Corynebacterium striatum에 의한 화농성 슬관절염

박상훈(Sang-Hoon Park),윤한국(Han-Kook Yoon),김현교(Hyunkyo Kim),최호준(Ho-Jun Choi) 대한정형외과학회 2022 대한정형외과학회지 Vol.57 No.2

Corynebacterium striatum (C. striatum)은 호기성 그람 양성 막대균으로 호흡기, 피부의 상재균이다. 병독성이 낮아 배양 검사에 나와도 대개 오염균으로 생각되지만 심내막염, 호흡기 감염을 일으킬 수 있으며 드물게 뇌수막염, 관절염을 유발할 수 있다. 면역력이 저하된 환자뿐만 아니라 도관을 유치하고 있거나 피부장벽이 파괴된 환자에서 C. striatum 에 의한 감염이 보고된다. C. striatum 감염 증례로 화농성 슬관절염이 보고된 예는 드물며 이전 septic arthritis로 관절경하 변연절제술을 시행받은 환자에서 C. striatum 에 의한 감염에 대해 보고된 바는 더욱 드물다. 이에 C. striatum 에 의한 화농성 슬관절염을 조기 발견과 관절경적 치료로 호전된 1예를 보고하고자 한다. Corynebacterium striatum (C. striatum) is an aerobic Gram-positive rod, which is an organism of the respiratory tract and skin. Because of its low virulence, it is usually thought to be a contaminant even if it is shown in culture tests, but it can cause endocarditis and respiratory infections, and rarely meningitis and arthritis. Infection with C. striatum has been reported in patients with reduced immunity, as well as in patients with catheter or broken skin barriers. Septic knee arthritis caused by C. striatum infection is rarely reported, and knee joint infection by C. striatum in patients who underwent arthroscopic debridement for previous septic arthritis is even more rare. Therefore, we report a case of septic knee arthritis caused by C. striatum that was improved by early diagnosis and arthroscopic treatment.

자발 운동 및 부유 환경 조성에 의한 선조체 내 신경세포 생성 유도

민경훈,임상희,배병우,김은상,박은숙,박창일,조성래 대한재활의학회 2008 Annals of Rehabilitation Medicine Vol.32 No.6

Objective: To investigate that neurogenesis in the subventricular zone (SVZ), which is already known as neurogenic area where neural stem/progenitor cells persist, and the striatum, which is non-neurogenic area, might be induced by voluntary exercise (VEx) or environmental enrichment (EE), and compare the extent of the neurogenesis with untreated controls. Method: Total 12 C57BL/6 mice, 2∼3 months old, were recruited as follows; voluntary wheel runner, EE and control. For 2 weeks, VEx group was housed in rat cage (48×26 cm) with 2 running wheels with 3∼4 animals/cage, and EE group was housed in the living condition of huge cage (86×76 cm), social interaction (13∼14 mice/cage) and objects such as toys, tunnels and running wheel, whereas control group was placed in the standard cage (30×18 cm).Results: VEx and EE tended to increase the densities of mitotic marker BrdU+ cells in SVZ and striatum. They also exhibited more BrdU+ cells (/mm3) into the striatum, even though they did not show statistical significance. Moreover, EE group showed significant increment of the newly generated neurons coexpressed with BrdU+ and βIII-tubulin+ (/mm3) in SVZ and striatum as compared to those of controls.Conclusion: Voluntary physical exercise and EE induced cell proliferation and neurogenesis in both SVZ and striatum. Characteristically, EE could significantly induce neurogenesis in striatum, non-neurogenic area as well as SVZ, typical neurogenic area. Therefore, this strategy might be used to activate neural regeneration in various central nervous system diseases. Objective: To investigate that neurogenesis in the subventricular zone (SVZ), which is already known as neurogenic area where neural stem/progenitor cells persist, and the striatum, which is non-neurogenic area, might be induced by voluntary exercise (VEx) or environmental enrichment (EE), and compare the extent of the neurogenesis with untreated controls. Method: Total 12 C57BL/6 mice, 2∼3 months old, were recruited as follows; voluntary wheel runner, EE and control. For 2 weeks, VEx group was housed in rat cage (48×26 cm) with 2 running wheels with 3∼4 animals/cage, and EE group was housed in the living condition of huge cage (86×76 cm), social interaction (13∼14 mice/cage) and objects such as toys, tunnels and running wheel, whereas control group was placed in the standard cage (30×18 cm).Results: VEx and EE tended to increase the densities of mitotic marker BrdU+ cells in SVZ and striatum. They also exhibited more BrdU+ cells (/mm3) into the striatum, even though they did not show statistical significance. Moreover, EE group showed significant increment of the newly generated neurons coexpressed with BrdU+ and βIII-tubulin+ (/mm3) in SVZ and striatum as compared to those of controls.Conclusion: Voluntary physical exercise and EE induced cell proliferation and neurogenesis in both SVZ and striatum. Characteristically, EE could significantly induce neurogenesis in striatum, non-neurogenic area as well as SVZ, typical neurogenic area. Therefore, this strategy might be used to activate neural regeneration in various central nervous system diseases.

줄무늬체 및 운동신경계에서 노화에 따른 Neuropeptide Y 신경세포의 변화에 관한 연구

차중익,홍진주,이영일,이병란,조사선,백상호 대한해부학회 1997 Anatomy & Cell Biology Vol.30 No.3

증례 : 감염 ; 수술 후 발생한 Corynebacterium Striatum 복강 내 감염

최현석 ( Hyun Seok Choi ),김주승 ( Ju Seung Kim ),정을식 ( Eul Sik Jung ),김애진 ( Ae Jin Kim ),정한 ( Han Jung ),박윤수 ( Yoon Soo Park ),서일혜 ( Yiel Hea Seo ) 대한내과학회 2012 대한내과학회지 Vol.82 No.4

Corynebacterium striatum is an aerobic, Gram-positive bacillus that is part of the resident flora of skin and mucosal membranes. C. striatum is usually considered a non-pathogenic contaminant, although infective endocarditis and respiratory infection, and less frequently arthritis and meningitis, due to C. striatum have been reported. C. striatum has been particularly associated with catheter-related infections and infections following conditions that resulted in disruption of the skin barrier in both immunocompromised and immunocompetent hosts. We describe a case of post-operative intra-abdominal infection caused by the rare pathogen, C. striatum. (Korean J Med 2012;82:516-519)

신생흰쥐에서 6-OHDA 투여 후 줄무늬체 Tyrosine Hydroxylase 면역반응성 신경세포의 출현

한후재(Hoo Jae Hann) 대한해부학회 2003 Anatomy & Cell Biology Vol.36 No.2

흰쥐 줄무늬체(striatum)에는 흑색질(substantia nigra)에서 투사되는 도파민성 신경말단이 분포하지만, 도파민성 신경세포체는 존재하지 않는다. 연구자는 신생흰쥐에서 선택적 신경독성물질인 6-hydroxydopamine (6-OHDA)으로 유발된 반파킨슨병(hemiparkinsonian) 동물모델을 만드는 과정에서, 줄무늬체 내에 tyrosine hydroxylase (TH)-면역반응성 신경세포들이 출현하는 것을 관찰하고 이를 보고하는 바이다. 실험동물은 신생 Fischer 344 흰쥐를 사용하였고, 각각 생후 7일과 14일군으로 나누어 오른줄무늬체에 6-OHDA를 주입하고 일정기간 후 희생시켜 TH 면역조직화학염색을 시행하였다. TH-면역반응성을 보이는 세포들은 6-OHDA 주입 후 3일째에 처음 출현하였고, 본 연구의 최장생존기간인 손상 8주 후에도 관찰되었다. 이들은 주로 배쪽가쪽줄무늬체 (ventrolateral striatum), 줄무늬체-창백핵경계부 (striato-pallidal junction)와 창백핵 (globus pallidus)에 분포하였고, 신경세포 표지자인 NeuN과의 이중면역염색을 통해 신경세포로 확인되었다. 6-OHDA 주입군에서는 양쪽 줄무늬체에서 TH-면역반응성 신경세포를 관찰할 수 있었으나, 정상대조군이나 용매주입 대조군에서는 전혀 관찰되지 않았다. 이들이 뇌실밑층 (subventricular zone) 또는 줄무늬체의 줄기세포 (stem cell)에서 기원하는가 알아보기 위하여 bromodeoxyuridine (BrdU)으로 분열중인 세포를 표지하였으나, TH와 BrdU 면역반응성은 같은 세포에서 관찰할 수 없었다. 즉, 흑색질줄무늬체경로(nigrostriatal pathway) 손상 후 출현하는 줄무늬체의 TH-면역반응성 신경세포들이 줄기세포에서 기원되었을 가능성을 배제할 수 있었다. 본 연구를 통하여 도파민성 신경계통 자체가 가진 손상에 대한 보상잠재력을 확인할 수 있었으며, 그 기전 및 이와 관련된 인자들에 관한 연구가 보강된다면, 파킨슨병 치료방향의 새로운 가능성을 열어주게 될 것으로 보인다. Tyrosine hydroxylase-immunoreactive (TH-IR) neurons are known to exist in the substantia nigra pars compacta (SNpc), but not in the striatum in normal rats. In this study, injection of 6-OHDA into the 7 or 14 day neonatal rat striatum resulted in the appearance of ectopic TH-IR neurons in striatum. TH-IR cells were observed as early as postlesion day 3 and confirmed as neurons by TH/NeuN double immunohistochemistry. One or two neurons were found in most striatal sections at post-lesion day 4 where they were preferentially located in the ventro-lateral striatum, striatopallidal junction and globus pallidus. A small portion of these neurons persisted at least until post-lesion day 56, the oldest age studied. TH-IR neurons were found bilaterally in 6-OHDA-lesioned animals, but never in normal or vehicle-injected controls. To determine if these neurons resulted from stem cells, bromodeoxyuridine (BrdU) was injected daily for the first five days to label dividing cells. There was no co-localization of TH and BrdU immunoreactivity, excluding the possibility of stem cells as the source of these neurons. Although the TH-IR neurons were not numerous, their appearance following injury to the nigrostriatal system suggests that there is a capacity in neonatal brain to compensate for this lesion by upregulating dopaminergic phenotypic characters in pre-existing cells. The mechanism underlying this interesting phenotypic plasticity is unknown, but may be relevant to developing novel therapies for Parkinson’s disease through stimulation of the brain’s own potential for repair.

2018-2021년에 분리된 Corynebacterium striatum의 항균제 감수성 양상과 임상적 특성

최인호,이양순 대한임상미생물학회 2022 Annals of clinical microbiology Vol.25 No.3

Background: Corynebacterium striatum is part of the normal flora of the skin, oral cavity,and intestine. However, it can be a pathogen causing endocarditis, pneumonia, arthritis, andmeningitis occasionally. We evaluated the clinical features and antimicrobial susceptibilitypattern of C. striatum cases. Methods: Patients infected with C. striatum, who consulted infectious disease physicians andwere admitted to Hanyang University hospital between January 2018 and January 2021, wereenrolled for an antimicrobial susceptibility test (AST). We reviewed medical records of selectedpatients for information on diagnosis, specimen types, and antibiotics used before and afterAST. AST was performed using E-test and interpreted according to the Clinical and LaboratoryStandards Institute M45 guidelines. Results: A total of 23 cases were evaluated, and average age of patients was 58.5 years. Tencases were diagnosed sepsis. Eight cases were complicated with cancer, and five cases hadwound infections. Four cases were treated with vancomycin prior to AST; in 13 cases, antibioticswere switched to vancomycin after AST. Resistance rates were highest for ciprofloxacin(93.3%), which was followed by cefotaxime (92.3%), penicillin G (87.0%), erythromycin (87.0%),trimethoprim/sulfamethoxazole (78.3%), and meropenem (76.5%). Conclusion: The patients infected by C. striatum were old and immunosuppressed, while manyhad cancer. Since C. striatum shows resistance to most drugs except vancomycin, we shouldconsider conducting AST prior to antibiotic treatment.

Two Cases of Medical Device-Related Corynebacterium striatum Infection: A Meningitis and A Sepsis

박설희,정혜선,서의교,문영철,이미애 대한임상미생물학회 2016 Annals of clinical microbiology Vol.19 No.1

Corynebacterium striatum is a commonly isolated contaminant in the clinical microbiology. However, it can be an opportunistic pathogen in immunocompromised and even immunocompetent hosts. The increasing prevalence of C. striatum infection has been associated with immunosuppression and prosthetic devices. We report a case of meningitis with cerebrospinal fluid drainage and a case of catheter-related bloodstream infection caused by C. striatum. The isolates were identified as nondiphtherial Corynebacterium species by VITEK 2 (bioMérieux, France) anaerobe and Corynebacterium card. The final identification by 16S rRNA gene sequencing analysis was C. striatum with 99.7% identity and 99.6% identity with C. striatum ATCC 6940, respectively. Both strains were sensitive to vancomycin and gentamicin, but multidrug- resistant to ciprofloxacin, penicillin, erythromycin and imipenem.

Striatal Inhibition of MeCP2 or TSC1 Produces Sociability Deficits and Repetitive Behaviors

이윤진,김하나,한평림 한국뇌신경과학회 2018 Experimental Neurobiology Vol.27 No.6

Autism spectrum disorder (ASD) is a heterogeneous group of neurobehavioral disorders characterized by the two core domains of behavioral deficits, including sociability deficits and stereotyped repetitive behaviors. It is not clear whether the core symptoms of ASD are produced by dysfunction of the overall neural network of the brain or that of a limited brain region. Recent studies reported that excessive glutamatergic or dopaminergic inputs in the dorsal striatum induced sociability deficits and repetitive behaviors. These findings suggest that the dorsal striatum plays a crucial role in autistic-like behaviors. The present study addresses whether functional deficits of well-known ASD-related genes in the dorsal striatum also produce ASD core symptoms. This study also examines whether these behavioral changes can be modulated by rebalancing glutamate and/or dopamine receptor activity in the dorsal striatum. First, we found that the siRNA-mediated inhibition of Shank3, Nlgn3, Fmr1, Mecp2, or Tsc1 in the dorsal striatum produced mild to severe behavioral changes in sociability, cognition, and/or repetitive behaviors. The knockdown effects of Mecp2 and Tsc1 on behavioral changes were the most prominent. Next, we demonstrated that behavioral changes induced by striatal inhibition of MeCP2 and TSC1 were rescued by D-cycloserine (an NMDA agonist), fenobam (an mGluR5 antagonist), SCH23390 (a D1 antagonist), and/or ecopipam (a D1 partial antagonist), pharmacological drugs that are known to regulate ASD-like symptoms in animal models. Collectively, these results suggest that the dorsal striatum is a critical brain region that, when dysfunctional, produces the core symptoms of ASD.

The Role of Adenosine Receptors on Acetylcholine Release in the Rat Striatum

Kim, Do-Kyung,Kim, Hyeon-A,Choi, Bong-Kyu The Korean Society of Pharmacology 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.1

As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1$ adenosine heteroreceptor and various evidence suggest that indicate the $A_2$ adenosine receptor is present in the striatum, this study was undertaken to delineate the role of adenosine receptors on the striatal ACh release. Slices from the rat striatum were equilibrated with $[^3H]$choline and then the release amount of the labelled product, $[^3H]$ACh, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, $5\;Vcm^{-1}$, 2 min), was measured, and the influence of various agents on the evoked tritium outflow was investigated. And also, quantitative receptor autoradiography and drug-receptor binding assay were performed in order to confirm the presence and characteristics of $A_1$ and $A_2$ adenosine receptors in the rat striatum. Adenosine $(10{sim}100\;{mu}M)$ and $N^6$-cyclopentyladenosine (CPA, $1{sim}100\;{mu}M)$ decreased the $[^3H]$ACh release in a dose-dependent manner without changing the basal rate of release in the rat striatum. The reducing effects of ACh release by adenosine and CPA were abolished by 8-cyclopentyl-1,3-dipropy-Ixanthine (DPCPX, 2 ${mu}M$), a selective $A_1$, adenosine receptor antagonist, treatment. The effect of adenosine was potentiated markedly by 3,7-dimethyl-1-propargylxanthine (DMPX, 10 ${mu}M$), a specific $A_2$ adenosine receptor antagonist. 2-P-(2-carboxyethyl)phenethylamimo-5'-N- ethylcarboxamidoadenosine hydrochloride (CGS-21680C), in concentrations ranging from 0.01 to 10 ${mu}M$, a recently introduced potent $A_2$ adenosine receptor agonist, increased the $[^3H]$ACh release in a dose related fashion without changing the basal rate of release. These effects were completely abolished by DMPX $(10\;{mu}M)$. In autoradiograrhy experiments, $[^3H]$2-chloro-$N^6$-cyclopentyladenosine ($[^3H]$ CCPA) bindings were highly localized in the hippocampus and the cerebral cortex. Additionally, lower levels of binding were found in the striatum. However, $[^3H]$CGS-21680C bindings were highly localized in the striatal region with the greatest density of binding found in the caudate nucleus and putamen. Lower levels of binding were also found in the nucleus accumbens and olfactory tubercle. In drug-receptor binding assay, binding of $[^3H]$ CCPA to $A_1$ adenosine receptors of rat striatal membranes was inhibited by CPA ($K_i$ = 1.6 nM) and N-ethylcarboxamidoadenosine (NECA, $K_i$ = 12.9 nM), but not by CGS-21680C ($K_i$ = 2609.2 nM) and DMPX ($K_i$ = 19,386 nM). In contrast, $[^3H]$CGS-21680C binding to $A_2$ denosine receptors was inhibited by CGS-21680C ($K_i$ = 47.6 nM) and NECA ($K_i$ = 44.9 nM), but not by CPA ($K_i$ = 2099.2 nM) and DPCPX ($K_i$ = 19,207 nM). The results presented here suggest that both types of $A_1$ and $A_2$ adenosine heteroreceptors exist and play an important role in ACh release in the rat striatal cholinergic neurons.

The Role of Adenosine Receptors on Acetylcholine Release in the Rat Striatum

Do Kyung Kim,Hyeon A Kim,Bong Kyu Choi 대한생리학회-대한약리학회 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.1

<P> As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic A<SUB>1</SUB> adenosine heteroreceptor and various evidence suggest that indicate the A<SUB>2</SUB> adenosine receptor is present in the striatum, this study was undertaken to delineate the role of adenosine receptors on the striatal ACh release. <P> Slices from the rat striatum were equilibrated with [<SUP>3</SUP>H]choline and then the release amount of the labelled product, [<SUP>3</SUP>H]ACh, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, 5 Vcm<SUP>-1</SUP><SUB>, </SUB>2 min), was measured, and the influence of various agents on the evoked tritium outflow was investigated. And also, quantitative receptor autoradiography and drug-receptor binding assay were performed in order to confirm the presence and characteristics of A<SUB>1</SUB> and A<SUB>2</SUB> adenosine receptors in the rat striatum. <P> Adenosine (10∼100 ㄍM) and N<SUP>6</SUP>-cyclopentyladenosine (CPA, 1∼100 ㄍM) decreased the [<SUP>3</SUP>H]ACh release in a dose-dependent manner without changing the basal rate of release in the rat striatum. The reducing effects of ACh release by adenosine and CPA were abolished by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 2 ㄍM), a selective A<SUB>1</SUB> adenosine receptor antagonist, treatment. The effect of adenosine was potentiated markedly by 3,7-dimethyl-1-propargylxanthine (DMPX, 10 ㄍM), a specific A<SUB>2</SUB> adenosine receptor antagonist. 2-P-(2-carboxyethyl)phenethylamimo-5 -N-ethylcarboxamidoadenosine hydrochloride (CGS-21680C), in concentrations ranging from 0.01 to 10 ㄍM, a recently introduced potent A<SUB>2</SUB> adenosine receptor agonist, increased the [<SUP>3</SUP>H]ACh release in a dose related fashion without changing the basal rate of release. These effects were completely abolished by DMPX (10 ㄍM). In autoradiography experiments, [<SUP>3</SUP>H]2-chloro-N<SUP>6</SUP>-cyclopentyladenosine ([<SUP>3</SUP>H]CCPA) bindings were highly localized in the hippocampus and the cerebral cortex. Additionally, lower levels of binding were found in the striatum. However, [<SUP>3</SUP>H]CGS-21680C bindings were highly localized in the striatal region with the greatest density of binding found in the caudate nucleus and putamen. Lower levels of binding were also found in the nucleus accumbens and olfactory tubercle. In drug-receptor binding assay, binding of [<SUP>3</SUP>H]CCPA to A<SUB>1</SUB> adenosine receptors of rat striatal membranes was inhibited by CPA (K<SUB>i</SUB> = 1.6 nM) and N-ethylcarboxamidoadenosine (NECA, K<SUB>i</SUB> = 12.9 nM), but not by CGS-21680C (K<SUB>i</SUB> = 2609.2 nM) and DMPX (K<SUB>i</SUB> = 19,386 nM). In contrast, [<SUP>3</SUP>H]CGS-21680C binding to A<SUB>2</SUB> adenosine receptors was inhibited by CGS-21680C (K<SUB>i</SUB> = 47.6 nM) and NECA (K<SUB>i</SUB> = 44.9 nM), but not by CPA (K<SUB>i</SUB> = 2099.2 nM) and DPCPX (K<SUB>i</SUB> = 19,207 nM). <P> The results presented here suggest that both types of A<SUB>1</SUB> and A<SUB>2</SUB> adenosine heteroreceptors exist and play an important role in ACh release in the rat striatal cholinergic neurons.