Disease relevance of MIF

• Expression of Toll-like receptors, interleukin 8, macrophage migration inhibitory factor, and osteopontin in tissues from pigs challenged with Salmonella enterica serovar Typhimurium or serovar Choleraesuis [1].
• The histamine suppression of cutaneous delayed hypersensitivity could be accounted for in part by its inhibitory effect on certain lymphocyte responses including antigen-induced migration inhibitory factor (MIF) production and proliferation [2].
• When synthetic polynucleotides were used as adjuvants and were injected into guinea pigs in combination with PPD, dermal reactions as well ad MIF assays gave evidence that these animals exhibited delayed-type hypersensitivity [3].
• All swine serologically negative for TGE antibodies (i.e., unexposed to TGE virus) were also negative for MIF production by lymphocytes from both sources [4].
• The tissue extracts obtained from lungs at various stages of granuloma formation were examined for macrophage migration inhibition (MIF) activity [5].

High impact information on MIF

• While the results indicate that MIF production is a valid qualitative assay for T-cell competence, since MIF can be produced by B and T cells, the degree of migration inhibition cannot be regarded as a quantitative measure of T-cell function [6].
• We conclude that B lymphocytes are incapable of being stimulated by antigen in the absence of T cells, and that MIF production is a thymus-dependent response [6].
• While spleen cells from both strains produced MIF after stimulation with DNP-PLL-Ova, in response to DNP-PLL only strain 2 spleens were able to produce MIF [6].
• Extracts of L2C tumor cells stimulated in vitro production of macrophage migration inhibitory factor (MIF) in peritoneal exudate cells from guinea pigs immunized with L2C tumor cells [7].
• Thus, lymphocytes bearing H-2 receptors modulate MIF production and probably lymphocyte proliferation as well [2].

Chemical compound and disease context of MIF

• Antigen-induced stimulation of glucosamine also occurred in peritoneal exudate cells (PEC) isolated from animals primed for cutaneous basophil hypersensitivity with certain strong antigens (KLH, vaccinia virus) in incomplete Freund's adjuvant (IFA), and lymphocytes from such animals elaborated MIF when cultured with specific antigen [8].
• These studies suggest that metabolites of niridazole, but not the parent compound itslef, suppress delayed hypersensitivity in guinea pigs and prevent MIF production by lymphocytes without affecting the macrophage response to MIF [9].
• Using a guinea pig model of liver injury induced by bioactivation of the anesthetic drug, halothane, we found that toxicity was commensurate with an increase in serum macrophage migration inhibitory factor (MIF), a pro-inflammatory signal and counter-regulator of glucocorticoids, but only in susceptible animals [10].
• Moreover, TAS-1D3 induced well both thymidine incorporation and the production of migration inhibitory factor (MIF) by the spleen cells from guinea pigs sensitized with BCG vaccine [11].
• The hypersensitivity induced in animals is detectable by factor Ei and PPD or OT tuberculins using MIF method [12].

Biological context of MIF

• Immunohistochemical staining with anti-human MIF polyclonal antibodies was carried out on placental sections from 11 stages of gestation (16-95 days postcoitus) and on nonpregnant uterus at 13 days postestrus [13].
• The high activity of MIF in the maternal and fetal tissues throughout placentation and its expression in the nonpregnant uterus indicate a regulatory role for MIF during embryo receptivity and epitheliochorial placentation [13].
• Functional activation of immune lymphocytes by antigenic stimulation in cell-mediated immunity. IV. Role of macrophage and its soluble factor in antigen-induced MIF production of immune T lymphocytes [14].
• Fc phagocytosis by refractory populations increased rapidly during 24-28 hr in vitro culture to levels equal to that of responsive cells which corresponded with an increase in their MMI response to MIF [15].
• These findings are compatible with the hypothesis that the inhibiton of macrophage migration by MIF is the result of reversible autotoxic damage by a yet unidentified product of the oxidative burst, possibly hypochlorous acid [16].

Anatomical context of MIF

• MIF, a proinflammatory cytokine with many actions on macrophages and monocytes, may play an important role in materno-fetal immuno-tolerance during placental establishment, modulation, and growth [13].
• The vasculature also showed staining for MIF, and an intense to moderate staining was shown in the nonpregnant uterus, mostly in the surface and glandular epithelium [13].
• By two in vitro criteria, PPD-induced lymphoproliferation and elaboration of migration inhibition factor (MIF), the responses of lymph node cells were equivalent to sensitized controls [17].
• Neuraminidase treatment of peritoneal exudate cells results in the abrogation of macrophage responsiveness to MIF [18].
• Pretreatment with desensitizing doses of mycobacteria prevented the EA-induced appearance of MIF in the peritoneal fluids [19].

Associations of MIF with chemical compounds

• At concentrations of 10(-3)-10(-5) M histamine reversibly inhibited MIF production and its action could be blocked by H-2 antagonists but not H-1 antagonists [2].
• MIF was purified approximately 30,000-fold from the culture fluid by using gel filtration, sucrose density gradient electrophoresis, isoelectric focusing, and hydrophobic affinity chromatography [20].
• After a single dose of hydrocortisone, peripheral lymphocyte migration inhibitory factor (MIF) production and antigen and mitogen-induced proliferation were unchanged [21].
• This LMWL has the ability, in the presence of PPD, to stimulate nonsensitive PEC to produce a heat-stable molecule(s) resembling MIF with a m.w. in the range 50,000 to 100,000 [22].
• Role of sialic acid in the macrophage glycolipid receptor for MIF [18].

Other interactions of MIF

• Feeding STG and SCR resulted in significant (P</=0.05) tissue specific effects for TLR5, TLR9, IL8, MIF and OPN [1].
• Next, we evaluated the time course of MIF, IL8, CCL20, and OPN mRNA expression induced by application of lipopolysaccharide (LPS), ST or SC in vitro using pig jejunal epithelial cells (IPEC-J2) [23].
• 1. The protein exhibited marked macrophage chemotactic activities (MCA) but no neutrophil chemotactic, lymphocyte chemotactic, and MIF activity in excess of that in vitro [24].
• The plasmin esterase inhibitors, epsilon-amino-n-caproic acid, tranexamic acid, and L-lysine, previously established to reverse the MMI response to MIF, FBP, and C3 activators were found to inhibit both Fc- and C3-dependent phagocytosis [15].

Analytical, diagnostic and therapeutic context of MIF

• Western blot analysis confirmed the specificity of the anti-human MIF polyclonal antibodies on pig tissues [13].
• In contrast Brown Norway (BN) rats, which lack the Ir-EAE gene, did not develop delayed skin tests to EF and their LNC were not stimulated and did not produce MIF when incubated in vitro with EF [25].
• Results of a guinea pig migration inhibition factor (MIF) assay, a terminal deoxyribonucleotidyl transferase (TdT) assay, and radioimmunoassay indicate that the N alpha-desacetylthymosin alpha 1 produced by deoxyribonucleic acid (DNA) cloning techniques has biological activity equivalent to that of the native hormone [26].
• Suppression of cutaneous delayed-type hypersensitivity was achieved by intraperitoneal injection of the MIF fraction into the animals bearing macrophage-rich peritoneal exudates [27].
• Lung lavage cells were harvested at 2, 3, 6 and 7 weeks following sensitization and tested for migration inhibitory factor (MIF) production in Mackaness chambers with purified protein derivative (PPD) [28].

References