PMID- 30106146 OWN - NLM STAT- MEDLINE DCOM- 20190109 LR - 20240331 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 18 IP - 4 DP - 2018 Oct TI - C‑C chemokine receptor type 3 gene knockout alleviates inflammatory responses in allergic rhinitis model mice by regulating the expression of eosinophil granule proteins and immune factors. PG - 3780-3790 LID - 10.3892/mmr.2018.9380 [doi] AB - The present study aimed to investigate the effects of C‑C chemokine receptor type 3 (CCR3) gene knockout on allergic rhinitis (AR) in mice, as well as the underlying molecular mechanisms. Ovalbumin was administrated to CCR3+/+ and CCR3‑/‑ BALB/c mice to establish an AR model. The mice were divided into four groups: i) Normal control (CG), ii) AR model (AR), iii) CCR3 knockout CG (CCR3‑/‑CG) and iv) AR model with CCR3 knockout (CCR3‑/‑AR). Histological sections of nasal mucosae were examined by hematoxylin and eosin staining, which revealed that CCR3 knockout suppressed the invasion of inflammatory cells and relieved the damage of nasal mucosae. Peripheral blood smear and nasal‑washing smears were evaluated by Wright's staining. Eosinophil (EOS) numbers in nasal mucosae, peripheral blood, and nasal washings of the various groups were ranked in the order: AR>CCR3‑/‑AR>CG>CCR3‑/‑. mRNA expression levels of CCR3, EOS peroxidase (EPO), EOS cationic protein (ECP), and major basic protein (MBP) in the peripheral serum and nasal washings were detected by reverse transcription‑polymerase chain reaction. Interferon‑gamma (IFN‑gamma), interleukin (IL)‑4, IL‑10, and immunoglobulin E (IgE) protein levels in the peripheral serum and nasal washings were investigated by ELISA. CCR3 mRNA expression was not detected in the CCR3‑/‑ and CCR3‑/‑AR groups, whereas expression levels in the AR group were markedly higher compared with expression in the CG group. Compared with the CG‑associated groups (i.e., the CG and CCR3‑/‑CG groups), the levels of EPO, ECP, MBP, IL‑4, and IgE were significantly increased in the AR‑associated groups (that is, R and CCR3‑/‑AR). In addition, the CCR3‑/‑AR group mice produced significantly lower levels of EPO, ECP, MBP, IL‑4 and IgE compared with the AR group, whereas the expression levels of IFN‑gamma and IL‑10 were increased. CCR3 gene knockout may alleviate EOS invasion and the inflammatory response in AR model mice by reducing the expression levels of EPO, ECP, MBP, IL‑4, and IgE, and increasing the expression of IL‑10 and IFN‑gamma. FAU - Zhu, Xinhua AU - Zhu X AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Liu, Ke AU - Liu K AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Wang, Jialin AU - Wang J AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Peng, Haisen AU - Peng H AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Pan, Qibin AU - Pan Q AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Wu, Shuhong AU - Wu S AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Jiang, Yinli AU - Jiang Y AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. FAU - Liu, Yuehui AU - Liu Y AD - Department of Otorhinolaryngology Head and Neck Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China. LA - eng PT - Journal Article DEP - 20180810 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (Ccr3 protein, mouse) RN - 0 (Eosinophil Granule Proteins) RN - 0 (Immunologic Factors) RN - 0 (Receptors, CCR3) SB - IM MH - Animals MH - Eosinophil Granule Proteins/genetics/*immunology MH - Female MH - Gene Expression Regulation MH - Gene Knockout Techniques MH - Immunologic Factors/genetics/*immunology MH - Inflammation/genetics/*immunology/pathology MH - Male MH - Mice, Inbred BALB C MH - Mice, Knockout MH - Nasal Mucosa/immunology/metabolism/pathology MH - Receptors, CCR3/genetics/*immunology MH - Rhinitis, Allergic/genetics/*immunology/pathology PMC - PMC6131541 EDAT- 2018/08/15 06:00 MHDA- 2019/01/10 06:00 PMCR- 2018/08/10 CRDT- 2018/08/15 06:00 PHST- 2017/04/18 00:00 [received] PHST- 2018/03/26 00:00 [accepted] PHST- 2018/08/15 06:00 [pubmed] PHST- 2019/01/10 06:00 [medline] PHST- 2018/08/15 06:00 [entrez] PHST- 2018/08/10 00:00 [pmc-release] AID - mmr-18-04-3780 [pii] AID - 10.3892/mmr.2018.9380 [doi] PST - ppublish SO - Mol Med Rep. 2018 Oct;18(4):3780-3790. doi: 10.3892/mmr.2018.9380. Epub 2018 Aug 10.