Pulmonary Interstitial Macrophages stIMulate Regulatory T Cell Responses
Am J Respir Cell Mol Biol. 2024 Mar 6. doi: 10.1165/rcmb.2024-0049ED. Online ahead of print.NO ABSTRACTPMID:38445963 | DOI:10.1165/rcmb.2024-0049ED (Source: Am J Respir Cell Mol...)
Source: Am J Respir Cell Mol... - March 6, 2024 Category: Respiratory Medicine Authors: Stephen A Schworer Timothy P Moran Source Type: research
Pulmonary Interstitial Macrophages stIMulate Regulatory T Cell Responses
Am J Respir Cell Mol Biol. 2024 Mar 6. doi: 10.1165/rcmb.2024-0049ED. Online ahead of print.NO ABSTRACTPMID:38445963 | DOI:10.1165/rcmb.2024-0049ED (Source: Am J Respir Cell Mol...)
Source: Am J Respir Cell Mol... - March 6, 2024 Category: Respiratory Medicine Authors: Stephen A Schworer Timothy P Moran Source Type: research
March Highlights/Papers by Junior Investigators/NIH News
Am J Respir Cell Mol Biol. 2024 Mar;70(3):iii-iv. doi: 10.1165/rcmb.70i3RedAlert.NO ABSTRACTPMID:38426711 | DOI:10.1165/rcmb.70i3RedAlert (Source: Am J Respir Cell Mol...)
Source: Am J Respir Cell Mol... - March 1, 2024 Category: Respiratory Medicine Source Type: research
March Highlights/Papers by Junior Investigators/NIH News
Am J Respir Cell Mol Biol. 2024 Mar;70(3):iii-iv. doi: 10.1165/rcmb.70i3RedAlert.NO ABSTRACTPMID:38426711 | DOI:10.1165/rcmb.70i3RedAlert (Source: Am J Respir Cell Mol...)
Source: Am J Respir Cell Mol... - March 1, 2024 Category: Respiratory Medicine Source Type: research
March Highlights/Papers by Junior Investigators/NIH News
Am J Respir Cell Mol Biol. 2024 Mar;70(3):iii-iv. doi: 10.1165/rcmb.70i3RedAlert.NO ABSTRACTPMID:38426711 | DOI:10.1165/rcmb.70i3RedAlert (Source: Am J Respir Cell Mol...)
Source: Am J Respir Cell Mol... - March 1, 2024 Category: Respiratory Medicine Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK Mediated Efferocytosis
Am J Respir Cell Mol Biol. 2024 Feb 22. doi: 10.1165/rcmb.2023-0390OC. Online ahead of print.ABSTRACTLung inflammation, caused by acute exposure to ozone (O3) - one of the six criteria air pollutants - is a significant source of morbidity in susceptible individuals. Alveolar macrophages (AMØs) are the most abundant immune cells in the normal lung and their number increases following O3 exposure. However, the role of AMØs in promoting or limiting O3-induced lung inflammation has not been clearly defined. Here, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human vo...
Source: Am J Respir Cell Mol... - February 22, 2024 Category: Respiratory Medicine Authors: Marissa A Guttenberg Aaron T Vose Anastasiya Birukova Kaitlyn Lewars R Ian Cumming Michaela C Albright Jasper I Mark Claudia J Salazar Suchitra Swaminathan Zhan Yu Yuliana V Sokolenko Elsie Bunyan Michael J Yaeger Michael B Fessler Loretta G Que Kymberly Source Type: research
Presenilin 1 Is a Therapeutic Target in Pulmonary Hypertension and Promotes Vascular Remodeling
Am J Respir Cell Mol Biol. 2024 Feb 21. doi: 10.1165/rcmb.2022-0426OC. Online ahead of print.ABSTRACTSmall muscular pulmonary artery remodeling is a dominant feature of PAH. PSEN1 affects angiogenesis, cancer and Alzheimer's disease. We aimed to determine the role of PSEN1 in the pathogenesis of vascular remodeling in PH. Haemodynamics and vascular remodeling in the Psen1-knockin and smooth muscle-specific Psen1-knockout mice were assessed. The functional partners of PSEN1 were predicted by bioinformatics analysis and biochemical experiments. The therapeutic effect of PH was evaluated by administration of the PSEN1-specifi...
Source: Am J Respir Cell Mol... - February 21, 2024 Category: Respiratory Medicine Authors: Tingting Shen Jiucheng Shi Xijuan Zhao Li Fu Na Wang Jiaxin Han Xiaodong Zheng Yingli Chen Minghui Li Cui Ma Pixu Liu Daling Zhu Source Type: research
Presenilin 1 Is a Therapeutic Target in Pulmonary Hypertension and Promotes Vascular Remodeling
Am J Respir Cell Mol Biol. 2024 Feb 21. doi: 10.1165/rcmb.2022-0426OC. Online ahead of print.ABSTRACTSmall muscular pulmonary artery remodeling is a dominant feature of PAH. PSEN1 affects angiogenesis, cancer and Alzheimer's disease. We aimed to determine the role of PSEN1 in the pathogenesis of vascular remodeling in PH. Haemodynamics and vascular remodeling in the Psen1-knockin and smooth muscle-specific Psen1-knockout mice were assessed. The functional partners of PSEN1 were predicted by bioinformatics analysis and biochemical experiments. The therapeutic effect of PH was evaluated by administration of the PSEN1-specifi...
Source: Am J Respir Cell Mol... - February 21, 2024 Category: Respiratory Medicine Authors: Tingting Shen Jiucheng Shi Xijuan Zhao Li Fu Na Wang Jiaxin Han Xiaodong Zheng Yingli Chen Minghui Li Cui Ma Pixu Liu Daling Zhu Source Type: research
Lysophospholipid Acyltransferase 9 Promotes Emphysema Formation via Platelet-activating Factor
Am J Respir Cell Mol Biol. 2024 Feb 20. doi: 10.1165/rcmb.2023-0253OC. Online ahead of print.ABSTRACTCigarette smoking is known to be the leading cause of chronic obstructive pulmonary disease (COPD). However, the detailed mechanisms have not been elucidated. Platelet-activating factor (PAF), a potent inflammatory mediator, is involved in the pathogenesis of various respiratory diseases, such as bronchial asthma or COPD. We focused on lysophospholipid acyltransferase 9 (LPLAT9), a biosynthetic enzyme of PAF, in the pathogenesis of COPD. LPLAT9 gene expression was observed in excised COPD lungs and single-cell RNA sequencin...
Source: Am J Respir Cell Mol... - February 20, 2024 Category: Respiratory Medicine Authors: Hiroaki Murano Sumito Inoue Tomomi Hashidate-Yoshida Hideo Shindou Takao Shimizu Yoichiro Otaki Yukihiro Minegishi Takumi Kitaoka Mitsuru Futakuchi Akira Igarashi Michiko Nishiwaki Takako Nemoto Masamichi Sato Maki Kobayashi Kento Sato Toshinari Hanawa Os Source Type: research
