Requirement of Mip-1α for an Inflammatory Response to Viral Infection

Cook, Donald N.; Beck, Melinda A.; Coffman, Thomas M.; Kirby, Suzanne L.; Sheridan, John F.; Pragnell, Ian B.; Smithies, Oliver

doi:10.1126/science.7667639

Cited by 590 publications

(321 citation statements)

References 14 publications

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“…Islet infiltration begins at 4 -6 wk of age in our colony of female NOD mice, and progression to destructive insulitis and overt diabetes occurs by 4 -6 mo of age. The incidence of diabetes in female NOD mice in our colony is 40 -50% at 15 wk of age and 80 -90% by 25 wk. C57BL/6J and 129/J mice were obtained from The Jackson Laboratory (Bar Harbor, ME).…”

Section: Methodsmentioning

confidence: 99%

“…Ϫ/Ϫ mice C57BL/6.MIP-1␣ Ϫ/Ϫ mice, previously shown to be resistant to virus-induced autoimmune inflammation, were generated in 129 embryonic stem cells by gene-targeted disruption (25). Mice were backcrossed six generations onto the NOD background (Ͼ98% NOD-like; Idd1-7, Idd10, Idd12, Idd14, and Idd15 positive) and intercrossed to generate mice with the NOD.MIP-1␣ Ϫ/Ϫ and NOD.MIP-1␣ ϩ/ϩ genotypes.…”

Section: Generation Of Nodmip-1␣mentioning

confidence: 99%

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Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes

Cameron

Arreaza

Grattan

et al. 2000

The Journal of Immunology

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133

107

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We investigated the biological role of CC chemokines in the Th1-mediated pathogenesis of spontaneous type I diabetes in nonobese diabetic (NOD) mice. Whereas an elevated ratio of macrophage inflammatory protein-1α (MIP-1α):MIP-1β in the pancreas correlated with destructive insulitis and progression to diabetes in NOD mice, a decreased intrapancreatic MIP-1α:MIP-1β ratio was observed in nonobese diabetes-resistant (NOR) mice. IL-4 treatment, which prevents diabetes in NOD mice by polarizing intraislet Th2 responses, decreased CCR5 expression in islets and potentiated a high ratio of MIP-1β and monocyte chemotactic protein-1 (MCP-1): MIP-1α in the pancreas. Furthermore, NOD.MIP-1α−/− mice exhibited reduced destructive insulitis and were protected from diabetes. Neutralization of MIP-1α with specific Abs following transfer of diabetogenic T cells delayed the onset of diabetes in NOD.Scid recipients. These studies illustrate that the temporal expression of certain CC chemokines, particularly MIP-1α, and the CCR5 chemokine receptor in the pancreas is associated with the development of insulitis and spontaneous type I diabetes.

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Section: Methodsmentioning

confidence: 99%

Section: Generation Of Nodmip-1␣mentioning

confidence: 99%

Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes

Cameron

Arreaza

Grattan

et al. 2000

The Journal of Immunology

Self Cite

133

107

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“…CCL3 -/-mice [54] were purchased from The Jackson Laboratory (Bar Harbor, ME). CCR1 -/-mice [12] and CCR5 -/-mice [55] were generated as described previously.…”

Section: Micementioning

confidence: 99%

Role of C‐C chemokine receptors 1 and 5 and CCL3/macrophage inflammatory protein‐1α in the cutaneous Arthus reaction: possible attenuation of their inhibitory effects by compensatory chemokine production

et al. 2004

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The deposition of immune complexes induces an acute inflammatory response with tissue injury. Immune complex-induced tissue injury is mediated by inflammatory cell infiltration that is highly regulated by multiple chemokines. To assess the role of the chemokine receptors CCR1 and CCR5, and a ligand for these receptors CCL3/macrophage inflammatory protein1a, in this pathogenic process, the reverse passive cutaneous Arthus reaction was induced in mice lacking CCR1, CCR5, or CCL3. Edema was significantly attenuated in CCR1-deficient (CCR1 -/-) and CCL3 -/-mice but not CCR5 -/-mice, compared with wild-type mice. Numbers of infiltrating neutrophils and mast cells were reduced in CCL3 -/-and CCR1 -/-mice, respectively, compared with wild-type mice. CCR1 and CCR5 were expressed on neutrophils and mast cells. Remarkably, the intradermal mRNA expression of CCL5/RANTES, another ligand for CCR1 and CCR5, was increased in CCR5 -/-and CCL3 -/-mice, compared with wild-type mice, while the cutaneous CCL3 mRNA expression was augmented in CCR1 -/-and CCR5 -/-mice. These results indicate that CCR1, CCR5, and CCL3 cooperatively contribute to the cutaneous Arthus reaction, and also suggest that enhanced expression of CCL3 and CCL5 compensates for the loss of CCR1, CCR5, and CCL3 in the reaction.

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“…MIP-1␣ is induced in patients with diverse inflammatory diseases, including bacterial sepsis (27,28), malaria (29), and interstitial lung diseases (30), and in vivo administration of MIP-1␣ to laboratory animals results in localized infiltration of monocytes (31)(32)(33). In animal models of infections, MIP-1␣ has been shown to play a critical role in the cellular recruitment and inflammatory response to coxsackie and influenza infections (34), endotoxemia (35), bacterial pneumonia (36), and cryptococcosis (37,38). Two previous studies have examined the expression of MIP-1␣ in response to Aspergillus species; one showed that rat alveolar macrophages express MIP-1␣ mRNA when exposed to A. fumigatus conidia in vitro (39), and another demonstrated that MIP-1␣ is induced in the lungs after intrapulmonary challenge with conidia (40).…”

Section: Macrophage Inflammatory Protein-1␣ Is a Critical Mediator Ofmentioning

confidence: 99%

Macrophage Inflammatory Protein-1α Is a Critical Mediator of Host Defense Against Invasive Pulmonary Aspergillosis in Neutropenic Hosts

Mehrad

Moore

Standiford

2000

The Journal of Immunology

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Invasive pulmonary aspergillosis is a devastating complication of immunosuppression that usually occurs in neutropenic patients. In this setting, augmentation of the antifungal activity of available immune cells may improve the outcome of the infection. Macrophage inflammatory protein-1α (MIP-1α) is a CC chemokine with potent chemotactic activity for various subsets of mononuclear leukocytes. We therefore tested the hypothesis that the influx of mononuclear cells into the lung in invasive pulmonary aspergillosis is in part mediated by MIP-1α, and the manipulation of this ligand alters the outcome of the infection. We found that in both immunocompetent and neutropenic mice, MIP-1α was induced in the lungs in response to intratracheal administration of Aspergillus fumigatus conidia. In neutrophil-depleted mice challenged with intratracheal conidia, there was evidence of invasive fungal pneumonia associated with a predominantly mononuclear leukocyte infiltrate. Ab-mediated depletion of MIP-1α resulted in a 6-fold increase in mortality in neutropenic mice, which was associated with a 12-fold increase in lung fungal burden. Studies of single-cell suspensions of whole lungs revealed a 36% decrease in total lung leukocyte infiltration as a result of MIP-1α neutralization. Flow cytometry on whole lung suspensions showed a 41% reduction in lung monocyte/macrophages as a result of MIP-1α neutralization, but no difference in other lung leukocyte subsets. These studies indicate that MIP-1α is a critical mediator of host defense against A. fumigatus in the setting of neutropenia and may be an important target in devising future therapeutic strategies against invasive aspergillosis.

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Requirement of Mip-1α for an Inflammatory Response to Viral Infection

Cited by 590 publications

References 14 publications

Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes

Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes

Role of C‐C chemokine receptors 1 and 5 and CCL3/macrophage inflammatory protein‐1α in the cutaneous Arthus reaction: possible attenuation of their inhibitory effects by compensatory chemokine production

Macrophage Inflammatory Protein-1α Is a Critical Mediator of Host Defense Against Invasive Pulmonary Aspergillosis in Neutropenic Hosts

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