LL-37 alone and in combination with IL17A enhances proinflammatory cytokine expression in parallel with hyaluronan metabolism in human synovial sarcoma cell line SW982—A step toward understanding the development of inflammatory arthritis

Kuensaen, Chakkrapong; Chomdej, Siriwadee; Kongdang, Patiwat; Sirikaew, Nutnicha; Jaitham, Rungnaree; Thonghoi, Supitcha; Ongchai, Siriwan

doi:10.1371/journal.pone.0218736

Cited by 8 publications

(12 citation statements)

References 52 publications

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“…SS typically occurs in young adults and has a poor prognosis, with a tendency to relapse and metastasize at a late stage. [ 3 ] Currently, surgery is the only option for comprehensive treatment. Radiotherapy, chemotherapy, and targeted molecular therapy are considered as additional options following surgery.…”

Section: Introductionmentioning

confidence: 99%

Primary renal synovial sarcoma

Zhang

Tian

et al. 2020

Medicine

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Rationale: Synovial sarcoma (SS) is a malignant neoplasm that arises from soft tissues proximal to the joints. It occurs primarily at the major joints of the extremities, but may also occur in the deep soft tissues around the joints. While primary renal synovial sarcoma (PRSS) is extremely rare, it is important to have a better understanding of their imaging and clinical features to establish an effective treatment plan. Correct identification of PRSS is also useful for treating renal neoplasms. Patient's concerns: A 56-year-old Chinese man was admitted to our hospital due to moderate, paroxysmal left-sided loin pain. Diagnosis: Renal enhanced computed tomography (CT) scanning showed a relatively hypovascular lesion with calcification in the left kidney. A radical nephrectomy was performed in the left kidney. Postoperative pathology indicated SS with necrosis. The immunohistochemical findings were as follows: 34βE12 (Epithelium+), Bcl-2(+), CD99(+), CK-pan((Epithelium+), EMA(Epithelium+), Ki-67(+60%), and Vimentin(+), CD34(−). Interventions: The patient underwent radical left nephrectomy with no complications. Outcomes: After discharge, a close review for 3 months showed no evidence of recurrence. Lessons: PRSS should be considered for the differential diagnosis of renal hypovascular tumors. When problems arise in distinguishing renal hypovascular tumors, surgical pathology is helpful in the final diagnosis and further treatment of the disease.

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Section: Introductionmentioning

confidence: 99%

Primary renal synovial sarcoma

Zhang

Tian

et al. 2020

Medicine

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“…Interestingly, LL-37 also induces IL-17A expression. Moreover, long activation of IL-17A by LL-37 and cooperation of these two mediators, prolong and enhance the main inflammatory processes in tissues [42]. Overall, the synergy of LL-37 and IL-17A, HBD-3 and HBD-4 supports the hypothesis that synergistic cooperation of different immune factors can lead to a higher response to pathogens and faster reduction of inflammation.…”

Section: Introductionmentioning

confidence: 55%

Local Defence System in Healthy Lungs

Lohova

Vitenberga-Verza

Kažoka

et al. 2021

Clinics and Practice

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Background: The respiratory system is one of the main entrance gates for infection. The aim of this work was to compare the appearance of specific mucosal pro-inflammatory and common anti-microbial defence factors in healthy lung tissue, from an ontogenetic point of view. Materials and methods: Healthy lung tissues were collected from 15 patients (three females and 12 males) in the age range from 18 to 86. Immunohistochemistry to human β defensin 2 (HBD-2), human β defensin 3 (HBD-3), human β defensin 4 (HBD-4), cathelicidine (LL-37) and interleukine 17A (IL-17A) were performed. Results: The lung tissue material contained bronchial and lung parenchyma material in which no histological changes, connected with the inflammatory process, were detected. During the study, various statistically significant differences were detected in immunoreactive expression between different factors in all lung tissue structures. Conclusion: All healthy lung structures, but especially the cartilage, alveolar epithelium and the alveolar macrophages, are the main locations for the baseline synthesis of antimicrobial proteins and IL-17A. Cartilage shows high functional plasticity of this structure, including significant antimicrobial activity and participation in local lung protection response. Interrelated changes between antimicrobial proteins in different tissue confirm baseline synergistical cooperation of all these factors in healthy lung host defence.

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“…Further in vitro studies had found that CAMP gene methylation inhibited the level of ROS and TNF-α in chondrocytes, promoted the level of TGF-β expression, inhibited the proliferation of chondrocytes, and promoted their apoptosis. The results of Kuensaen et al [36] found that high levels of CAMP promote the expression of downstream pro-in ammatory cytokines (especially IL17A), which was related to the pathogenesis of in ammatory arthritis. Hu et al [37] found that CAMP regulated the production of in ammatory cytokines such as TNF-α and inhibited cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

CAMP Gene Promoter Methylation Induces Chondrocyte Apoptosis By Inhibiting ROS Levels And Inflammatory Response

Wang

Liu

Yang

et al. 2021

Preprint

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Objective: The occurrence of osteoarthritis is related to genetic and environmental factors. Among them, the change of chondrocyte gene expression pattern regulated by epigenetic modification is an important participant. This study analyzed the effect of CAMP gene methylation on the level of oxidative stress and inflammation of chondrocytes. Methods: We analyzed the changes of the transcriptome in the articular cartilage tissue of osteoarthritis patients (OA) from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. MTT assay and flow cytometry analysis of short hairpin RNA (shRNA) silencing CAMP gene and 5μM 5-Aza-2’-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human Chondrocytes Osteoarthritis (HC-OA) cells. The DCFH-DA assay was used to detect the level of reactive oxygen species (ROS), and the expression level of inflammatory factors was analyzed by Western Blot. Results: The expression of CAMP in cartilage tissue of OA patients was up-regulated, and the level of methylation was down-regulated. CAMP was highly expressed in osteoarthritis articular cartilage cells. Silencing CAMP inhibited the proliferation of HC-OA cells and promoted their apoptosis. CAMP gene methylation inhibited ROS levels and TNF-α expression levels in HC-OA cells, and promoted TGF-β expression. CAMP gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis. Conclusion: CAMP gene promoter methylation induces chondrocyte apoptosis by inhibiting ROS levels and inflammation.

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LL-37 alone and in combination with IL17A enhances proinflammatory cytokine expression in parallel with hyaluronan metabolism in human synovial sarcoma cell line SW982—A step toward understanding the development of inflammatory arthritis

Cited by 8 publications

References 52 publications

Primary renal synovial sarcoma

Primary renal synovial sarcoma

Local Defence System in Healthy Lungs

CAMP Gene Promoter Methylation Induces Chondrocyte Apoptosis By Inhibiting ROS Levels And Inflammatory Response

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