-HIV Agents↗
PubMed1998

Three-dimensional microanatomy of perineuronal proteoglycan nets enveloping motor neurons in the rat spinal cord.

Spinal motor neurons possess reticular coats of extracellular matrix proteoglycans on their somata and proximal dendrites. In order to define the anatomical background of the network, spatial relationships of the perineuronal proteoglycans with synaptic boutons and astrocyte processes were analyzed in rat motor neurons by TEM after histochemical detection of the substances with cationic iron colloid, and by SEM after exposure of the cytoarchitecture with NaOH maceration. Narrow intercellular channels filled with proteoglycan were found to extend along the surface of the neurons to form a homogeneous network of a mesh size of about 1 microm. The system of perineuronal channels consisted of two parts: a primary intervaricose net which meandered among synaptic boutons on the surface of the motor neuron, and secondary subvaricose nets which irrigated interfaces between larger boutons and the neuron. No elements in the perineuronal cytoarchitecture coincided with the meshwork of proteoglycan, indicating the involvement of postsynaptic factors in the distribution of the substance. Thin astrocyte processes surrounding the neurons formed a distinct network with heterogeneous meshes corresponding to boutons of various sizes. The perineuronal glial nets extended their surface area in contact with the intervaricose nets of proteoglycan by complex cellular interdigitations. The subvaricose nets of proteoglycan compartmentalized multiple synapses on large boutons, suggesting an involvement in the division of the synapses during development.

Animals↗
PubMed1998

Molecular analyses of the Cu/Zn superoxide dismutase gene in patients with familial amyotrophic lateral sclerosis (ALS) in Japan.

1. Amyotrophic lateral sclerosis (ALS) is a degenerative disorder characterized by selective damage to the neural system that mediates voluntary movement. Although the pathophysiologic process of ALS remains unknown, about 5 to 10% of cases are familial. According to genetic linkage studies, the familial ALS (FALS) gene has been mapped on chromosome 21 in some families and recent work identified some different missense mutations in the Cu/Zn superoxide dismutase gene in FALS families. 2. We recently identified five mutations in six FALS families. The mutations identified in our FALS families are H46R, L84V, I104F, S134N, and V148I. The H46R mutation that locates in the active site of Cu/Zn SOD gene is associated with two Japanese families with very slow progression of ALS. On the other hand, the L84V mutation associated with a rapidly progressive loss of motor function with predominant lower motor neuron manifestations. 3. In the family with the V148I, the phenotype of the patient varied very much among the affected members. One case had weakness of the lower extremities at first and died without bulbar paresis. The second case first noticed wasting of the upper limbs with bulbar symptoms, but the third had weakness of upper extremities without developing dysarthria nor dysphagia until death. These mutations account for 50% of all FALS families screened, although Cu/Zn SOD gene mutations are responsible for less than about 13-21% in the Western population. 4. Our results indicate that the progression of disease with mutations of Cu/Zn SOD is well correlated with each mutation. The exact mechanism by which the abnormal Cu/Zn SOD molecules selectively affect the function of motor neurons is still unknown.

Adult↗
PubMed1998

Stress protein inductions after brain ischemia.

1. Hippocampal CA1 neurons are the most vulnerable to transient cerebral ischemia. However, the mechanism has not been fully understood. 2. The mRNAs for 72-kd (HSP72) and 73-kd (HSC73) heat shock proteins (HSPs), which are located mainly in the cytoplasm, were greatly induced together in CA1 cells, with a peak at 1-2 days in gerbils. However, immunoreactive HSP72 protein was only minimally expressed in CA1 neurons. 3. The mRNA for mitochondrial HSP60 began to increase at 3 hr in CA1 cells and was sustained until 1 day. 4. The level of mRNA for cytochrome c oxidase subunit I (COX-I) progressively decreased in CA1 neurons after a transient ischemia and completely disappeared at 7 days. The activity of cytochrome c oxidase (COX) protein also showed an early decrease in CA1 cells and was followed by a reduction in the level of COX-I DNA after 2 days. 5. These results suggest that HSP gene inductions were inhibited at the translational level but that mitochondrial DNA expression was disturbed at the transcriptional level. A disturbance of mitochondrial DNA expression could cause progressive failure of energy production of CA1 cells that eventually results in neuronal cell death.

Animals↗
PubMed1998

DNA fragmentation and HSP72 gene expression by adenovirus-mediated gene transfer in postischemic gerbil hippocampus and ventricle.

A replication defective adenoviral vector containing the E. coli lacZ gene (AdCMVnLacZ) was directly injected into right hippocampus and lateral ventricle immediately after 5 min of transient global ischemia in gerbils. The relations between the lacZ gene expression and DNA fragmentation or heat shock protein 72 (HSP72) immunoreactivity were examined up to 21 days post ischemia. The lacZ gene was transiently expressed at 1 day in the hippocampus except around the CA1 region, while a large number of the periventricular cells strongly expressed the lacZ gene from 8 h to 7 days. In CA1 layer, terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) positive cells, which were present only adjacent to the needle track at 8 h to 1 day, became more extensive in the whole CA1 layer at 3 to 7 days. TUNEL-positive cells were also detected around the DG at 1 day, around the needle track at 8 h to 3 days, and in the choroid plexus cells at 7 days. HSP72 staining was detected in the subiculum at 1 to 3 days, the dentate granule cells at 8 h to 1 day, and in the CA3 or CA4 pyramidal cells at 1 to 3 days. Some lacZ expressing cells were double-positive with HSP72 in DG, while the majority of those were distinguished from the TUNEL-positive cells. Pyramidal neurons were almost completely lost in the CA1 sector at 7 days after the ischemia. The present study demonstrates the successful LacZ gene transfer into the hippocampus and ventricle of postischemic gerbil brain except in the vulnerable CA1 layer by adenoviral vector injection. However, adenovirus-mediated gene transfer may induce indirect apoptotic cell death in the DG and ventricle, in addition to direct traumatic injury around the needle track.

Adenoviridae↗
PubMed1998

Functional and morphological damage of endothelium in rabbit ear artery following irradiation with cobalt60.

1. The relaxant actions of acetylcholine and A23187 were examined in the rabbit central ear artery at different intervals following exposure to different doses of radiation with a cobalt60 unit. The artery was irradiated with a dose of 10 Gy, 20 Gy and 45 Gy. Radiation caused dose- and time-dependent impairment of the endothelium-dependent relaxations. The impaired endothelium-dependent relaxations occurred as early as 1 week postirradiation and persisted throughout the experimental period (10 weeks). 2. The endothelium-independent response to sodium nitroprusside was well preserved up to 6 weeks after irradiation. The contractile response to noradrenaline was unaltered by irradiation throughout the experimental period, but in contrast to control vessels, an increase in the sensitivity to noradrenaline in the presence of the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine was not observed in the irradiated vessels. 3. The impaired endothelium-dependent relaxations in the irradiated vessels were not improved by pretreatment with the NOS substrate L-arginine, the cyclo-oxygenase inhibitor indomethacin or the free radical scavengers superoxide dismutase and catalase. 4. Scanning electron microscopy indicated morphologically intact endothelial cells within the first 4 weeks after irradiation. 5. Western blot analysis showed a significant decrease in the expression of endothelial NOS (eNOS) in the irradiated vessels. 6. These data indicate that endothelial cell function is specifically impaired in the irradiated vessels before morphological endothelial cell damage can be detected. This impairment may be related to diminished eNOS expression.

Animals↗
PubMed1998

Role of thyroid-stimulating blocking antibody in patients who developed hypothyroidism within one year after 131I treatment for Graves' disease.

OBJECTIVE: We recently reported that thyroid-stimulating blocking antibody (TSBAb) may not contribute to the development of hypothyroidism more than six years after 131I treatment. In the present study, we attempted to determine whether hypothyroidism that develops within a shorter period of time following 131I therapy is associated with TSBAb. DESIGN: Retrospective study. PATIENTS: Sera were obtained from 8 patients who developed hypothyroidism within 6 months after 131I therapy (Group 1), 8 patients who became euthyroid one year after 131I therapy (Group 2), and 7 patients who developed transient hypothyroidism (Group 3). MEASUREMENTS: Thyroid stimulating antibody (TSAb) activity was measured as the amount of cyclic adenosine monophosphate (cAMP) produced by cultured FRTL-5 cells, and TSBAb activity as the inhibition of cAMP produced in response to 100 mU/l bovine TSH. RESULTS: At about 3 months after 131I treatment, TSAb activity increased significantly in Groups 2 and 3, but did not change in Group 1. In contrast, TSBAb activity in Group 1 increased significantly and was positive in 6 patients at that time. At 12-18 months after 131I treatment, TSBAb activity tended to decrease and remained positive in 3 patients but became negative in 3 patients. It did not change in the patients in Groups 2 and 3. The patients in Group 1 were treated with levothyroxine, 75-125 micrograms/day. Levothyroxine was discontinued in the 3 patients whose TSBAb activity disappeared. Two of them remained euthyroid, and 1 became hypothyroid. CONCLUSION: Results indicate that the hypothyroidism that develops within a short time after 131I treatment may be caused by TSBAb activity. Thyroid function may be recovered when TSBAb activity disappears.

Analysis of Variance↗
PubMed1998

Involvement of both donor cytotoxic T lymphocytes and host NK1.1+ T cells in the thymic atrophy of mice suffering from acute graft-versus-host disease.

It has been reported that a dramatic decrease in the number of thymocytes (thymic atrophy) in mice suffering from acute graft-versus-host disease (GVHD) is ascribed to glucocorticoids. In this study, we examined the possibility that cellular immune responses may thus be involved in thymic atrophy. In contrast to chronic GVHD mice, acute GVHD (C57BL/6 X DBA/2) F1 (BDF1) hybrid mice, which were injected intravenously with both spleen and lymph node cells from C57BL/6 mice, showed a dramatic decrease in the number of CD4 CD8 double-positive thymocytes 2 or 3 weeks after the induction of GVHD. A flow cytometric analysis revealed the donor-derived T cells with either CD4 or CD8 molecules to infiltrate the thymus of the mice undergoing acute GVHD for 10 days. In a cytolytic assay, such thymus-containing cells exhibited a cytolytic activity specific to the host cells. In addition, anti-H-2d cytolytic T cells showed a high level of cytolytic activity against BDF1 (H-2bXd) thymocytes, whereas they also showed a low level of cytolytic activity against C57BL/6 (H-2b) thymocytes, thus suggesting that the thymus-infiltrating donor-derived T cells killed the host thymocytes through both anti-H-2d-specific and non-specific mechanisms. Interestingly, a flow cytometric analysis revealed both the percentage and the absolute cell number of host-derived NK1.1+ CD3+ cells to increase in the thymus of mice suffering from acute GVHD for 10 days. In addition, they also showed the cytolytic activity against YAC-1 cells and the mRNA expression of interleukin-12 (IL-12) in the thymus to be also significantly augmented on day 7 after the induction of acute GVHD. Collectively, our results indicate that the cellular immune responses such as donor cytotoxic T lymphocytes and host NK1.1+ T cells are therefore involved in the thymic atrophy of mice suffering from acute GVHD.

Acute Disease↗
PubMed1998

Expression of endothelial and inducible nitric oxide synthase in human glomerulonephritis.

The presence of nitric oxide (NO) in the kidney has been implicated in the pathogenesis of human glomerulonephritis. However, the exact type of glomerular cells that express NO synthase (NOS) and the NOS isoform involved in the local production of NO has not been identified in the human diseased kidney. We examined the expression of three isoforms of NOS, inducible NOS (iNOS), endothelial NOS (eNOS) and brain NOS (bNOS) in the renal tissue of patients with IgA nephropathy (IgAN, N = 10), lupus nephritis (LN, N = 5), membranous nephropathy (MN, N = 5) and minimal change nephrotic syndrome (MCNS, N = 5). Sections were immunostained and the correlation between the expression of each NOS and the degree of glomerular injury in that section was also examined. Normal portions of surgically resected kidneys served as controls. eNOS was present in glomerular endothelial cells and endothelium of cortical vessels in the control and diseased kidneys. iNOS was localized in mesangial cells, glomerular epithelial cells and infiltrating cells in the diseased glomeruli, whereas immunostaining for iNOS was hardly detected in control kidneys. In addition, the expression pattern of eNOS in each glomerulus was the reverse of that of iNOS. In IgAN and LN, the extent of staining for eNOS correlated negatively with the degree of glomerular injury, while the extent of staining for iNOS correlated positively with the degree of glomerular injury in the same tissues. bNOS was not detected in normal or nephritic glomeruli. Our results indicate the presence of a NO pathway in human diseased kidney, and suggest that NO derived from eNOS and iNOS may be involved in the progression of renal diseases and that NO derived from each NOS may play an important role in different way in human inflamed glomeruli.

Adult↗
PubMed1998

Expression of decay accelerating factor mRNA and complement C3 mRNA in human diseased kidney.

BACKGROUND: Decay accelerating factor (DAF), a product of mesangial cells in vitro, is expressed on the surface of cells and is a candidate for the focal suppression of complement activation. It is not clear at present whether the levels of expression of DAF and intrarenal C3 synthesis correlate with the level of tissue injury. METHODS: Immunohistochemistry for DAF and C3 and nonradioactive in situ hybridization with digoxigenin-labeled oligonucleotide probe for DAF and C3 mRNA were performed in 22 tissue samples of kidneys from patients with IgA nephropathy (IgAN), 6 with membranous nephropathy (MN), 6 with lupus nephritis (LN), and five normal kidneys. RESULTS: In the normal kidney, DAF was confined to the juxtaglomerular apparatus and little or no C3 was detected; however, a few glomerular cells were positive for DAF mRNA but no C3 mRNA positive cells were detected. In diseased kidneys, DAF and C3 as well as their mRNAs were detected in mesangial cells, tubular cells and infiltrating cells. Glomerular epithelial cells and Bowman's capsule cells contained little or no DAF and C3 but were positive for their mRNAs. The mean percentages of mesangial cells positive for DAF and C3 mRNAs were 49.3 +/- 11.5% and 50.7 +/- 10.3% in IgAN, and 17.0 +/- 6.3% and 19.4 +/- 9.0% in MN, respectively. The percentage of mesangial cells positive for DAF and C3 mRNAs among intraglomerular cells correlated positively with the degree of mesangial proliferation and glomerular sclerosis in IgAN. In contrast, in LN the percentage of glomerular cells positive for DAF mRNA correlated negatively with the degree of glomerular injury, while the percentage of cells positive for C3 mRNA did not change with the progression of the disease. The ratio of C3 mRNA/DAF mRNA of glomerular cells correlated with the degree of glomerular injury in both IgAN and LN. In the tubulointerstitium, the percentage of cells expressing mRNA, and C3 mRNA/DAF mRNA radio correlated with the degree of tubular atrophy and interstitial broadening in both IgAN and LN. CONCLUSIONS: We conclude that DAF and C3 mRNAs are synthesized in human diseased kidneys, and that a balance between locally synthesized DAF and C3 may be important in the progression of glomerulonephritis.

Adult↗
PubMed1998

Control of the pulmonary arterial resistance by the use of the oscillated assist flow.

In the clinical application of supporting circulation, the treatment of a patient with pulmonary hypertension is very important. We developed the electromagnetically driven vibrating flow pump (VFP) as a totally implantable type ventricular assist system. The artificial heart driven by electromagnetic forces creates high speed oscillation flow around 10-50 Hz. Assistance by high-speed oscillation flow has an interesting influence on the cardiovascular system. In this study, we carried out research on the influence such oscillation flow had on the pulmonary arterial vessels, and the supporting flow wave-form that controlled pulmonary vascular resistance was considered. Six healthy adult goats of both sexes were used in the experiments. We carried out inhalation anesthesia and performed intubation. The thorax was opened through left fourth rib resection. Right heart bypass was performed from the right atrium to the pulmonary artery. The flow of right heart assistance was maintained within 20-25% of total flow. Our purpose was to add flow of a specific high frequency to the right heart circulation. The hemodynamic parameters were recorded on a magnetic tape data recorder and input into a computer through an A-D converter. A result identified was that the pulmonary vascular resistance changed according to the alteration of the driving frequency of the VFP even during the same flow assistance. The resistance of the pulmonary arterial vessels became smaller when the driving of the VFP of 30 Hz was added to the right heart circulation. This was significant even when compared with continuous flow right heart assist. The characteristics of impedance appeared to have interesting alterations as well. Control of pulmonary vascular resistance by right heart assistance becomes possible if these results are applied. Accordingly, it may become one of the choices for treatment of a patient with pulmonary hypertension.

Animals↗
PubMed1998

Arterial changes following single-dose irradiation.

In this reported experiment, the serial morphologic changes in the rabbit ear central artery, following a single dose of 45 Gy 60Co gamma-ray irradiation, were investigated using light and scanning electron microscopy. Under light microscopy, mild intimal proliferation, disorganization of smooth muscle, and severe perivascular fibrosis were observed. These appeared to be caused by increased intimal cell death and lower repair capability after large single-dose irradiation. Under scanning electron microscopy, the endothelial cells did not show significant morphologic changes during the first 4 weeks. At 6 and 10 weeks after irradiation, the endothelial cells shrank in all directions and detached from the basement membrane. These changes accord with the theory that radiation damage following therapeutic dosage occurs within the DNA of the cell, and that there is no significant change until the cell attempts to divide.

Animals↗
PubMed1998

Ameliorative effect of glial cell line-derived neurotrophic factor on brain edema formation after permanent middle cerebral artery occlusion in rats.

Glial cell line-derived neurotrophic factor (GDNF) was applied topically on the brain surface immediately after permanent middle cerebral artery (MCA) occlusion in rats. In contrast to the cases treated with vehicle, a formation of brain edema was significantly reduced at one day by the treatment with GDNF. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) staining was markedly reduced in the cases with GDNF treatment at 12 h after MCA occlusion. However, the induction of immunoreactive 70-kd heat shock protein (HSP70) was slightly ameliorated by the GDNF treatment. The present results suggest that the treatment with GDNF has a significant effect on ameliorating brain edema formation after continuous brain ischemia, and the effect is greatly associated with the reduction of apoptotic changes, but slightly with that of stress response of cells.

Administration, Topical↗
PubMed1998

A change of P-selectin immunoreactivity in rat brain after transient and permanent middle cerebral artery occlusion.

Although the role of an adhesion molecule such as P-selectin may be important in the pathogenesis of stroke, temporal, spatial, and cellular profiles of the expression of such a protein has not been fully studied in the case of the middle cerebral artery (MCA) occlusion and reperfusion in rat brain. Change in expression of immunoreactive P-selectin was examined in rat brain after transient MCA occlusion (MCAO) in comparison to that of permanent occlusion with an anti-P-selectin monoclonal antibody. Western blot analyses were performed to ensure the selective detection of immunoreactive P-selectin protein with the monoclonal antibody using brain homogenates before and after MCAO. Temporal, spacial, and cellular changes of P-selectin expressions were evaluated with rat brain sections at 2, 8h, 1 and 3 days of permanent MCAO, and at 2, 8h, 1, 3 and 7 days of reperfusion after 1 h of transient MCAO. Western blot showed a single band with a molecular weight of 140 kDa for both cases with permanent occlusion and reperfusion. P-selectin immunoreactivity was not normally present in rat brain sections. However, it was expressed mainly in the post-capillary venules of the cerebral cortex and caudate in the MCA territory with a peak at 2-8h after permanent occlusion and at 8h to 1 day after the reperfusion. The expression was diminished by 1 day of permanent occlusion and 3 days of reperfusion. The maximum staining in the case of permanent MCAO was stronger than the case with reperfusion. However, spacial distribution of the staining was similar in the cerebral cortex and caudate between the cases with permanent of transient MCAO. These results suggest a different temporal but similar spacial and cellular expression of P-selection immunoreactivity between permanent occlusion and reperfusion of MCA in rat brain.

Animals↗
PubMed1998

Temporal profile of adenovirus-mediated E. coli lacZ gene expression in normal and post-ischemic gerbil hippocampus and ventricle.

A replication-defective adenoviral vector containing the E. coli lacZ gene was directly injected into normal and post-ischemic gerbil right hippocampus and lateral ventricle, and temporal profiles of the exogenous gene expression were compared. In case of ischemia, common carotid arteries (CCA) were transiently occluded for 5 min, and the adenoviral vector was administered just after the reperfusion. The animals were recovered for 8 h, 1, 3, 7 or 21 days. A small to moderate number of neural cells in the normal hippocampus expressed the gene from 1-3 days except for the cells around dentate gyrus (DG) and the needle route that began to express from 8 h of injection. Some normal hippocampal cells persisted the expression until 7 days. A moderate to large number of ventricular cells expressed the lacZ gene from 8 h to 7 days in the normal brain. On the other hand, no expression of the lacZ gene was observed in the post-ischemic hippocampus at 8 h including cells at DG and the needle route. Hippocampal CA1 neurons, that were selectively lost at 7 days of reperfusion, never expressed the gene throughout the post-ischemic course. The other hippocampal cells such as CA3 and dentate granule cells that survived ischemia expressed the gene only transiently at 1 day. A robust expression of the gene persisted in the ventricular cells from 8 h to 7 days. The majority of brain cells in the hippocampus that expressed the lacZ gene was not the pyramidal neurons, but small neurons at around the pyramidal layers of DG. Some astroglial, but no microglial, cells expressed the lacZ gene in the hippocampus. The present study shows that an expression of the lacZ gene was limited in the post-ischemic gerbil hippocampus especially at the vulnerable CA1 layer in contrast to the strong and persistent expression in the ventricular cells, and that the majority of beta-gal positive cells were not the pyramidal neurons but small neurons at around the cell layer both in the control and post-ischemic gerbil hippocampus.

Adenoviridae↗
PubMed1998

Differences in glomerular leukocyte infiltration between IgA nephropathy and membranoproliferative glomerulonephritis.

BACKGROUND: An important aspect in glomerular nephritic processes is the enhanced influx of leukocytes into the glomerulus. METHODS: To investigate the mechanisms of intraglomerular leukocyte infiltration in IgA nephropathy (IgA-N) and membranoproliferative glomerulonephritis type I (MPGN-I), we immunohistochemically examined the intraglomerular expression of leukocyte function-associated antigen-1 (LFA-1, CD11a/CD18), macrophage-1 (Mac-1, CD11b/CD18) and intercellular adhesion molecule-1 (ICAM-1, CD54) together with glomerular deposition of C3c and fibrinogen. RESULTS: In IgA-N (n=42), LFA-1+ cells were distributed mainly in glomeruli with intense expression of ICAM-1, and there was a positive correlation (P<0.001) between the number of LFA-1+ cells and the degree of ICAM-1 expression. Mac-1+ cells had no correlation with glomerular C3c deposition, but had a significant correlation with fibrinogen deposition (P<0.05). The number of LFA-1+ cells was significantly greater than of Mac-1+ cells (P<0.05). The number of LFA-1+ cells was strongly correlated with that of CD68+ cells (P<0.00001). In MPGN-I (n= 43), on the contrary, Mac-1+ cells correlated only with C3c deposition (P<0.001), and they were observed mainly in peripheral loops of glomerular capillaries where C3c was deposited with a similar distribution. However, there was no relationship between LFA-1+ cells and ICAM-1 expression. The number of Mac-1+ cells was greater than that of LFA-1+ cells (P<0.0001), and most Mac-1+ cells were identical to CD15+ cells. CONCLUSION: These results indicate the possibility that different mechanisms may cause glomerular leukocyte infiltration in various forms of human glomerulonephritis. The LFA-1/ICAM-1 pathway may play an important role in glomerular leukocyte infiltration in IgA-N, while the Mac-1/complement pathway may be important in MPGN-I. The former may promote mainly the infiltration of CD68+ cells, and the latter may promote that of CD15+ cells. In addition, Mac-1+ cells may act as fibrinogen and complement receptors in IgA-N and MPGN-I, respectively.

Antigens, CD↗