Significantly elevated expression of PF4 (platelet factor 4) and eotaxin in the NOA mouse, a model for atopic dermatitis

Watanabe, Otsu; Natori, Kyoko; Tamari, Mayumi; Shiomoto, Yasuhisa; Kubo, Shuji; Nakamura, Yusuke

doi:10.1007/s100380050136

Cited by 45 publications

(19 citation statements)

References 21 publications

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“…Furthermore, as compared with other chemokines, PF-4 displays an exceptionally high degree of sequence identity between isoforms of different species (43,44), e.g., human and murine PF-4 share Ͼ64% identity on the protein level. This may explain why human PF-4 functionally cross-reacted with murine macrophages with an efficacy comparable with that of human cells.…”

Section: Discussionmentioning

confidence: 99%

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

Первушина¹,

Scheuerer²,

Reiling

et al. 2004

The Journal of Immunology

105

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Platelet factor 4 (PF-4), a platelet-derived CXC chemokine, is known to prevent human monocytes from apoptosis and to promote differentiation of these cells into HLA-DR− macrophages. In this study, we investigated the role of PF-4 in the control of acute monocyte proinflammatory responses involved in the direct combat of microbial invaders. We show that PF-4 increases monocyte phagocytosis and provokes a strong formation of oxygen radicals but lacks a chemotactic activity in these cells. Compared with FMLP, PF-4-induced oxidative burst was later in its onset but was remarkably longer in its duration (lasting for up to 60 min). Furthermore, in PF-4-prestimulated cells, FMLP- as well as RANTES-induced burst responses became synergistically enhanced. As we could show, PF-4-mediated oxidative burst in monocytes does not involve Gi proteins, elevation of intracellular free calcium concentrations, or binding to CXCR3B, a novel PF-4 receptor recently discovered on endothelial cells. Moreover, we found that PF-4 acts on macrophages in a dual manner. On the one hand, very similar to GM-CSF or M-CSF, PF-4 treatment of monocytes generates macrophages with a high capacity for unspecific phagocytosis. On the other hand, short term priming of GM-CSF-induced human macrophages with PF-4 substantially increases their capability for particle ingestion and oxidative burst. A comparable effect was also observed in murine bone marrow-derived macrophages, indicating cross-reactivity of human PF-4 between both species. Taken together, PF-4 may play a crucial role in the induction and maintenance of an unspecific immune response.

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Section: Discussionmentioning

confidence: 99%

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

Первушина¹,

Scheuerer²,

Reiling

et al. 2004

The Journal of Immunology

105

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“…Evidence, in animals, suggests that PF4 may contribute significantly to the development of atopic dermatitis (7). Throughout their preliminary studies the authors have recorded increased plasma level of PF4 in 9 male AEDS patients.…”

Section: Introductionmentioning

confidence: 98%

Enhanced Platelet Activation in Patients with Atopic Eczema/Dermatitis Syndrome

2004

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Data gathered prove that circulating platelets are activated upon human allergic inflammation, partly as a result of direct IgE-mediated process. It has been indicated that platelets may contribute to pathogenesis of atopic eczema/dermatitis syndrome (AEDS). Authors of the recent study have investigated systemic platelet activation in patients with AEDS on the basis of blood level of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4), which are recognized markers of platelet activation, also belonging to C-X-C chemokine family. Plasma levels of beta-TG and PF4 were measured by enzyme-linked immunoassay (ELISA) in 18 AEDS patients with moderate disease activity and 23 healthy, nonatopic individuals. No differences in peripheral platelet count of the two groups were noted. Only four (33.3%) AEDS patients represented beta-TG and PF4 within the control range; plasma beta-TG and PF4 were significantly increased (p < 0.001) in the AEDS group compared as a whole with the control subjects. No association between circulating concentrations of beta-TG or PF4 and total IgE levels in AEDS patients was proved. The results suggest that some patients with AEDS may have enhanced blood platelet activity as expressed by beta-TG and PF4 level.

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“…nOA mice are hairless, and a specialized diet exacerbates the dermatitis. A major gene responsible for the dermatitis is present on murine chromosome 14 [29].…”

Section: Noa (Naruto Research Institute Otsuka Atrichia) Micementioning

confidence: 99%

Recent Findings in Mouse Models for Human Atopic Dermatitis

et al. 2012

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Atopic dermatitis (AD) is a chronic inflammatory skin disease, with its major clinical feature being persistent itch sensation in the skin. There are extremely few animal models to reproduce the complicated condition of a patient with AD; therefore researchers have been confronted with some difficulties in pathologic analysis and drug development for AD. Although various models have been proposed and developed, there is no doubt that the spontaneous mouse model, NC mice, gave the greatest impact. NC mice enabled us to analyze pathogenesis of allergic skin abnormalities as well as development of new drugs for AD. However, many questions still remain in the pathogenesis of AD. In recent years, the study of the itch has attracted our attention because itch is one of the most unbearable symptoms of AD. For development of an effective treatment to overcome the itch, not only a precise animal model but also an accurate evaluation protocol are needed. This review summarizes some mouse models of AD, particularly focusing on NC mice, together with a novel evaluation system for scratching behavior of mice to help the understanding of researchers.

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Significantly elevated expression of PF4 (platelet factor 4) and eotaxin in the NOA mouse, a model for atopic dermatitis

Cited by 45 publications

References 21 publications

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

Platelet Factor 4/CXCL4 Induces Phagocytosis and the Generation of Reactive Oxygen Metabolites in Mononuclear Phagocytes Independently of Gi Protein Activation or Intracellular Calcium Transients

Enhanced Platelet Activation in Patients with Atopic Eczema/Dermatitis Syndrome

Recent Findings in Mouse Models for Human Atopic Dermatitis

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