M-CSF transgenic mice: Role of M-CSF in infection and autoimmunity

Bernier, Tanja; Halter, Roman; Paul, Dieter; Rittinghausen, Susanne; Emmendörffer, Andreas

doi:10.1078/0940-2993-00172

Cited by 5 publications

(2 citation statements)

References 35 publications

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“…In this context, we previously defined the dynamic changes in the various mononuclear phagocyte populations during experimental Gram-negative pneumonia and reported that CCR2 was necessary not only to the recruitment of monocyte-derived lineage cells but, unexpectedly, also controlled the number and phenotype of alveolar macrophages and all DC populations in this infection (17). Little is known about the role of the M-CSF/IL-34 biologic axis in the context of infection and many of the published studies in the field pre-date current understanding of the lineages of mononuclear phagocytes (21–25). To our knowledge, this mechanism has not been investigated in pulmonary infections to date.…”

Section: Introductionmentioning

confidence: 99%

M-CSF Mediates Host Defense during Bacterial Pneumonia by Promoting the Survival of Lung and Liver Mononuclear Phagocytes

Bettina

Zhang

Michels

et al. 2016

The Journal of Immunology

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Gram-negative bacterial pneumonia is a common and dangerous infection with diminishing treatment options due to increasing antibiotic resistance among causal pathogens. The mononuclear phagocyte system is a heterogeneous group of leukocytes composed of tissue-resident macrophages, dendritic cells and monocyte-derived cells that are critical in defense against pneumonia, but mechanisms that regulate their maintenance and function during infection are poorly defined. Macrophage-colony stimulating factor (M-CSF) has myriad effects on mononuclear phagocytes but its role in pneumonia is unknown. We therefore tested the hypothesis that M-CSF is required for mononuclear phagocyte-mediated host defenses during bacterial pneumonia in a murine model of infection. Genetic deletion or immunoneutralization of M-CSF resulted in reduced survival, increased bacterial burden and greater lung injury. M-CSF was necessary for the expansion of lung mononuclear phagocytes during infection but did not affect the number of bone marrow or blood monocytes, the proliferation of precursors or the recruitment of leukocytes to the lungs. In contrast, M-CSF was essential to survival and anti-microbial functions of both lung and liver mononuclear phagocytes during pneumonia and its absence resulted in bacterial dissemination to the liver and hepatic necrosis. We conclude that M-CSF is critical to host defenses against bacterial pneumonia by mediating survival and anti-microbial functions of mononuclear phagocytes in the lungs and liver.

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Section: Introductionmentioning

confidence: 99%

M-CSF Mediates Host Defense during Bacterial Pneumonia by Promoting the Survival of Lung and Liver Mononuclear Phagocytes

Bettina

Zhang

Michels

et al. 2016

The Journal of Immunology

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show abstract

“…Studies on MRL- Faslpr mice demonstrate that M-CSF plays a pivotal role in kidney injury 2 – 4. Increased glomerular expression of M-CSF mRNA and protein was also reported in lupus nephritis patients 5.…”

mentioning

confidence: 99%

Increase in the level of macrophage colony-stimulating factor in patients with systemic lupus erythematosus

Yang

Xiao

Zhao

et al. 2008

Annals of the Rheumatic Diseases

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MAbs Targeting Soluble Mediators in Phase 1 and 2 Clinical Studies Immunological Disorders

Brennan

2014

Handbook of Therapeutic Antibodies

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M-CSF transgenic mice: Role of M-CSF in infection and autoimmunity

Cited by 5 publications

References 35 publications

M-CSF Mediates Host Defense during Bacterial Pneumonia by Promoting the Survival of Lung and Liver Mononuclear Phagocytes

M-CSF Mediates Host Defense during Bacterial Pneumonia by Promoting the Survival of Lung and Liver Mononuclear Phagocytes

Increase in the level of macrophage colony-stimulating factor in patients with systemic lupus erythematosus

MAbs Targeting Soluble Mediators in Phase 1 and 2 Clinical Studies Immunological Disorders

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