Cigarette smoke-induced pulmonary inflammation is attenuated in CD69-deficient mice

Tsuyusaki, Junichi; Kuroda, Fuminobu; Kasuya, Yoshitoshi; Ishizaki, Shunsuke; Yamauchi, Keita; Sugimoto, Hidekatsu; Kono, Toru; Iwamura, Chiaki; Nakayama, Toshinori

doi:10.3109/10799893.2011.631929

Cited by 13 publications

(14 citation statements)

References 22 publications

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“…CS is a strong inflammatory stimulus that induces the release of proinflammatory mediators in the bronchoalveolar lavage fluid (BALF) (32). To investigate whether cellular changes induced by the DC subset modulated cytokine production, proinflammatory mediators were measured in BALF.…”

Section: Effect Of DC Subset Modulation On the Release Of Proinflammamentioning

confidence: 99%

Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice

Givi

Akbari

Boon

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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The recruitment and activation of inflammatory cells into the respiratory system is considered a crucial feature in the pathophysiology of chronic obstructive pulmonary disease (COPD). Because dendritic cells (DCs) have a pivotal role in the onset and regulation of immune responses, we investigated the effect of modulating DC subsets on airway inflammation by acute cigarette smoke (CS) exposure. CS-exposed mice (5 days) were treated with fms-like tyrosine kinase 3 ligand (Flt3L) and 120g8 antibody to increase total DC numbers and deplete plasmacytoid DCs (pDCs), respectively. Flt3L treatment decreased the number of inflammatory cells in the bronchoalveolar lavage (BALF) of the smoke-exposed mice and increased these in lung tissue. DC modulation reduced IL-17 and increased IL-10 levels, which may be responsible for the suppression of the BALF cells. Furthermore, depletion of pDCs led to increased infiltration of alveolar macrophages while restricting the presence of CD103(+) DCs. This study suggests that DC subsets may differentially and compartment-dependent influence the inflammation induced by CS. pDC may play a role in preventing the pathogenesis of CS by inhibiting the alveolar macrophage migration to lung and increasing CD103(+) DCs at inflammatory sites to avoid extensive lung tissue damage.

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Section: Effect Of DC Subset Modulation On the Release Of Proinflammamentioning

confidence: 99%

Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice

Givi

Akbari

Boon

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…7 However, CD69-deficient mice showed enhanced inflammatory responses in models of allergic asthma, skin contact hypersensitivity, 8 collagen-induced arthritis, 9 NK-sensitive tumors, 10 and experimental autoimmune myocarditis. 11 In contrast, CD69-deficient mice were found to have less inflammation in models of dextran sulfate sodium-induced acute and chronic colitis, 12 cigarette smoke-induced pulmonary inflammation, 13 bleomycininduced lung inflammation and fibrosis, 14 another study of collagen-induced arthritis, 15 and allergic airway inflammation, 16 and they were also protected from vaccinia virus infection. 17 These results suggest that the role of CD69 depends on the type of disease and the cell types involved, and it may also depend on the strain of CD69-deficient mice used.…”

Section: Introductionmentioning

confidence: 99%

CD69 Plays a Beneficial Role in Ischemic Stroke by Dampening Endothelial Activation

Brait

Miró-Mur

Pérez-de-Puig

et al. 2019

Circulation Research

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Rationale: CD69 is an immunomodulatory molecule induced during lymphocyte activation. Following stroke, T lymphocytes upregulate CD69 but its function is unknown. Objective: We investigated whether CD69 was involved in brain damage following ischemic stroke. Methods and Results: We used adult male mice on the C57BL/6 or BALB/c backgrounds, including wild type mice and CD69-/mice, and CD69 +/+ and CD69-/lymphocyte-deficient Rag2-/mice, and generated chimeric mice. We induced ischemia by transient or permanent middle cerebral artery occlusion. We measured infarct volume, assessed neurological function, and studied CD69 expression, as well as platelet function, fibrin(ogen) deposition, and von Willebrand factor (vWF) expression in brain vessels and vWF content and activity in plasma, and performed the tail-vein bleeding test and the carotid artery FeCl3-induced thrombosis model. We also carried out primary glial cell cultures, and sorted brain CD45-CD11b-CD31 + endothelial cells for mRNA expression studies. We blocked vWF by i.v. administration of anti-vWF antibodies. CD69-/mice showed larger infarct volumes and/or worse neurological deficits than the wild type mice after ischemia. This worsening effect was not attributable to lymphocytes or other hematopoietic cells. CD69 deficiency lowered the time to thrombosis in the carotid artery despite platelet function not being affected. Ischemia upregulated Cd69 mRNA expression in brain endothelial cells. CD69-deficiency increased fibrin(ogen) accumulation in the ischemic tissue, and plasma vWF content and activity, and vWF expression in brain vessels. Blocking vWF reduced infarct volume and reverted the detrimental effect of CD69-/deficiency. Conclusion: CD69 deficiency promotes a pro-thrombotic phenotype characterized by increased vWF and worse brain damage after ischemic stroke. The results suggest that CD69 acts as a down-regulator of endothelial activation.

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“…There are some discrepancies in the implication of the role for CD69 in the pathogenesis of inflammation using these two lines of Cd69 −/− mice. As we discussed in the earlier sections, our Cd69 −/− (a) mice showed limited inflammatory responses in several mouse models such as OVA-induced allergic airway inflammation, 70 DSS-induced colitis, 73 anti-type II collagen Ab induced arthritis, 69 cigarette smoke-induced pulmonary inflammation 74 and bleomycin-induced lung injury fibrosis. 75 In contrast, the other line of Cd69 −/− (b) mice showed enhanced inflammation in OVA-induced allergic airway inflammation 77 and no difference in inflammatory responses in anti-type II collagen Ab induced arthritis.…”

Section: Two Lines Of Cd69 −/− Mice With Some Variations In Implicamentioning

confidence: 71%

“…Other disease models such as cigarette smoke-induced pulmonary inflammation 74 and bleomycin-induced lung injury fibrosis 75 were also ameliorated in Cd69 −/− mice. In both models, the authors demon-…”

Section: Roles Of Cd69 In Murine Models Of Inflammatory Diseasementioning

confidence: 93%

“…Other disease models such as cigarette smoke‐induced pulmonary inflammation and bleomycin‐induced lung injury fibrosis were also ameliorated in Cd69 −/− mice. In both models, the authors demonstrated that infiltration of macrophages, neutrophils and lymphocytes (lymphocytes are only in bleomycin‐induced fibrosis) to the inflamed lung was significantly impaired in Cd69 −/− mice.…”

Section: Cd69 and Inflammatory Diseasesmentioning

confidence: 94%

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Crucial role for CD69 in allergic inflammatory responses: CD69‐Myl9 system in the pathogenesis of airway inflammation

Kimura

Hayashizaki

Tokoyoda

et al. 2017

Immunological Reviews

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CD69 has been known as an early activation marker of lymphocytes; whereas, recent studies demonstrate that CD69 also has critical functions in immune responses. Early studies using human samples revealed the involvement of CD69 in various inflammatory diseases including asthma. Moreover, murine disease models using Cd69 mice and/or anti-CD69 antibody (Ab) treatment have revealed crucial roles for CD69 in inflammatory responses. However, it had not been clear how the CD69 molecule contributes to the pathogenesis of inflammatory diseases. We recently elucidated a novel mechanism, in which the interaction between CD69 and its ligands, myosin light chain 9, 12a and 12b (Myl9/12) play a critical role in the recruitment of activated T cells into the inflammatory lung. In this review, we first summarize CD69 function based on its structure and then introduce the evidence for the involvement of CD69 in human diseases and murine disease models. Then, we will describe how we discovered CD69 ligands, Myl9 and Myl12, and how the CD69-Myl9 system regulates airway inflammation. Finally, we will discuss possible therapeutic usages of the blocking Ab to the CD69-Myl9 system.

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Cigarette smoke-induced pulmonary inflammation is attenuated in CD69-deficient mice

Cited by 13 publications

References 22 publications

Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice

Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice

CD69 Plays a Beneficial Role in Ischemic Stroke by Dampening Endothelial Activation

Crucial role for CD69 in allergic inflammatory responses: CD69‐Myl9 system in the pathogenesis of airway inflammation

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