• Asian-Australasian Journal of Animal Sciences
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• v.28 no.9
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• pp.1354-1361
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• 2015

The complement system is a part of the natural immune regulation mechanism against invading pathogens. Complement activation from three different pathways (classical, lectin, and alternative) leads to the formation of C5-convertase, an enzyme for cleavage of C5 into C5a and C5b, followed by C6, C7, C8, and C9 in membrane attack complex. The C9 is the last complement component of the terminal lytic pathway, which plays an important role in lysis of the target cells depending on its self-polymerization to form transmembrane channels. To address the association of C9 with traits related to disease resistance, the complete porcine C9 cDNA was comparatively sequenced to detect single nucleotide polymorphisms (SNPs) in pigs of the breeds Hampshire (HS), Duroc (DU), Berlin miniature pig (BMP), German Landrace (LR), Pietrain (PIE), and Muong Khuong (Vietnamese potbelly pig). Genotyping was performed in 417 $F_2$ animals of a resource population (DUMI: $DU{\times}BMP$) that were vaccinated with Mycoplasma hyopneumoniae, Aujeszky diseases virus and porcine respiratory and reproductive syndrome virus at 6, 14 and 16 weeks of age, respectively. Two SNPs were detected within the third exon. One of them has an amino acid substitution. The European porcine breeds (LR and PIE) show higher allele frequency of these SNPs than Vietnamese porcine breed (MK). Association of the substitution SNP with hemolytic complement activity indicated statistically significant differences between genotypes in the classical pathway but not in the alternative pathway. The interactions between eight time points of measurement of complement activity before and after vaccinations and genotypes were significantly different. The difference in hemolytic complement activity in the both pathways depends on genotype, kind of vaccine, age and the interaction to the other complement components. These results promote the porcine C9 (pC9) as a candidate gene to improve general animal health in the future.

• Childhood Kidney Diseases
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• v.10 no.1
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• pp.45-51
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• 2006

Hypocomplementemia is found in all types of membranoproliferative glomerulonephritis (MPGN) but not in all patients. Hypocomplementemia can be ascribed to at least two circulating complement reactive modalities. The activation of the classical pathway produced by circulating immune complexes and the presence in the blood of anticomplement autoantibodies, called 'nephritic factor'(NF). The activation of the classical pathway by circulating immune complexes is probably the major mechanism responsible for hypocomplementemia in idiopathic MPGN type I. Nephritic factors have been shown to be responsible for the hypocomplementemia in both MPGN type II and III. NFa is probably the major mechanism responsible for the hypocomplementemia of idiopathic MPGN type II. NFt appears to be solely responsible for the hypocomplementemia in MPGN type III. Judging from the complement profile, NFt also may be present in some patients with MPGN type I. Although infection by meningococcus has been associated with deficiency of any of the plasmatic proteins of complement, it more commonly involves deficiency of the terminal components of the complement pathway(C5-C9). We experienced a patient who had MPGN and meningococcal meningitis. We examined the complement level and significantly lower levels of C3, C5 were found persistently. C7 was low at first and it returned to normal range after 2 months. C9 was normal at first, and was low after 2 months. This is the first reported case in which MPGN with meningococcal meningitis occurred.

• Journal of Chest Surgery
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• v.32 no.11
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• pp.978-983
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• 1999

Background: Complement activation with transpulmonary leukocyte sequestration is considered a main mediator leading to ischemia-reperfusion lung(I-R) injury. We studied the role of leukocytes in the formation of I-R injury in ovine cardiopulmonary bypass(CPB) model with a membrane oxygenator. Material and Method: Five sheep were used. CPB circuitry consisted of a roller pump(American Optical Corp., Greenwich, CT, USA) and a membrane oxygenator(UNIVOX-IC, Bentley, Baxter Health Corp, Irvine, CA, USA). The CPB time was fixed at 120 min. Ten minutes after the start of CPB, total CPB was established. Thereafter a total CPB of 100 min was performed, followed by another 10 min of partial CPB. The CPB was discontinued and the animals were fully recovered. For measuring left and right atrial leukocyte counts, blood samples were taken before thoracotomy, 5 min and 109 in after the start of CPB, and 30 min and 120 min after weaning. C3a was measured before thoracotomy, 109 min after the start of CPB, and 30 min and 120 min after weaning. Plasma malondialdehyde(MDA) was checked before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. One to two grams of lung tissue were taken for water content measurement before thoracotomy, 109 min after the start of CPB, and 30 min after weaning. Lung biopsy specimens were examined by light and electron microscopy. Result: Of 5 animals, 4 survived the experimental procedures. Of these, 3 animals survived on a long-term basis. No significant differences in transpulmonary gradients of leukocyte were found and no significant complement activation was expressed by C3a levels. MDA level did not show significant changes related to lung reperfusion despite an increase after the start of CPB. On both light and electron microscopic examinations, mild to moderate acute lung change was observed. Interstitial edema, leakage of erythrocytes into the alveolar space and endothelial cell swelling were the main findings. Water content of the lung showed a slight increase after the start of CPB, but there was no statistical significance. Conclusion: These findings indicate that ischemia-repersusion lung injury may not be from complement activation-leukocyte sequestration but from another source of oxygen free radicals related to CPB.

• The Korean Journal of Pain
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• v.37 no.2
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• pp.91-106
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• 2024

The mechanisms of the chronic pain and depression comorbidity have gained significant attention in recent years. The complement system, widely involved in central nervous system diseases and mediating non-specific immune mechanisms in the body, remains incompletely understood in its involvement in the comorbidity mechanisms of chronic pain and depression. This review aims to consolidate the findings from recent studies on the complement system in chronic pain and depression, proposing that it may serve as a promising shared therapeutic target for both conditions. Complement proteins C1q, C3, C5, as well as their cleavage products C3a and C5a, along with the associated receptors C3aR, CR3, and C5aR, are believed to have significant implications in the comorbid mechanism. The primary potential mechanisms encompass the involvement of the complement cascade C1q/C3-CR3 in the activation of microglia and synaptic pruning in the amygdala and hippocampus, the role of complement cascade C3/C3a-C3aR in the interaction between astrocytes and microglia, leading to synaptic pruning, and the C3a-C3aR axis and C5a-C5aR axis to trigger inflammation within the central nervous system. We focus on studies on the role of the complement system in the comorbid mechanisms of chronic pain and depression.

• Journal of the Korean Institute of Rural Architecture
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• v.6 no.2
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• pp.11-20
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• 2004

The rural area is activated and if it does to sleep, that versatility the reading is necessary from the side which is various it sees. Only expansion or improvement of namely base facility it will have and there is not a possibility becoming the basic activation countermeasure. With this with the instance investigation against the traditional market activation which is developed the Gamgok from same background has both the quality of the rural and the city in the center it joins in and the far it will be able to complement a problem point it presents. Also it presents the activation plan which considers the regional quality which from the research which it sees relates with a traditional market to sleep and it does.

• Childhood Kidney Diseases
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• v.21 no.2
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• pp.160-164
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• 2017

C3 glomerulopathy (C3G) is a recently defined pathological entity characterized by C3 accumulation with absent or scant immunoglobulin deposition, leading to variable glomerular inflammation. The clinical presentation of patients with C3G is highly variable, as they may present with symptoms ranging from microscopic or mild proteinuria to full-blown nephrotic syndrome, with or without renal impairment. However, there is no consensus recommendation for specific treatment in children with C3G. Recently, new therapies have been suggested to target complement pathways, owing to an improvement in the understanding of the pathogenesis of C3G. C3G complement blockade with eculizumab, a monoclonal antibody targeted against complement C5, inhibits activation of the alternative complement pathway. We could not use eculizumab owing to its high price; thus, we administered oral prednisolone and mycophenolate mofetil (MMF). MMF was replaced with cyclosporine because proteinuria persisted, with a consistently low serum C3 level; we tapered off the prednisolone because of a Cushingoid appearance and amenorrhea. Thereafter, proteinuria improved, and the serum C3 level returned to normal. Thus, we report the effectiveness of cyclosporine in a patient with C3G and an inadequate response to prednisolone and MMF, who was detected via school urinary screening.

• Korean Journal of Food Science and Technology
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• v.34 no.2
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• pp.290-295
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• 2002

Among 12 lactic acid bacteria examined for their abilities to activate the complement system by hemolytic complement assay $(TCH_{50})$, Lactobacillus plantarum previously isolated from Kimchi showed high anti-complementary activity. The anti-complementary activity of the cell wall fraction of L. plantarum was more potent than that of the cytosol fraction, and both activities showed dose dependency. These high activities of the cytosol and the cell wall fractions were relatively resistant to the digestion with pronase, but sharply decreased after the treatment of $NaIO_4$. These results suggested that the complement activation by the cytosol and the cell wall fractions was mainly due to their polysaccharides. By the cross-immunoelectrophoresis using anti-human C3, the C3 activation products from both fractions were identified in $Ca^{++}$-free condition. Anti-complementary activity $(ITCH_{50})$ of the cell wall fraction was retained under the same condition, whereas that of the cytosol fraction was reduced considerably. From these results, it was inferred that the mode of complement activation by the cell wall fraction was mainly via alternative pathway, and that of the cytosol fraction was via both alternative and classical pathways.

• Clinical and Experimental Pediatrics
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• v.48 no.1
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• pp.81-84
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• 2005

Henoch-$Sch{\ddot{o}}nlein$ purpura (HSP) is a systemic disorder characterized by leukocytoclastic vasculitis that can affect multiple organs predominantly the skin, joints, gastrointestinal tract and kidney. Although the specific pathogenesis of HSP is not known, there are several hypotheses. Although the importance of the complement activation in glomerular injury in HSP has been suggested, the complement levels and the blood pressure in those patients are usually normal and massive proteinuria is not common. And pathologic renal changes also have been reported to show a large variety of glomerular changes. However, to our knowledge, a membranoproliferative glomerulo-nephritis (MPGN) is a rare renal clinicopathologic manifestation of HSP. We report a 6-year-old boy with HSP who developed MPGN with hypertension, massive proteinuria, and hypo-complementemia revealed activation of the classical complement pathway, although we could not exclude the possibility of other hypocomplementemic glomerulonephritis including post-streptococcal acute glomerulonephritis.

• Journal of Preventive Medicine and Public Health
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• v.18 no.1
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• pp.91-97
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• 1985

The capacity of tobacco infusions of Korean cigarettes to activate the complement pathway was investigated in vitro by hemolytic assay. Complement activity was studied using samples of normal rabbit serum incubated at $37^{\circ}C$ with tobacco infusions. In all mixtures containing tobacco infusion A, B, C, D, E, F, G, H and I at a concentration of 0.1 : 1, total hemolytic complement showed a progressive decrease of 55.92%, 48.62%, 42.89%, 49.12%, 42.26%, 52.26%, 71.96%, 60.90%, and 61.14% respectively, after 60min of incubation. This study suggests that all tobacco infusions of Korean cigarettes are activators of complement.

• Clinical and Experimental Pediatrics
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• v.50 no.10
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• pp.931-937
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• 2007

The hemolytic uremic syndrome (HUS) is a rare disease of microangiopathic hemolytic anemia, low platelet count and renal impairment. HUS usually occurs in young children after hemorrhagic colitis by shigatoxin-producing enterohemorrhagic E. coli (D+HUS). HUS is the most common cause of acute renal failure in infants and young children, and is a substantial cause of acute mortality and morbidity; however, renal function recovers in most of them. About 10% of children with HUS do not reveal preceding diarrheal illness, and is referred to as D- HUS or atypical HUS. Atypical HUS comprises a heterogeneous group of thrombomicroangiopathy (TMA) triggered by non-enteric infection, virus, drug, malignancies, transplantation, and other underlying medical condition. Emerging data indicate dysregulation of alternative complement pathway in atypical HUS, and genetic analyses have identified mutations of several regulatory genes; i.e. the fluid phase complement regulator Factor H (CFH), the integral membrane regulator membrane cofactor protein (MCP; CD46) and the serine protease Factor I (IF). The uncontrolled activation of the complement alternative pathway results in the excessive consumption of C3. Plasma exchange or plasma infusion is recommended for treatment of, and has dropped the mortality rate. However, overall prognosis is poor, and many patients succumb to end-stage renal disease. Clinical presentations, response to plasma therapy, and outcome after renal transplantation are influenced by the genotype of the complement regulators. Thrombotic thrombocytopenic purpura (TTP), another type of TMA, occurs mainly in adults as an acquired disease accompanied by fever, neurologic deficits and renal abnormalities. However, less frequent cases of congenital or hereditary TTP associated with ADAMTS-13 (a disintegrin and metalloprotease, with thrombospondin 1-like domains 13) gene mutations have been reported, also. Recent advances in molecular genetics better allow various HUS to be distinguished on the basis of their pathogenesis. The genetic analysis of HUS is important in defining the underlying etiology, predicting the genotype-related outcome and optimizing the management of the patients.