Disease relevance of IFNG

• Gradual development of the interferon-gamma response of swine to porcine reproductive and respiratory syndrome virus infection or vaccination [1].
• Effect of interferon-alpha, interferon-gamma and tumour necrosis factor on African swine fever virus replication in porcine monocytes and macrophages [2].
• Supplementation of CLA in the diet before the induction of colitis decreased mucosal damage; maintained cytokine profiles (i.e., interferon-gamma and interleukin-10) and lymphocyte subset distributions (i.e., CD4+ and CD8+), resembling those of noninfected pigs; enhanced colonic expression of PPAR-gamma; and attenuated growth failure [3].
• Engineering by PCR-based exon amplification of the genomic porcine interferon-gamma DNA for expression in Escherichia coli [4].
• The effect of recombinant porcine interferon-gamma (IFN-gamma) on the immunogenicity in vivo of inactivated suid herpesvirus-1 (SHV-1, Phylaxia strain) was studied applying two successive i.m. immunizations [5].

High impact information on IFNG

• When either native or recombinant porcine somatotropin or native rat somatotropin was administered to hypophysectomized rats in vivo, activation of peritoneal macrophages, as measured by release of O2- in response to opsonized zymosan, was equivalent to that of macrophages from rats primed with the macrophage-activating factor interferon-gamma [6].
• CD4+ T cells proliferate after MHC class II molecules are induced with swine interferon-gamma [7].
• In addition, we have found that these cells express, after activation with interferon-gamma and lipopolysaccharide, an inducible Ca2(+)-independent NO synthase that is distinct from the constitutive enzyme [8].
• No statistical differences were detected between diabetic and control subjects with respect to lymphocyte subsets and the recognition mechanisms or to interferon-gamma/interleukin-10 production in response to islet cells [9].
• During proliferation in response to islet cells, interleukin-10 increased 43-fold (p<0.01) but interferon-gamma increased only slightly [9].

Chemical compound and disease context of IFNG

• Changes in swine macrophage phenotype after infection with African swine fever virus: cytokine production and responsiveness to interferon-gamma and lipopolysaccharide [10].
• Circulating cortisol, tumor necrosis factor-alpha interleukin-1beta, and interferon-gamma in pigs infected with Actinobacillus pleuropneumoniae [11].
• Collectively, these results indicate that increasing antioxidant defenses by feeding high levels of vitamin E did not ameliorate the effects of PRRSV on decreased growth, leukopenia, and increased serum IL-1beta and IFN-gamma [12].
• Antiviral effect of Saccharomyces cerevisiae beta-glucan to swine influenza virus by increased production of interferon-gamma and nitric oxide [13].

Biological context of IFNG

• Furthermore, the genes for mucin and interferon gamma were physically localized to porcine chromosome 5q2.3 and 5p1.2-q1.1 by fluorescence and radioactive in situ hybridization, respectively, thereby assigning four new markers to chromosome 5 [14].
• The compound microsatellites IFNG and S0215 were unaffected by size homoplasy (SH) within our material [15].
• Efforts to enhance Th1 immunity, by utilizing an expression plasmid encoding porcine IFNA (pINA) as an adjuvant, resulted in a temporary increase in the frequency of PRRSV-specific IFNG SC but only minor changes overall in the expression of Th1 associated cytokine or innate immune marker mRNA by virus-stimulated PBMC [16].
• Induction of the IFN-gamma gene and protein is linked to the establishment of cell polarity in a porcine epithelial cell line [17].
• Interferon-gamma gene and protein are spontaneously expressed by the porcine trophectoderm early in gestation [18].

Anatomical context of IFNG

• Interferon gamma bound to extracellular matrix changes the hyporesponsiveness to LPS in crypt but not villous intestinal epithelial cells [19].
• Genetic analysis of the gene for porcine submaxillary gland mucin: physical assignment of the MUC and interferon gamma genes to chromosome 5 [14].
• In contrast, in the mesenteric lymph node (MLN), only expression of IRF1 and IFNG was significantly upregulated [20].
• Our report represents the first example of an inducible expression of IFN-gamma by a polarized epithelial cell [17].
• The number of viral particles released from endothelial cells was 10 to 5 x 10 viral particles/mL after cellular activation with tumor necrosis factor-alpha, interferon-gamma, or lipopolysaccharide, as shown by PBRT analysis [21].

Associations of IFNG with chemical compounds

• METHODS: Primary and immortalized porcine aortic EC cultures were stimulated with phorbol-myristate acetate/ionomycin, lipopolysaccharide, tumor-necrosis factor-alpha, or interferon-gamma [22].
• In contrast, prostaglandin accumulation was not enhanced by interferon-gamma or interleukin-2 [23].
• Furthermore, we have characterized three different molecular species of recombinant porcine interferon-gamma that are formed under non-optimal refolding conditions (1 M guanidine/HCl) and that differ from each other in specific activity, size and stability [24].
• Serum was harvested and frozen until assayed for cortisol, tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma [11].
• We found that soluble high molecular weight beta-glucan could increase IFNgamma-producing cell frequency in a dose-dependent manner in the enzyme-linked immunospot assay (ELISPOT) in the absence of antigenic restimulation [25].

Regulatory relationships of IFNG

• Interleukin-6 and interleukin-15 are selectively regulated by lipopolysaccharide and interferon-gamma in primary pig adipocytes [26].
• We previously showed that treatment of polarized TBA B4-3 cells with the strong protein kinase C (PKC) agonist phorbol 12-myristate-13-acetate (PMA) induced 3-4 days later a transient IFN-gamma mRNA expression and apical IFN-gamma protein secretion [27].
• Porcine interleukin-12 fusion protein and interleukin-18 in combination induce interferon-gamma production in porcine natural killer and T cells [28].

Other interactions of IFNG

• Administration of pINA, however, did correlate with decreased IL1B secretion by cultured, unstimulated PBMC but had no effect on their ability to release IFNG [16].
• PROCEDURE: Alveolar macrophages were incubated for 48 hours with APP (1 X 10(4) colony-forming units/mL), interleukin-1beta, (IL-1beta; 5 U/mL), tumor necrosis factor-alpha (TNFalpha; 500 U/mL), interferon-gamma (IFN-gamma, 100 U/mL), or lipopolysaccharide (LPS; 10 microg/mL) [29].
• Thus, when induced by IFN-gamma or other inflammatory mediators, IL-15 may be a significant homeorhetic factor that mobilizes and directs energy away from the adipocyte to other cells during the acute phase of the inflammatory response [30].
• A strong correlation between rejection and up-regulation of the IFN-gamma gene was observed, whereas animals with long-term tolerance showed low levels of IFN-gamma, but high levels of IL-10 gene transcription [31].
• This is a simple method that allows reliable determination of the differing regulation of cytokine mRNAs specific for porcine interleukin (IL)-2, -4 and -10, interferon gamma (IFN-gamma) and the housekeeping gene, GAPDH, as an endogenous control [32].

Analytical, diagnostic and therapeutic context of IFNG

• Here we used a coculture system of RAW 264.7 macrophage cells and tubular LLC-PK(1) cells to establish that lipopolysaccharide- and interferon-gamma-stimulated but not resting macrophages elicited HIF-1alpha accumulation in LLC-PK(1) cells [33].
• In order to construct the porcine IFN-gamma DNA without intervening sequence, the four exons were separately amplified by the polymerase chain reaction (PCR) using primers matching the exon-termini [4].
• No (2',5')-oligoadenylate synthetase activity could be measured on the trophoblast, even after treatment with IFN-gamma or spI IFN [34].
• We observed prominent myocardial interferon-gamma gene expression only in Group 1.CONCLUSION: Despite differences in myocardial interferon-gamma gene expression, the histology and severity of the vascular lesions in CAV did not vary significantly with different histoincompatibilities or treatment protocols [35].
• Through the use of isotype-specific antibody secreting cell ELISPOT assays, interferon-gamma ELISPOT assays and isotype-specific ELISAs on serum, nasal wash and bronchoalveolar lavage samples, we defined the humoral and cellular immune responses, both locally in the respiratory tract and systemically, to this viral infection [36].

References