Allograft inflammatory factor-1 in the pathogenesis of bleomycin-induced acute lung injury

Nagahara, Hidetake; Yamamoto, Aihiro; Seno, Taiko; Obayashi, Hiroshi; Kida, Takashi; Nakabayashi, Amane; Kukida, Y.; Fujioka, Kazuki; Fujii, Wataru; Murakami, Ken; Kohno, Masataka; Kawahito, Yutaka

doi:10.5582/bst.2016.01027

Cited by 13 publications

(12 citation statements)

References 36 publications

(36 reference statements)

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“…An automated MATLAB algorithm was implemented to accurately isolate the red stain in the protein also acts as an independent inflammatory stimulus. IBA/AIF-1 induces IL-6, TNF, and CXCL1 (KC) production by pulmonary macrophages and fibroblasts (8,36). The increased neutrophils in the HC3-treated animals would be consistent with increased pulmonary CXCL1(54).…”

Section: Discussionmentioning

confidence: 91%

“…We used Iba1 as a marker of overall inflammation (8,29,(36)(37)(38) to determine the effect of HC3 treatment during the later stage of infection (Fig 7). Fluorescent signal from immunofluorescence stained slides was quantified spatially to determine the degree of inflammation at set time points.…”

Section: Blocking Ach Synthesis Increases Pulmonary Inflammationmentioning

confidence: 99%

“…A growing body of research indicates that acetylcholine (ACh) produced by specialized lymphocytes plays a critical role in regulating inflammation and immunity(1-6). It is now understood that roughly 60% of the ACh content of whole blood is sequestered within mononuclear leukocytes (MNLs), a group comprised of mostly lymphocytes and a small number of monocytes (5)(6)(7)(8). Immune cells preform and store ACh in a similar fashion to neurons (9), allowing for quick and efficient release following appropriate stimulation.…”

Section: Introductionmentioning

confidence: 99%

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Acetylcholine regulates pulmonary inflammation and facilitates the transition from active immunity to tissue repair during respiratory viral infection

Horkowitz

Schwartz

Álvarez

et al. 2020

Preprint

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ABSTRACTInflammatory control is critical to recovery from respiratory viral infection. Acetylcholine (ACh) secreted from non-neuronal sources, including lymphocytes, plays an important, albeit underappreciated, role in regulating immune-mediated inflammation. This study was designed to explore the role of ACh in acute viral infection and recovery. Using the murine model of influenza A, cholinergic status in the lungs and airway was examined over the course of infection and recovery. The results showed that airway ACh remained constant through the early stage of infection and increased during the peak of the acquired immune response. As the concentration of ACh increased, cholinergic lymphocytes appeared in the airway and lungs. Cholinergic capacity was found primarily in CD4 T cells, but also in B cells and CD8 T cells. The cholinergic CD4+ T cells bound to influenza-specific tetramers at the same frequency as their conventional (i.e., non-cholinergic) counterparts. In addition, they were retained in the lungs throughout the recovery phase and could still be detected in the resident memory regions of the lung up to two months after infection. Histologically, cholinergic lymphocytes were found in direct physical contact with activated macrophages throughout the lung. When ACh production was inhibited, mice exhibited increased tissue inflammation, altered lung architecture, and delayed recovery. Together, these findings point to a previously unrecognized role for ACh in the transition from active immunity to recovery and pulmonary repair following respiratory viral infection.

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Section: Discussionmentioning

confidence: 91%

Section: Blocking Ach Synthesis Increases Pulmonary Inflammationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Acetylcholine regulates pulmonary inflammation and facilitates the transition from active immunity to tissue repair during respiratory viral infection

Horkowitz

Schwartz

Álvarez

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Bronchoalveolar lavage fluid analysis. At each time point, bronchoalveolar lavage fluid (BALF) of killed mice was assessed as previously described (30). Briefly, the lungs were exposed and lavaged three times with 1 ml ice-cold phosphate-buffered saline (PBS) through a 20-gauge intravenous catheter inserted in the trachea.…”

Section: Methodsmentioning

confidence: 99%

“…Isolation and stimulation of primary lung fibroblasts. Primary lung fibroblasts were isolated from healthy C57BL/6 mice and cultured as previously described (30). Briefly, lungs were excised, cut up into pieces with a diameter of 1-2 mm, and cultured in a 10-cm culture dish containing DMEM supplemented with 10% fetal bovine serum, 100 U/ml penicillin, and 100 g/ml streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Roles of high-mobility group box 1 and thrombin in murine pulmonary fibrosis and the therapeutic potential of thrombomodulin

Kida

Seno

Nagahara

et al. 2018

American Journal of Physiology-Lung Cellular and Molecular Phys

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Cross talk between inflammation and coagulation plays important roles in acute or subacute progressive pulmonary fibrosis characterized by diffuse alveolar damage. Thrombomodulin is a physiological inhibitor of high-mobility group box 1 (HMGB1), and thrombin and may be effective for this condition. This study investigated the roles of HMGB1 and thrombin in the pathophysiology of bleomycin-induced pulmonary fibrosis and the efficacy of recombinant human soluble thrombomodulin (rhTM). Pulmonary fibrosis was induced in wild-type C57BL/6 mice by intratracheal instillation of bleomycin. We first assessed HMGB1, thrombin, transforming growth factor (TGF)-β1, and α-smooth muscle actin (SMA) levels in bronchoalveolar lavage fluid and lung tissue sections over time. Expression of HMGB1 and thrombin was elevated before that of TGF-β1 and α-SMA and remained high during the fibrotic phase after bleomycin instillation. We next examined whether in vitro stimulation with HMGB1 and thrombin induced expression of TGF-β1 and α-SMA in cultured alveolar macrophages and lung fibroblasts, respectively, by performing quantitative PCR, enzyme-linked immunosorbent assay, Western blot, and immunofluorescence analyses. HMGB1 and thrombin stimulation induced TGF-β1 production by alveolar macrophages, and thrombin stimulation also induced α-SMA expression in lung fibroblasts. Finally, we evaluated the effect of rhTM on bleomycin-induced pulmonary fibrosis. Compared with the vehicle control, both early and late-phase administration of rhTM suppressed the fibrotic process. Our results suggest that HMGB1 and thrombin were involved in the pathophysiology of pulmonary fibrosis via production of profibrotic proteins and that rhTM attenuated bleomycin-induced pulmonary fibrosis. rhTM may be a therapeutic option for acute or subacute pulmonary fibrosis.

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Type I/II Immune Balance Contributes to the Protective Effect of AIF-1 on Hepatic Immunopathology Induced by Schistosoma japonicum in a Transgenic Mouse Model

Lei,

Feng,

Zheng

et al. 2024

Inflammation

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Allograft inflammatory factor-1 in the pathogenesis of bleomycin-induced acute lung injury

Cited by 13 publications

References 36 publications

Acetylcholine regulates pulmonary inflammation and facilitates the transition from active immunity to tissue repair during respiratory viral infection

Acetylcholine regulates pulmonary inflammation and facilitates the transition from active immunity to tissue repair during respiratory viral infection

Roles of high-mobility group box 1 and thrombin in murine pulmonary fibrosis and the therapeutic potential of thrombomodulin

Type I/II Immune Balance Contributes to the Protective Effect of AIF-1 on Hepatic Immunopathology Induced by Schistosoma japonicum in a Transgenic Mouse Model

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