Cloning and characterization of cDNAs for murine macrophage inflammatory protein 2 and its human homologues.

Tekamp-Olson, Patricia; Gallegos, C; Bauer, Diane; McClain, Joyce; Sherry, Barbara; Fabre, Myriam; Deventer, Sander van; Cerami, Anthony

doi:10.1084/jem.172.3.911

Cited by 267 publications

(148 citation statements)

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“…Similar to H. pylori infection in human gastric mucosa, 44 H. felis infection markedly enhanced gene expression of IL-1b, TNF-a, IL-7, and MIP-2, a mouse counterpart for human IL-8, 45 in the stomach of WT mice. Although IL-1b and TNF-a mRNA expression was significantly lower in TRX-1-TG mice than in WT mice, gene expression of IL-7 and MIP-2 was not different from WT mice.…”

Section: Discussionmentioning

confidence: 97%

Helicobacter felis-induced gastritis was suppressed in mice overexpressing thioredoxin-1

Kawasaki

Nishio

Nakamura

et al. 2005

Laboratory Investigation

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Thioredoxin-1 (TRX-1) is a redox-active protein involved in scavenging reactive oxygen species and regulating redox-sensitive transcription factors. TRX-1 is induced in various inflammatory conditions and shows cytoprotective action. We investigated the roles of TRX-1 in the host defense mechanism against Helicobacter felis (H. felis) infection. Transgenic (TG) mice overexpressing human TRX-1 and wild-type (WT) mice were orally inoculated with H. felis. After 2 months, histology, oxidative damage, and gene expression of several cytokines, including macrophage inflammatory protein-2 (MIP-2), a murine equivalent to interleukin (IL)-8, in the gastric mucosa were investigated. Furthermore, the effects of TRX-1 on oxidative stress and neutrophil migration were studied both in vivo and in vitro. The gastric mucosa was thickened in H. felis-infected WT mice, but not in infected TRX-1-TG mice. Histologically, all H. felis-infected WT mice developed moderate-to-severe gastritis, whereas the development of gastritis was significantly suppressed in infected TRX-1-TG mice. Oxidative damage markers, 8-hydroxy-2 0 -deoxyguanosine and malondialdehyde, increased in the stomach of infected WT mice, but not TRX-1-TG mice. Upregulation of IL-1b and tumor necrosis factor-a gene expression in H. felisinfected TRX-1-TG mice was significantly lower than in WT mice. However, upregulation of MIP-2 and IL-7 was not different between the two groups. TRX-1 suppressed oxidative cytotoxicity and DNA damage, and inhibited neutrophil migration both in vivo and in vitro. The present study suggests that overexpression of TRX-1 suppresses H. felis-induced gastritis by inhibiting chemotaxis of neutrophils and reducing oxidative stress.

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Section: Discussionmentioning

confidence: 97%

Helicobacter felis-induced gastritis was suppressed in mice overexpressing thioredoxin-1

Kawasaki

Nishio

Nakamura

et al. 2005

Laboratory Investigation

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“…A 351-bp fragment of MIP-2 was amplified by reverse transcriptasepolymerase chain reaction from total cellular RNA from LPS-treated RAW 264.7 cells, using the primers ACCAACCACCAGGCTACAG and CAGCGAG-GCACATCAGG. The amplified product was cloned into pCR2.1 (Invitrogen, Carlsbad, CA) and verified by sequencing to be identical to nt 107-457 of the murine MIP-2 cDNA [7]. We previously used as a constitutive control an S2 probe (CHOb) derived from Chinese hamster ovary cells.…”

Section: Plasmids and Probesmentioning

confidence: 99%

“…The best-studied ELR ϩ CXC chemokine is human interleukin-8 (IL-8). However, six additional human ELR ϩ CXC chemokines have been described: neutrophil-activating peptide-2 (NAP-2) [5]; growth-related oncogenes/melanoma growth stimulating activity (GRO/ MGSA)-␣, -␤, and -␥ [6,7]; epithelial cell-derived neutrophil-activating peptide-78 (ENA-78) [8]; and granulocyte chemotactic protein-2 (GCP-2) [9,10]. Two human receptors for the ELR ϩ CXC chemokines have been identified, CXCR1 and CXCR2 [11,12].…”

Section: Introductionmentioning

confidence: 99%

“…However, mouse neutrophils express a receptor homologous to human CXCR2 that mediates neutrophil chemotaxis in response to human IL-8 and to the murine ELR ϩ CXC chemokines KC and macrophage inflammatory protein 2 (MIP-2) [13,14]. KC and MIP-2 are related to the three human GRO chemokines [7,15]. Neutrophils from mice with a targeted deletion of CXCR2 fail to respond to KC, MIP-2, or human IL-8, but exhibit normal chemotaxis in response to the complement fragment C5a [14].…”

Section: Introductionmentioning

confidence: 99%

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The murine neutrophil-chemoattractant chemokines LIX, KC, and MIP-2 have distinct induction kinetics, tissue distributions, and tissue-specific sensitivities to glucocorticoid regulation in endotoxemia

Rovai

Herschman

Smith

1998

Journal of Leukocyte Biology

165

144

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Lipopolysaccharide-induced CXC chemokine (LIX) is a novel murine neutrophil-chemoattractant CXC chemokine cloned as a glucocorticoidattenuated response gene. We investigated LIX message expression in an acute endotoxemia model. LIX message peaks later than KC or macrophage inflammatory protein-2 (MIP-2) and remains elevated longer in almost all tissues. Induced LIX message expression in heart is 5-to 6-fold greater than in lung and spleen, and 20-fold greater than in liver. In contrast, KC expression is equal in heart, lung, and liver, whereas MIP-2 expression is strongest in the lung. Glucocorticoid regulation of these genes also differs. Endotoxemia-induced LIX message expression in the lung is markedly enhanced in adrenalectomized mice and strongly attenuated by dexamethasone, whereas lung KC and MIP-2 expression are unaffected by glucocorticoids. It is surprising to note that endotoxemia-induced brain expression of LIX (but not KC or MIP-2) is increased by dexamethasone. These observations suggest that LIX may have biological roles distinct from KC and MIP-2. J. Leukoc. Biol. 64: 494-502; 1998.

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“…MIP-I and MlP-2 represent two families of structurally related proteins, and are part of the proinflammatory supergene 'intererine' cytokine family [17]. MIP-la/MlP-I// have been shown to exert a variety of important effects, including modulation of rnacrophage function, pyrogenic activity i>j vivo, as well as T cell adhesion and chemoiaxis [18][19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Alveolar macrophages from subjects infected with HIV-1 express macrophage inflammatory protein-1α (MIP-1α): contribution to the CD8+ alveolitis

Michel

Ghadirian

1994

Clinical and Experimental Immunology

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SUMMARY We examined the synthesis and release of MIP‐1α in alveolar macrophages obtained from normal subjects or subjects infected with HIV‐1, at different stages of the disease. HIV‐1‐infected subjects in groups II, III and IV all had significant interstitial pneumonitis, featuring a significant infiltration of CD8+ lymphocytes in the bronchoalveolar lavage. Alveolar macrophages from HIV‐1‐infected subjects were shown to express significant levels of MIP‐1α via immunohistochemistry, both spontaneously and in response to lipopolysaccharide (LPS), whereas cells from normal subjects expressed very low levels of the cytokine. Supernatants of alveolar macrophages from HIV‐1‐infected subjects exerted strong chemotactic activity for purified activated blood CD8+ T lymphocytes, which was strongly inhibited by neutralizing MIP‐1α. Studies of patients with HIV‐1 infection at different stages of the disease showed that MIP‐1α secretion increased as viral infection developed, There was a significant positive correlation between MIP‐1α secretion and the CD8+ alveolitis in HIV‐1‐infected subjects. Infection of alveolar macrophages in vitro with three distinct strains of HIV‐1 which replicated profusely in macrophages did not induce the expression of MIP‐1α. Collectively, these data suggest that HIV‐1 infection in vivo induces MIP‐1α expression and release in alveolar macrophages, and this appears to contribute significantly to the alveolar lymphocytosis seen in HIV‐1‐infected subjects.

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Cloning and characterization of cDNAs for murine macrophage inflammatory protein 2 and its human homologues.

Cited by 267 publications

References 56 publications

Helicobacter felis-induced gastritis was suppressed in mice overexpressing thioredoxin-1

Helicobacter felis-induced gastritis was suppressed in mice overexpressing thioredoxin-1

The murine neutrophil-chemoattractant chemokines LIX, KC, and MIP-2 have distinct induction kinetics, tissue distributions, and tissue-specific sensitivities to glucocorticoid regulation in endotoxemia

Alveolar macrophages from subjects infected with HIV-1 express macrophage inflammatory protein-1α (MIP-1α): contribution to the CD8+ alveolitis

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