Journal of Pathology and Translational Medicine

Original Articles

Blocking Toll-like receptor 9 attenuates bleomycin-induced pulmonary injury: Badr Alzahrani, Mohamed M. S. Gaballa, Ahmed A. Tantawy, Maha A. Moussa, Salma A. Shoulah, Said M. Elshafae; J Pathol Transl Med. 2022;56(2):81-91. Published online March 2, 2022; DOI: https://doi.org/10.4132/jptm.2021.12.27

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Background
Acute respiratory distress syndrome (ARDS) is one of the most common complications in coronavirus disease 2019 patients suffering from acute lung injury (ALI). In ARDS, marked distortion of pulmonary architecture has been reported. The pulmonary lesions in ARDS include hemodynamic derangements (such as alveolar edema and hemorrhage), vascular and bronchiolar damage, interstitial inflammatory cellular aggregations, and eventually fibrosis. Bleomycin induces ARDS-representative pulmonary damage in mice and rats; therefore, we used bleomycin model mice in our study. Recently, Toll-like receptor 9 (TLR9) was implicated in the development of ARDS and ALI.
Methods
In this study, we evaluated the efficiency of a TLR9 blocker (ODN2088) on bleomycin-induced pulmonary damage. We measured the apoptosis rate, inflammatory reaction, and fibroplasia in bleomycin- and bleomycin + ODN2088-treated mice.
Results
Our results showed a significant amelioration in bleomycin-induced damage to pulmonary architecture following ODN2088 treatment. A marked decrease in pulmonary epithelial and endothelial apoptosis rate as measured by cleaved caspase-3 expression, inflammatory reaction as indicated by tumor necrosis factor α expression, and pulmonary fibrosis as demonstrated by Van Gieson staining and α-smooth muscle actin immunohistochemistry were observed following ODN2088 treatment.
Conclusions
All these findings indicate that blocking downstream TLR9 signaling could be beneficial in prevention or mitigation of ARDS through hemodynamic derangements, inflammation, apoptosis, and fibrosis.

Citations

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A novel mouse model of myositis-associated interstitial lung disease was established by using TLR9 agonist combined with muscle homogenate
Ling Bai, Jiarui Zhu, Wenlan Ma, Peipei Zhao, Feifei Li, Cen Zhang, Sigong Zhang
Clinical and Experimental Immunology.2025;[Epub] CrossRef
Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis
Glenda Trujillo, Alicia Regueiro-Ren, Chunjian Liu, Buqu Hu, Ying Sun, Farida Ahangari, Vitoria Fiorini, Genta Ishikawa, Karam Al Jumaily, Johad Khoury, John McGovern, Chris J. Lee, Xue Yan Peng, Taylor Pivarnik, Huanxing Sun, Anjali Walia, Samuel Woo, Sh
American Journal of Respiratory and Critical Care Medicine.2025; 211(1): 91. CrossRef
CD103+ dendritic cell–fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis
Hannah Carter, Rita Medina Costa, Taylor S. Adams, Talon M. Gilchrist, Claire E. Emch, Monica Bame, Justin M. Oldham, Steven K. Huang, Angela L. Linderholm, Imre Noth, Naftali Kaminski, Bethany B. Moore, Stephen J. Gurczynski
JCI Insight.2025;[Epub] CrossRef
Mechanisms underlying dose-limiting toxicities of conventional chemotherapeutic agents
Mohammad Amin Manavi, Mohammad Hosein Fathian Nasab, Razieh Mohammad Jafari, Ahmad Reza Dehpour
Journal of Chemotherapy.2024; 36(8): 623. CrossRef
Innate Immune Response-Mediated Inflammation in Viral Pneumonia
Weiwei Ni, Xin Wei, Rui Wu
Journal of Pediatric Infectious Diseases.2024; 19(03): 140. CrossRef
Combination of losartan with pirfenidone: a protective anti-fibrotic against pulmonary fibrosis induced by bleomycin in rats
Arian Amirkhosravi, Maryamossadat Mirtajaddini Goki, Mahmoud Reza Heidari, Somayyeh Karami-Mohajeri, Maryam Iranpour, Maryam Torshabi, Mitra Mehrabani, Ali Mandegary, Mehrnaz Mehrabani
Scientific Reports.2024;[Epub] CrossRef
Suppression of miR-17 Alleviates Acute Respiratory Distress-associated Lung Fibrosis by Regulating Mfn2
Mei-xia Xu, Tao Xu, Ning An
Current Medical Science.2024; 44(5): 964. CrossRef
TLR9: A friend or a foe
Mona M. Saber, Nada Monir, Azza S. Awad, Marwa E. Elsherbiny, Hala F. Zaki
Life Sciences.2022; 307: 120874. CrossRef

Vascular Endothelial Growth Factor Bioactivity and Its Receptors in Patients with Acute Respiratory Distress Syndrome.: Simona Gurzu, Ioan Jung, Leonard Azamfirei, Bong Young Shin, Raluca Solomon, Daria Demian, Judith Kovacs, Han Kyeom Kim; Korean J Pathol. 2011;45(2):139-145.; DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.2.139

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Abstract PDF

BACKGROUND
Pathogenesis of acute respiratory distress syndrome (ARDS) is a controversial issue. Few studies have analyzed the possible role of vascular endothelial growth factor (VEGF) and its receptors in this lesion.
METHODS
We compared the immunohistochemical expression of VEGF, its receptors (VEGFR1, VEGFR2) and CD68, in normal lungs and lungs with ARDS. Fifty necropsy cases and 12 lung biopsies with ARDS were analyzed. In total, eight cases were in the early stage and 54 cases were in late stage of ARDS. In addition, the serum level of VEGF165 was also determined.
RESULTS
In normal lungs, all antibodies marked the endothelial cells (EC) and pneumocytes (PC), except for CD68, which was expressed in the alveolar macrophages. In early ARDS, the intensity of VEGF165 and VEGFR2 decreased in both EC and PC. VEGF121 was absent in PC but its expression increased in bronchial epithelium. VEGFR1 was expressed in the integral PC. In late ARDS, VEGF165 down-regulation was more significant in PC and EC but its intensity increased in hyaline membranes (HM). In some cases, HM were CD68 positive. The serum level of VEGF165 was up-regulated, while VEGF165 intensity in PC decreased and the HM appeared in alveolar spaces.
CONCLUSIONS
Sporadic positivity of HM for CD68 and decreasing of VEGF165 expression in EC proved that VEGF165 is produced by PC, destroyed macrophages, and extravasated serum.

Citations

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Hallazgos similares al COVID-19 en un caso fatal de neumonía intersticial descamativa asociada con glomerulonefritis por IgA en una niña de 13 meses de edad
Simona Gurzu, Catalin-Bogdan Satala, Lorena Elena Melit, Adrian Streinu-Cercel, Dan Otelea, Brandusa Capalna, Claudiu Ioan Puiac, Janos Szederjesi, Ioan Jung
Kompass Neumología.2021; 3(2): 69. CrossRef
COVID-19 Like Findings in a Fatal Case of Idiopathic Desquamative Interstitial Pneumonia Associated With IgA Glomerulonephritis in a 13-Month-Old Child
Simona Gurzu, Catalin Bogdan Satala, Lorena Elena Melit, Adrian Streinu-Cercel, Dan Otelea, Brandusa Capalna, Claudiu Ioan Puiac, Janos Szederjesi, Ioan Jung
Frontiers in Pediatrics.2020;[Epub] CrossRef

Morphological Study on the Mechanism of the Central Nervous System Dysfunction Induced by Unipolar Pulsating Magnetic Field in Mice.: Ro Hyun Sung, Gyeong Hoon Kang, Chong Heon Lee, Suk Keun Lee, Young Hae Chung, Yoo Hurn Suh, Jeong Wook Seo, Je G Chi; Korean J Pathol. 1996;30(12):1073-1082.

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Abstract PDF: The morphologic change of the mouse brain after exposure to magnetic field is studied. Our magnetic field model was a pulsed unipolar magnetic field with the flux density of 0.2 - 0.3 tesla and the frequency of 60 hertz. Twelve adult male mice were exposed to the magnetic field for 2, 4, 8, 12, 18 and 24 hours. After the exposure to the magnetic field mice were anesthetized with chloral hydrate, and paraformaldehyde was infused through the left ventricle for fixation. During exposure to the magnetic field, behavioral and weight changes of mice were observed. Mice became irritable and restless, especially during first 2 hours of the exposure. Microscopic and ultrastructural examination on the brain revealed nuclear chromatin clumping of the neuron in mice exposed to the magnetic field for more than four hours. The change was proportional to the exposed time and more prominent in the cerebral cortex. An immunohistochemical study for amyloid precursor protein (APP) was also performed. There was an increased expression of APP in the neuronal cytoplasm of the mouse brain exposed to the magnetic field for 4 hours or more. But the reaction was not proportional to the exposure time and reactive neuron was diffusely distributed through the whole brain. Anti-APP antibody reactivity was not correlated with the chromatin clumping. The mechanism of APP induction was postulated as stress-induced APP-gene induction, and the role of APP was presumed to protect the neuron against hazardous environment.

Case Report

Fine Needle Aspiration Cytology of Salivary Duct Carcinoma: A Case Report.: A Young Park, Hyun Jung Kim, Dong Won Kim, Dong Wha Lee; Korean J Cytopathol. 1997;8(2):143-149.

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Abstract PDF: PURPOSE: To investigate renal toxicity of high-dose intravenous immunoglobulin(IVIG) in children with Kawasaki disease and idiopathic thrombocytopenic purpura. METHODS: 23 children with Kawasaki disease and 7 children with idiopathic thrombocytopenic purpura who were treated with high-dose IVIG(2 g/kg) were evaluated for the change of urine output, blood urea nitrogen(BUN), serum creatinine(Scr), creatinine clearance(Ccr), tubular reabsorption of phosphorus(TRP), fractional excretion of sodium(FENa), 24hour urine b2-microg1obuin/creatinine(b2MG/cr) ratio and urine microalbumin/creatinine(MA/cr) ratio at post-IVIG 1 and 3 day. RESULTS: There was no significant change of urine output, BUN, Scr, Ccr, TRP, 24hour urine b2MG/cr and MA/cr ratio after high-dose IVIG treatment. Transient increase of FENa at post-IVIG 1 day was the only significant change.
CONCLUSION
There was no significant renal toxicity of high-dose IVIG in children with Kawasaki disease and idiopathic thrombocytopenic purpura who had normal renal function.

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