Literature DB >> 24273921

Expression of CC chemokines CCL2, CCL5, and CCL11 is associated with duration of disease and complications in type-1 diabetes: a study on Iranian diabetic patients.

Zahra Jamali1, Mahmood Nazari, Hossein Khoramdelazad, Elham Hakimizadeh, Mehdi Mahmoodi, Mojgan Noroozi Karimabad, Gholamhossein Hassanshahi, Mohsen Rezaeian, Parisa Balaei, Shokoofeh Darakhshan, Nahideh Masood Poor.   

Abstract

BACKGROUND: Type-1 diabetes (T1D) is defined as a heterogeneous autoimmune disease. Immune system related factors are important in the pathogenesis of T1D. Chemokines are important factors in the pathogenesis of several autoimmune diseases, including T1D. They are potent chemotactic cytokines with various functions such as maturation, trafficking of leukocytes, angiogenesis, and homing of stem cells. Therefore, the current study was aimed to examine whether expression of CC chemokines CCL2, CCL5, and CXCL11 is associated with disease duration and complications in Iranian T1D patients.
METHODS: In this experimental study, blood samples were collected from 108 T1D patients and 189 healthy controls in EDTA pre-coated tubes. The serum levels of CC chemokines were measured by ELISA. Demographic data were also collected along with experimental examinations in a questionnaire which was designed specifically for this study.
RESULTS: Results of the present study demonstrated that the expression of CCL2 was decreased while CCL5 and CCL11 were increased in T1D patients in comparison to controls. These results demonstrated that CCL2, CCL5, and CCL1 were elevated in T1D patients with duration of disease. Again, our findings demonstrated that CCL2, CCL5, and CCL11 were elevated in T1D patients with age. But there was not a significant difference between circulating level of CC chemokines studied in T1D patients regarding their gender and they have followed a similar pattern of expression in both genders. Our findings also showed that all three CC chemokines were elevated in TID patients suffering from diabetes complications.
CONCLUSIONS: According to the results of our study, elevated levels of CCL5 and CCL11 are in parallel with decreased level of CCL2 and are useful tools in the differential diagnosis of T1D from other types of metabolic disorders. Elevated levels of these CC chemokines probably could be implicated as predictive factors for occurrence of T1D complications. These results may also re-emphasize the prominent therapeutic role(s) of these CC chemokines in control of either T1D or its associated complications.

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Year:  2013        PMID: 24273921     DOI: 10.7754/clin.lab.2012.120810

Source DB:  PubMed          Journal:  Clin Lab        ISSN: 1433-6510            Impact factor:   1.138


  10 in total

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2.  Syntaxin 4 Enrichment in β-Cells Prevents Conversion to Autoimmune Diabetes in Non-Obese Diabetic (NOD) Mice.

Authors:  Eunjin Oh; Erika M McCown; Miwon Ahn; Pablo A Garcia; Sergio Branciamore; Shanshan Tang; De-Fu Zeng; Bart O Roep; Debbie C Thurmond
Journal:  Diabetes       Date:  2021-09-23       Impact factor: 9.461

3.  CCR2 upregulation in DRG neurons plays a crucial role in gastric hyperalgesia associated with diabetic gastropathy.

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Journal:  Sci Rep       Date:  2021-04-15       Impact factor: 4.379

5.  Chemokines in Type 1 Diabetes Mellitus.

Authors:  Xiongfeng Pan; Atipatsa C Kaminga; Sanjay Kinra; Shi Wu Wen; Hongying Liu; Xinrui Tan; Aizhong Liu
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Journal:  Vaccines (Basel)       Date:  2022-08-11

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9.  Loss of NOX-Derived Superoxide Exacerbates Diabetogenic CD4 T-Cell Effector Responses in Type 1 Diabetes.

Authors:  Lindsey E Padgett; Brian Anderson; Chao Liu; Douglas Ganini; Ronald P Mason; Jon D Piganelli; Clayton E Mathews; Hubert M Tse
Journal:  Diabetes       Date:  2015-08-12       Impact factor: 9.461

10.  Orally administered anti-eotaxin-1 monoclonal antibody is biologically active in the gut and alleviates immune-mediated hepatitis: A novel anti-inflammatory personalized therapeutic approach.

Authors:  Tawfik Khoury; Dory Rotnemer-Golinkin; Lidya Zolotarev; Yaron Ilan
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  10 in total

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