• Title/Summary/Keyword: 노출치료

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The Review of Environment, Food and Exercise on Allergy Anaphylaxis (환경, 음식 및 운동 알레르기 반응에 대한 고찰)

  • Kwak, Yi-Sub;Baek, Young-Ho;Kim, Seung-Hyun;Kim, Young-Il;Yoo, Byung-In
    • Journal of Life Science
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    • v.20 no.1
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    • pp.147-152
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    • 2010
  • Exercise-induced anaphylaxis (EIA) is a physical allergy, sometimes severe, triggered by exertion following specific food intake. It was defined for the first time in 1980. EIA is associated with different kinds of exercise. The clinical manifestations progress from itching, erythema and urticaria to some combination of cutaneous angioedema and vascular collapse. Mast cell participation in the pathogenesis of this syndrome has been proved by the findings of an elevated serum histamine level during exhaustive exercise. As predisposing factors of EIA, a specific or even nonspecific sensitivity to food has been reported. Food-dependent exercise-induced anaphylaxis (FDEIA) is a distinct form of food allergy induced by physical exercise. It is typified by the onset of anaphylaxis during exercise which was preceded by the ingestion of the causal food allergens. The diagnosis of FDEIA is heavily dependent on clinical history. Allergy tests may need to be performed using a broad panel of food and food additives. As with food allergies, FDEIA diagnosis is based on interview, biological test and skin test. Prophylaxis aims to prevent a recurrence; the patient should be given an emergency kit to deal with any recurrent episodes. After the food allergen has been identified, it should be avoided for at least 4 to 5 hours before any exercise. Two cases of EIA are presented (EIA to circumstances; FDEIA) in this paper, The diagnosis, pathophysiology and therapy of FDEIA are also reviewed.

Achieving Health Equity Through Health Promotion (건강증진사업의 효율성과 형평성: 건강증진을 통한 건강 형평성 제고)

  • Moskowitz, Joel M.
    • Proceedings of The Korean Society of Health Promotion Conference
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    • 2005.09a
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    • pp.91-119
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    • 2005
  • 오타와 헌장에 따르면 건강증진은 건강형평성을 성취하는 것이다. 건강격차를 감소시키고, 모든 사람들이 건강잠재력을 달성할 수 있도록 동등한 기회와 자원이 제공되어야 한다. 또한 각 개인들은 자신의 건강에 대한 결정요인들에 대한 통제능력을 가져야 한다. 미국의 조기사망은 40%가 행동양식에 의하여, 30%가 유전적인 문제로, 15%가 사회적 환경에 의하여, 10%는 의료적 치료의 부족으로, 그리고 5%는 환경위해 물질에 대한 노출로 발생한다. 건강불평등을 발설시키는 사회적 요인으로는 경제적 요인을 들 수 있다. 이러한 요인으로 야기되는 건강불평등의 문제를 해결하여 건강형평성을 달성하기 위해서는 절대적 목표들과 평등관련 목표들이 모두 필요하다. 건강형평성은 인구집단의 건강과 함께 향상되는 것으로 나은 건강상태에 있는 사람들의 건강을 악화시키면서 건강형평성을 달성하는 것은 아니다. 각자의 관심이 형평성을 어떻게 규정하는가에 영향을 미친다. 혜택을 받은 사람들은 성과/투입의 정의를 선호하며, 소외계층은 똑같은 성과 또는 요구에 기반한 정의를 선호한다. Healthy People 2010은 미국의 국가적 예방체계를 의미하며, 가장 중요하며 예방 가능한 건강위협들을 파악하고 이러한 위협들을 감소하기 위한 목적들이 설정되어 있다. 궁극적인 목적은 건강한 삶의 질적인 면과 양적인 측면을 향상시키는 것이며, 건강불평등을 제거하는 것이다. 그러나 미국이 유럽의 국가들에 비해서 사회 프로그램에 대한 투자가 적은 이유는 재분배는 소수인종만을 위한 것이라는 믿음과, 우리는 개방되고 공정한 사회에 살고 있기 때문에 가난하다는 것은 가난한 사람들 자신들의 잘못으로 인한 것이라는 믿음 그리고 재분배를 방지하는 정치체계 때문이다. 국가기관인 CDC의 예방연구센터(Prevention Research Centers)는 지역사회 파트너들과 함께 건강증진, 질병예방, 그리고 질병과 상해로 인한 합병증을 관리하게 위한 효과적인 예방 전략을 개발하고 있다. 예방연구센터의 프로그램들은 지역사회 기반 참여연구와 소외된 계층에 중점을 두며, 다학제 간 접근방법을 활용하고, 교육기관, 공공보건기관 그리고 지역사회의 파트너들 간의 네트웍을 형성을 통한 협력관계를 강조하고 있다. 지역사회 위원회가 구성되어 있으며, 또한 근거중심 프로그램을 개발하고 있다. 이들은 건강 결정요인에 관한 연구, 형성적 연구, 개입 프로그램 및 프로그램의 확산에 관한 연구를 진행한다. UC Berkeley의 가족/지역사회 보건센터(Center for Family & Community Health)는 1993년에 설립되었다. 사업의 대상이 되는 주요 지역사회는 한국교민사회이며, 한국교민사회 자문위원회(Korean Community Advisory Board, KCAB)가 구성되어 있다. 1993년부터 2003년까지는 'Health is Strength' 사업이 시범연구사업으로 진행되었는데, 그 내용은 유방암과 자궁경부암 검진 프로그램이었다. 2003년부터 2009년까지 진행될 'Quitting is Winning'이라는 두 번째 시범연구사업은 남성들의 금연에 중점을 둔 사업이다. 'Health is Strength'는 아시아 보건서비스 및 한국교민사회 자문위원회가 함께 협력하여 진행된 사업으로, 주요 목표는 18세 이상 여성의 자궁암 조기 검진(Pap test)과 자가 유방검진 실천을 증가시키는 것이며, 50세 이상여성의 유방 임상검사와 유방 X선촬영 비율을 증가시키는 것이었다. 한 지역의 카운티에 거주하는 한국 여성들은 4년간의 개입프로그램의 대상이 되었으며, 이들을 대상으로 횡단적인 전화조사를 3번(사전, 중간, 사후)실시하였다. 개입 프로그램은 교회에서 워크샵 개최, Tell-A-Friend Form 작성하기, 포스터 및 책자 발행, 신문광고 등과 함께 자궁암 조기 검진(Pap test)과 유방 X선 촬영권을 무료로 제공하는 것으로 구성되었다. 'Quitting is Winning'은 지역사회 기반 참여 연구모형으로 한국교민사회 자문위원회는 흡연을 1순위의 사업으로 선정하였고, 근거에 기반한 금연 프로그램에 대한 연구들을 검토하여, 기존의 보편적 방법이 아닌 인터넷을 활용하는 프로그램을 진행하는 것으로 결정되었다. 이는 무작위 임상실험으로 연구대상으로 미국에 거주하는 한국인 남성흡연자 2300명을 모집하였다. 이들의 1/2은 실험군인 인터넷 프로그램 집단에, 또 다른 1/2은 대조군인 인쇄책자 집단에 무작위 할당되었다. 12개월 동안 11번의 진단이 인터넷을 통하여 진행되었으며, 참여와 참여유지에 대한 금전적인 보상이 제공되었다.

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Shear bond strength of ceramic and resin brackets used with visible light-cured adhesives (도재 및 레진 브라켓에 대한 광중합 접착제의 전단 접착 강도)

  • Hwang, Yu-Sun;Row, Joon;Hwaang, Chung-Ju
    • The korean journal of orthodontics
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    • v.26 no.2 s.55
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    • pp.233-244
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    • 1996
  • The purpose of this study was to compare the shear bond strength obtained from ceramic and plastic brackets bonded with various light-cured adhesives and to evaluate their debonded failure sites. Plastic brackets, Transcend 6000, Signature and Starflre TMB brackets were bonded with Orthobond, Light Bond and Transbond on one hundred forty extracted human premolar teeth as manufacturer's descriptions. After thermocycling the brackets were debonded with an Instron universal testing machine and the debonded bracket base surfaces were inspected under stereoscope to evaluate the failure sites. Also the shear bond strength and failure patterns with different curing time and with two different source of light were compared. The results were as follows. 1. There were no statistically significant differences among the mean shear bond strength of Orthobond, Light Bond and Transbond in a same bracket group except Plastic bracket group(p<0.05). 2. The mean shear bond strength of each adhesive with different bracket groups showed statistically significant differences. Stafire TMB showed the highest shear bond strenght among the brackets in this study, but there was no statistically singnificant difference with Transcend 6000 while there was statistically significant difference with Signature.(p<0.05) 3. The various bonding failure patterns were occurred among different bracket groups but most of failure sites were bracket base -adhesive interfaces. 4. There were no statistically significant differences in shear bond strength between the groups with curing time of 10 second and 20 second, and between the groups with two different sources of light as long as sufficient light intensity(above $400mWcm^2$) were provided(p<0.05). According to the result, it should be considered in clinical use of ceramic bracket with light-cured adhesives that the shear strengths of ceramic brackets were influenced by the retention from of bracket base as well as the composition of bracket and there was no difference in the shear bond strenght among various light-cured adhesives used in this study.

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In vitro cytotoxicity of self-etching primers (자가 산부식 프라이머의 세포독성에 관한 실험적 연구)

  • Rhee, Chang-Hoon;Kim, In-Ryeon;Kim, Gyoo-Cheon;Kim, Seong-Sik;Son, Woo-Sung
    • The korean journal of orthodontics
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    • v.36 no.6
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    • pp.422-433
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    • 2006
  • Objective: Several ions and components are released from self-etching primers in the oral cavity. This may cause injury to the periodontal tissues throughout orthodontic treatment. The purpose of this study was to assess the cytotoxicity of self-etching primers to HGF-1, HaCaT, and RHEK cells. Method: Transbond XT Primer (3M Unitek, Monrovia, CA, USA), and self-etching primers, Clearfil SE Bond (Kuraray, Osaka, Japan), Transbond Plus SEP (3M Unitek, Monrovia, CA, USA), and Adper Prompt L-Pop (3M Unitek, Monrovia, CA, USA), were evaluated by MTT assay, and cellular changes were also observed. Results: In all cells after 72 hours with all primers, severe morphological changes such as atrophy and necrosis were observed. In the MTT assay using HGF-1, Clearfil SE Bond, Transbond XT Primer, Transbond Plus SEP, and Adper Prompt L-Pop were lined up in order of ascending cytotoxicity When using HaCaT, Clearfil SE Bond, Adper Prompt L-Pop, Transbond Plus SEP, and Transbond XT Primer were lined up in order of ascending cytotoxicity. When using RHEK, Clearfil SE Bond, Transbond XT Primer, Adper Prompt L-Pop, and Transbond Plus SEP were lined up in order of ascending cytotoxicity. Conclusion: The result of this study shows that care is needed because self-etching primers show cytotoxic properties similar to conventional primers.

Expression of Growth Factors and Secretory Leukocyte Protease Inhibitor (SLPI) in RAW264.7 Cells after Lipopolysaccharide (LPS) Stimulation (대식세포주 (RAW264.7)에서 박테리아성 지질다당류 (LPS) 자극에 의한 분비백혈구단백분해효소억제제 (SLPI)와 성장인자들의 발현)

  • Son, Wook-Hee;Choi, Baik-Dong;Jeong, Soon-Jeong;Wang, Guan-Lin;Hwang, Ho-Keel;Jeong, Moon-Jin
    • Applied Microscopy
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    • v.37 no.2
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    • pp.93-102
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    • 2007
  • Secretory leukocyte protease inhibitor (SLPI) was known as one of bacterial lipopolysaccharide (LPS)-induced products of macrophage. Macrophages play an important role in the development of inflammatory responses by secreting an array of cytokines and chemokines in a tissue microenvironment. To identify the function and relationship between potent growth factors and SLPI after LPS stimulation, we conducted reverse transcriptase polymerase chain reaction (RT-PCR) and Western blots for the detection of mRNA and protein expression of SLPI and growth factors such as VEGF, PDGF, bFGF after 100 ng LPS stimulation on the RAW264.7 cells. The result of RT-PCR was showed SLPI mRNA expression was increased from 60 min to 48h in RAW 264.7 cells after incubation with LPS. VEGF and PDGF mRNA was expressed highly at initial stage by LPS stimulation. The mRNA of bFGF and type I collagen was very weakly expressed after LPS stimulation. SLPI protein level was increased likely the mRNA levels in RAW 267.7 cells. Additionally, phase contrast and scanning electron microscopic observation demonstrated that the LPS induce the change of morphology of the RAW264.7 cells. From these results, it suggest that expression of SLPI by LPS treatment may associate with VEGF and PDGF expression in RAW264.7 cells.

Cytotoxicity and Apoptosis of Various Concentrations of Doxorubicin in Methylcholanthrene- induced Rat Fibrosarcoma(MCA) Cells (Methylcholanthrene 유도 섬유육종세포주에서 Doxorubicin 농도에 따른 세포독성과 자멸사의 변화)

  • 정진용;왕영필;나석주
    • Journal of Chest Surgery
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    • v.34 no.6
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    • pp.447-453
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    • 2001
  • Background: Although pulmonary resection is the standard approach for the management of pulmonary metastases from soft tissue sarcoma, most of them are unresectable and chemotherapy remains the only option. The effectiveness of the cytotoxic drugs may be limited by the toxicities that occur before the therapeutic dose is reached. The regional administration of doxorubicin using pulmonary arterial perfusion in a rodent model can produce 10 to 25 times higher concentrations in the lung than systemic administration with minimal systemic toxicities. However, it is unclear whether a high concentration of doxorubicin has beneficial effects for killing cancer cells. Material and Method: We studied this to evaluate the dose-dependent cytotoxic and apoptotic effects of doxorubicin on methylcholanthrene-induced rat fibrosarcoma(MCA) cells. This study examined the cytotoxicity and apoptosis-related gene expressions(Fas, FasL, Bax, caspase 1, caspase 2, caspase 8, Bcl-2, Bcl-xL, Bcl-xS) in MCA cells after 24 hours exposure to various concentrations of doxorubicin such as 1, 5, 10, 50, and 100 $\mu$M. Result: Dose-dependent cytotoxicity was observed after 24 hours exposure to doxorubicin. However, peak apoptosis after 24 hours exposure was observed at 5 $\mu$M of doxorubicin. Above 5 $\mu$M, apoptotic activity was decreased with dose-increment. All mRNA levels of apoptosis-related genes after 24 hours exposure were up-regulated above the control level at 1 $\mu$M of doxorubicin and then decreased by doxorubicin dose-increment except caspase 8, which showed higher levels than the control level at 5 $\mu$M. Apoptosis-related protein levels were highest at 1 $\mu$M of doxorubicin and then decreased by doxorubicin dose-increment. However, Bax and Bcl-xL proteins steadily showed higher levels than the control throughout the different concentrations of doxorubicin. Conclusion: These results suggest that apoptosis is the main cytotoxic mechanism in low concentrations of doxorubicin in MCA cells and apoptosis-related genes, such as Bax, caspase 8, and Bcl-xL, are involved. At high concentrations, doxorubicin still can kill MCA cells, even when apoptosis is inhibited, and have its propriety for achieving much cytotoxicity against MCA cells.

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Protective Effect of the Ethyl Acetate-fraction of Methanol Extract of Ophiophogon japonicus on Amyloid beta Peptide-induced Cytotoxicity in PC12 Cells (소엽맥문동-에틸아세테이트 분획물의 아밀로이드 베타단백질-유발 세포독성에 대한 억제 효능)

  • Moon, Ja-Young;Kim, Eun-Sook;Choi, Soo-Jin;Kim, Jin-Ik;Choi, Nack-Shik;Lee, Kyoung;Park, Woo-Jin;Choi, Young-Whan
    • Journal of Life Science
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    • v.29 no.2
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    • pp.173-180
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    • 2019
  • Amyloid ${\beta}$-protein ($A{\beta}$) is the principal component of senile plaques characteristic of Alzheimer's disease (AD) and elicits a toxic effect on neurons in vitro and in vivo. Many environmental factors, including antioxidants and proteoglycans, modify $A{\beta}$ toxicity. It is worthwhile to isolate novel natural compounds that could prove therapeutic for patients with AD without causing detrimental side effects. In this study, we investigated the in vitro neuroprotective effects of the ethyl acetate fraction of methanol extract of Ophiophogon japonicas (OJEA fraction). We used an MTT reduction assay to detect protective effects of the OJEA fraction on $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells. We also used a cell-based ${\beta}$-secretase assay system to investigate the inhibitory effect of the OJEA fraction on ${\beta}$-secretase activity. In addition, we performed an in vitro lipid peroxidation assay to evaluate the protective effect of the OJEA fraction against oxidative stress induced by $A{\beta}_{25-35}$ in PC12 cells. The OJEA fraction had strong protective effects against $A{\beta}_{25-35}$-induced cytotoxicity to PC12 cells and was strongly inhibitory to ${\beta}$-secretase activity, which resulted in the attenuation of $A{\beta}$ generation. In addition, the OJEA fraction significantly decreased malondialdehyde (MDA) content, which is induced by the exposure of PC12 cells to $A{\beta}_{25-35}$. Our results suggested that the OJEA fraction contained active compounds exhibiting a neuroprotective effect on $A{\beta}$ toxicity.

The Protective Role of Gleditsiae fructus against Streptococcus pneumoniae (폐렴 구균에 대한 조협의 보호 역할 연구)

  • Jun-ki Lee;Se-Hui Lee;Dong Ju Seo;Kang-Hee Lee;Sojung Park;Sun Park;Taekyung Kim;Jin-Young Yang
    • Journal of Life Science
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    • v.33 no.2
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    • pp.158-168
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    • 2023
  • Natural products have been used to mitigate the effects of cancer and infectious diseases, as they feature diverse bioactivities, such as antioxidant, antibacterial, anti-inflammatory, and immunomodulatory effects. Here, we chose 10 natural products that are well-known as pulmonary enhancers and investigated their bactericidal effects on Streptococcus pneumoniae. In the disk diffusion assay, the growth of S. pneumoniae was significantly regulated by G. fructus treatment regardless of extraction method used. We first adopted spraying as a novel delivery method for G. fructus. Interestingly, mice exposed to G. fructus three times a day for 2 weeks were resistant to S. pneumoniae intranasal infection (shown both through body weight loss and survival rates compared to the control group). Moreover, we confirmed that exposure to G. fructus regulated the colonization of the bacteria despite the sustained inflammation in the lung after exposure to S. pneumoniae, indicating that migrated inflammatory immune cells may involve a host defense mechanism against pulmonary infectious diseases. While a similar number of granulocytes (CD11b+Ly6C+Ly6G+), neutrophils (CD11b+Ly6CintLy6G+), and monocytes (CD11b+Ly6CintLy6G-) were found between groups, a significantly increased number of alveolar macrophages (CD11b+CD11chiF4/80+) was detected in BAL fluids of mice pre-exposed to G. fructus at 5 days after S. pneumonia infection. Taken together, our data suggest that this usage of G. fructus can induce protective immunity against bacterial infection, indicating that facial spray may be helpful in enhancing the defense mechanism against pulmonary inflammation and in evaluating the efficacy of natural products as immune enhancers against respiratory diseases.

Attenuation of Oxidative Stress-Induced HepG2 Cellular Damage by Cirsiumjaponicum Root Extract (HepG2 세포에서 대계 추출물에 의한 산화적 스트레스 유발 세포 손상의 억제)

  • Da Jung Ha;Seohwi Kim;Byunwoo Son;Myungho Jin;Sungwoo Cho;Sang Hoon Hong;Yung Hyun Choi;Sang Eun Park
    • Journal of Life Science
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    • v.33 no.12
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    • pp.1002-1014
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    • 2023
  • The root of Cirsium japonicum var. maackii (Maxim.) has long been used in traditional medicine to prevent the onset and progression of various diseases and has been reported to exert a wide range of physiological effects, including antioxidant activity. However, research on its effects on hepatocytes remains scarce. This study used the human hepatocellular carcinoma HepG2 cell line to investigate the antioxidant activity of ethanol extract of C. japonicum root (EECJ) on hepatocytes. Hydrogen peroxide (H2O2) was used to mimic oxidative stress. The results showed that EECJ significantly reverted the decrease in cell viability and suppressed the release of lactate dehydrogenase in HepG2 cells treated with H2O2. Moreover, an analysis of changes in cell morphology, flow cytometry, and microtubule-associated protein light chain 3 (LC3) expression showed that EECJ significantly inhibited HepG2 cell autophagy induced by H2O2. Furthermore, it attenuated H2O2-induced apoptosis and cell cycle disruption by blocking intracellular reactive oxygen species and mitochondrial superoxide production, indicating strong antioxidant activity. EECJ also restored the decreased levels of intracellular glutathione (GSH) and enhanced the expression and activity of superoxide dismutase and GSH peroxidase in H2O2-treated HepG2 cells. Although an analysis of the components contained in EECJ and in vivo validation using animal models are needed, these findings indicate that EECJ is a promising candidate for the prevention and treatment of oxidative stress-induced liver cell damage.

Research on Immune Responses Induced by Salmonella Typhimurium Infectionin CRIP1-Deficient Condition (CRIP1결손조건 하에서 Salmonella Typhimurium 감염에 의해 유도되는 면역반응에 관한 연구)

  • Dongju Seo;Se-Hui Lee;Sun Park;Hyeyun Kim;Jin-Young Yang
    • Journal of Life Science
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    • v.34 no.1
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    • pp.48-58
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    • 2024
  • Salmonella is a common food-borne intracellular bacterial pathogen that has triggered significant public health concerns. Salmonella hosts' genetic factors play a pivotal role in determining their susceptibility to the pathogen. Cysteine-rich intestinal protein 1 (CRIP1), a member of LIM/double zinc finger protein family, is widely expressed in humans, such as in the lungs, spleen, and especially the gut. Recently, CRIP1 has been reported as a key marker of several immune disorders; however, the effect of CRIP1 on bacterial infection remains unknown. We aimed to elucidate the relationship between Salmonella infection and CRIP1 gene deficiency, as Salmonella spp. is known to invade the Peyer's patches of the small intestine, where CRIP1 is highly expressed. We found that CRIP1-deficient conditions could not alter the characteristics of bone marrow-derived myeloid cells in terms of phagocytosis on macrophages and the activation of costimulatory molecules on dendritic cells using ex vivo differentiation. Moreover, flow cytometry data showed comparable levels of MHCII+CD11b+CD11c+ dendritic cells and MHCII+F4/80+CD11b+ macrophages between WT and CRIP1 knockout (KO) mice. Interestingly, the basal population of monocytes in the spleen and neutrophils in MLNs is more abundant in a steady state of CRIP1 KO mice than WT mice. Here, we demonstrated that the CRIP1 genetic factor plays dispensable roles in host susceptibility to Salmonella Typhimurium infections and the activation of myeloid cells. In addition, differential immune cell populations without antigen exposure in CRIP1 KO mice suggest that the regulation of CRIP1 expression may be a novel immunotherapeutic approach to various infectious diseases.