Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays an important role in host defense against a variety of microorganisms including protozoan parasites. Interestingly, some microbial pathogens also express a MIF-like protein, although its role in disease pathogenesis is not well understood. The aim of this study was to compare an Eimeria-encoded MIF (E.MIF) protein with chicken MIF (C.MIF) on the basis of their structural, immunological, and biological properties. E.MIF and C.MIF proteins, each with a glutathione S-transferase epitope tag, were expressed in Escherichia coli or COS-7 cells and purified by glutathione affinity chromatography. Rabbit antisera against the purified proteins demonstrated their mutual immunological cross-reactivity on Western blots, and immunolocalized intracellular native E.MIF to the Eimeria schizont, merozoite, and oocyst life cycle stages. HD11 chicken macrophages treated in vitro with C.MIF recombinant protein expressed increased levels of transcripts encoding interleukin-6 (IL-6), IL-17, and tumor necrosis factor superfamily member 15 (TNFSF15), but decreased levels of IL-8 transcripts, compared with cells treated with the PBS control; similar treatment with E.MIF only down-regulated IL-8 transcripts. Unlike recombinant E.MIF, C.MIF exhibited in vitro chemotactic activity for HD11 cells. Conversely, E.MIF, but not C.MIF, enhanced protection against experimental Eimeria infection, compared with the PBS control. These studies provide evidence for overlapping structural and antigenic properties, but distinct immunoregulatory roles, of E.MIF and C.MIF.
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PMID:Distinct immunoregulatory properties of macrophage migration inhibitory factors encoded by Eimeria parasites and their chicken host. 2194 52

Listeria monocytogenes can be carried by and infect poultry, although the clinical disease in birds is rare. Escape from macrophage phagocytosis is a key step in pathogenesis for L. monocytogenes. Therefore, we investigated the infection of the chicken macrophage-like cell line HD11 with 2 strains of L. monocytogenes EGD-e and Scott A. After infection, L. monocytogenes was quantified by spread plating and HD11 was quantified with trypan blue exclusion stain before enumeration. The standard macrophage killing protocols require washing the cell monolayers 3 times with PBS, which was found to negatively influence HD11 monolayers. Maximum bacterial densities within macrophages were not different between the 2 Listeria strains. HD11 required more than 11 h to effectively reduce intracellular L. monocytogenes Scott A, and Scott A was more susceptible to HD11 killing than EGD-e. It appears that Listeria infection initially causes attenuation of HD11 growth, and infected HD11 cells do not begin to lyse until at least 11 h post infection. These results suggest that there are subtle strain to strain differences in response to HD11 macrophage phagocytosis. The long lead-time required for HD11 to kill L. monocytogenes cells means that there is sufficient time available for chicken macrophages to circulate in the blood and transfer the intracellular Listeria to multiple tissues.
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PMID:Listeria monocytogenes infection of HD11, chicken macrophage-like cells. 2773 21