Acute effects of smoke exposure on the cellular and cytokine profile in isolated perfused lungs

Kyi, Min; Miyazaki, Yasunari; Inoue, Takeshi; Miyake, Shuji; Matsukawa, Akihiro; Yoshizawa, Yasuyuki

doi:10.1016/s0034-5687(00)00147-x

Cited by 3 publications

(8 citation statements)

References 25 publications

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“…1D). To assess the extent of lung epithelium damage we measured the total protein content in BAL fluid (21) and found increased protein concentrations in the BAL fluid of CD200 Ϫ/Ϫ mice (Fig. 1E).…”

Section: Lack Of Cd200 Causes Severe Pathology At Subclinical Doses Omentioning

confidence: 99%

Lack of CD200 Enhances Pathological T Cell Responses during Influenza Infection

Rygiel

Rijkers

Ruiter

et al. 2009

The Journal of Immunology

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Influenza virus infection can be accompanied by life-threatening immune pathology most likely due to excessive antiviral responses. Inhibitory immune receptors may restrain such overactive immune responses. To study the role of the inhibitory immune receptor CD200R and its ligand CD200 during influenza infection, we challenged wild-type and CD200−/− mice with influenza virus. We found that CD200−/− mice in comparison to wild-type controls when inoculated with influenza virus developed more severe disease, associated with increased lung infiltration and lung endothelium damage. CD200−/− mice did develop adequate adaptive immune responses and were able to control viral load, suggesting that the severe disease was caused by a lack of control of the immune response. Interestingly, development of disease was completely prevented by depletion of T cells before infection, despite dramatically increased viral load, indicating that T cells are essential for the development of disease symptoms. Our data show that lack of CD200-CD200R signaling increases immune pathology during influenza infection, which can be reduced by T cell depletion.

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Section: Lack Of Cd200 Causes Severe Pathology At Subclinical Doses Omentioning

confidence: 99%

Lack of CD200 Enhances Pathological T Cell Responses during Influenza Infection

Rygiel

Rijkers

Ruiter

et al. 2009

The Journal of Immunology

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“…Of the 29 papers, 18 reported that cigarette smoke activated MU [42-50, 52-55, 58, 59, 61, 65, 67]. In contrast, of the 29 studies, 11 reported that cigarette smoke did not activate MU [24,40,41,51,56,57,60,[62][63][64]66].…”

Section: Analysis Of the Retrieved Literaturementioning

confidence: 99%

“…These included international reference cigarettes (e.g., KY 1R3F) (N = 11) [24, 40, 42, 44-47, 51, 54, 58, 66] and popular market brands (N = 10) [41,43,49,50,52,56,[60][61][62][63]. In many cases, the cigarettes were not defined (N = 8) [48,53,55,57,59,64,65,67].…”

Section: Analysis Of the Retrieved Literaturementioning

confidence: 99%

“…Others stored smoke test material for indefinite periods. In some studies (N = 11) [40,44,45,47,50,53,56,61,64,66,67], whole fresh cigarette smoke was passed over MU cultures. In other instances, the cigarette smoke was bubbled through tissue culture medium (cigarette smoke extract, CSE), usually RPMI 1640 without serum (N = 8) [24,41,43,49,52,54,62,63].…”

Section: Analysis Of the Retrieved Literaturementioning

confidence: 99%

“…1). Of the 19 papers that used MU from the lung, 11 reported a pro-inflammatory response [43-47, 50, 52-54, 58, 61], whereas eight papers reported no response [40,41,56,57,59,60,62,63]. Seven papers reported the results of studies that employed MU cell lines.…”

Section: Diversity Of Mu Used As Bioassay Cellsmentioning

confidence: 99%

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Inflammatory response of lung macrophages and epithelial cells to tobacco smoke: a literature review of ex vivo investigations

et al. 2010

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Chronic inflammation contributes to the initiation and progression of tumors and tobacco smoke-associated inflammation is associated with malignant and certain non-neoplastic lung diseases. Reported herein are the results of an interpretative synthesis review of the literature assessing the inflammatory response of lung macrophages (MPhi) and epithelial cells to tobacco smoke as measured ex vivo. Papers were retrieved using Boolean operations from PubMed and Scopus. Many writings reported the results of assays of human MPhi from fresh surgically excised human lung tissue, bronchoalveolar lavage, activated blood monocytes, long-term cell lines and MPhi from different laboratory animals. Some publications reported the findings of comparative studies of lung MPhi freshly isolated from the lungs of smokers and non-smokers. Other papers described the effect of tobacco smoke on lung epithelial cells. Most investigators quantified the response of the target cells to tobacco smoke by measuring the production of pro-inflammatory mediators; these included chemokines, cytokines, reactive oxygen species and enzymes. Investigators have reported conflicting observations of the response of human and animal MPhi and epithelial cells to tobacco smoke. The spectrum included papers describing robust production of various inflammatory mediators, significant reduction of a pro-inflammatory response to a known stimulant and overt cytotoxicity. This literature review documents that there exists no consensus, and no emerging trend line, of the reproducible effect(s) of cigarette smoke. This discrepancy reflects the absence of standardized protocols for collecting, processing and bioassaying the smoke, a highly complex aerosol, and identifies the need for establishing collaborative research schemes.

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