The multi-organ origin of interleukin-5 in the mouse

Ryan, Phil; Willson, Tracy A.; Ws, Alexander; Rago, L Di; Mifsud, Sandra; Metcalf, Donald

doi:10.1038/sj.leu.2402173

Cited by 9 publications

(9 citation statements)

References 28 publications

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“…If this process was to become more evident with the extremely high cell concentrations in an intact organ, this might be the reason for complete failure of IL-3 production to occur. The present study reinforces earlier data (11,12) that T lymphocytes are not a major cellular source of organ CSFs, nonetheless their curious functional responses to cell crowding are intriguing and may be relevant for cell behavior in other organs.…”

Section: Discussionsupporting

confidence: 92%

“…This difference is most evident for IL-3 that has never been detected in whole organs or organ fragments (11,12). The nonlinear behavior of cell suspensions clearly indicates that accessory cells assist, or are necessary for, CSF production but an excess of such cells appears to be inhibitory.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, studies on murine organs have shown that T lymphocytes are not the exclusive source of these CSFs and, further, that no organ produces detectable IL-3 or contains detectable IL-3 mRNA (11,12). Although caution is clearly needed in interpreting in vitro data from lymphoid cell suspensions, the system is a robust one for producing CSFs and the induction systems involved remain to be characterized.…”

mentioning

confidence: 99%

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Crowding-dependent production of colony-stimulating factors by cultured syngeneic or allogeneic hematopoietic cells

Metcalf¹,

Rago²,

Mifsud³

2003

Proc. Natl. Acad. Sci. U.S.A.

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Mitogenic stimulation in vitro of mouse T lymphocytes induces the production of the hematopoietic cytokines granulocyte–macrophage colony-stimulating factor and IL-3. The present experiments showed that simple crowding of murine spleen or lymph node cells was a sufficient inducing stimulus. Crowding did not have this consequence for thymus or marrow cells or spleen cells from nu/nu or Rag-1 −/− mice lacking T lymphocytes. Crowding for as short a period as 24 h was sufficient to allow subsequent cytokine production in sparse cultures. Purified T lymphocytes also exhibited low levels of crowding induction of cytokine production and cytokine production was enhanced by IL-2 and IFN-γ. However, IFN-γ−/− spleen cells exhibited similar crowding-induced colony-stimulating factor production to that of control spleen cells. Excess cell crowding inhibited cytokine production. This inhibition was not caused by receptor internalization of cytokines but may contribute to the failure to observe IL-3 production in lymphoid organs in vivo . Coculture of allogeneic spleen or peritoneal cells was a strong inducing signal for colony-stimulating factor production but this parameter was unable to detect autoreactivity of T lymphocytes in mice that lack suppressor of cytokine signaling 1 and exhibit T lymphocyte activation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Crowding-dependent production of colony-stimulating factors by cultured syngeneic or allogeneic hematopoietic cells

Metcalf¹,

Rago²,

Mifsud³

2003

Proc. Natl. Acad. Sci. U.S.A.

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“…All methods for estimating cytokine production in tissues have their limitations and can be subjected to criticism (14,15). The present estimates of the capacity of various organs to produce cytokines in vitro share some of these limitations, although the validity and specificity of the bioassays used have been established.…”

Section: Discussionmentioning

confidence: 99%

“…For the specific assay of G-CSF, M-CSF, and IL-5, stable Ba/F3 sublines expressing inserted murine G-CSF, M-CSF, or IL-5␣ chain receptors (Ba/F3GR, Ba/F3MR, Ba/F3IL-5R, respectively, cell lines) were used as previously described (13)(14)(15). Because no organ-conditioned medium in fact contained detectable IL-3, these cell lines were able to provide specific assays for their respective ligands and were able to detect concentrations as low as 100 pg/ml for G-CSF and M-CSF and 2.5 pg/ml for IL-5.…”

Section: Assay Cell Linesmentioning

confidence: 99%

Production of Colony-Stimulating Factors and IL-5 by Organs from Three Types of Mice with Inflammatory Disease Due to Loss of the Suppressor of Cytokine Signaling-1

Metcalf

Alexander

Ryan

et al. 2001

The Journal of Immunology

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Organs from neonatal mice dying from IFN-γ-dependent inflammatory disease initiated by loss of the gene encoding the suppressor of cytokine signaling-1 (SOCS-1) had a normal capacity to produce G-CSF in vitro but a reduced capacity to produce GM-CSF, most evident with the lung, and some reduction in the production of M-CSF by muscle tissue. In contrast, organs from mice lacking the genes for both SOCS-1 and IFN-γ had a normal capacity to produce CSFs. Organs from young adult mice dying with polymyositis and myocarditis that lacked SOCS-1 but were heterozygous for IFN-γ had a normal capacity to produce GM-CSF and M-CSF, but muscle tissue produced significantly increased amounts of G-CSF and IL-5 with IL-5 production also being elevated for the salivary gland, thymus, and heart. Loss of the IFN-γ gene alone had no impact on organ production of these cytokines in vitro. In none of the inflammatory disease models was IL-3 production detected. The SOCS-1 protein appears to have no direct influence on the cellular production of these cytokines and the abnormalities observed either depend on the coaction of IFN-γ, or more likely, are linked with the invasion and destruction of tissue by T lymphocytes, macrophages, eosinophils, and neutrophils. The ability of local organs to produce these proinflammatory cytokines could contribute to the development and progression of these inflammatory lesions.

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Metabolic effects of host defence responses during gastrointestinal parasitism in sheep

Colditz¹

2003

Aust. J. Exp. Agric.

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Following stimulation of the immune system, tissue trauma, or exposure to some stressors, there can be activation of the acute phase response (APR). This is a primitive defence reaction that helps protect the host against noxious insults. Part of the response involvess a change in priorities for nutrient utilisation, when the pro-inflammatory cytokines IL-1α/β, TNFα, IL-6 and IFNα/β override the normal hypothalamic-somatotropic control of nutrient utilisation. The pro-inflammatory cytokines reduce protein synthesis and increase protein catabolism in muscle, induce synthesis of acute phase proteins in liver, and decrease de novo fatty acid synthesis and increase lipolysis in adipose tissue. In the central nervous system there is induction of fever, which increases metabolic rate, and induction of sickness behaviour. There are few reports in the literature of studies on the APR during gastrointestinal nematode (GIN) infection in sheep. However, IL-6 message is present in mucosa during Trichostrongylus colubriformis infection and mast cells in many species contain preformed TNFα. The changes in appetite, growth and nitrogen metabolism seen during GIN parasitism in sheep are in accord with the systemic effects of the APR. This review reports studies on activation of the APR in mastitis and fly strike, and the effects of APR on wool growth in high and low tensile strength genotypes and during Haemonchus contortus infection. The modified capacity of tissues to take up amino acids during pro-inflammatory cytokine perturbation of nutrient utilisation may limit the capacity for dietary supplementation to remedy the cost of host defence. Genetic variation may occur in production of pro-inflammatory cytokines or in tissue sensitivity to pro-inflammatory cytokines during GIN infection and may provide a basis for selection for resilience. Some questions for future research are identified.

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The multi-organ origin of interleukin-5 in the mouse

Cited by 9 publications

References 28 publications

Crowding-dependent production of colony-stimulating factors by cultured syngeneic or allogeneic hematopoietic cells

Crowding-dependent production of colony-stimulating factors by cultured syngeneic or allogeneic hematopoietic cells

Production of Colony-Stimulating Factors and IL-5 by Organs from Three Types of Mice with Inflammatory Disease Due to Loss of the Suppressor of Cytokine Signaling-1

Metabolic effects of host defence responses during gastrointestinal parasitism in sheep

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