RESUMEN
Antimicrobial peptides (AMPs) protect host from pathogens as first line of defense. Especially, ß-defensins shows antimicrobial activity and immune modulation effects. Avian species also have ß-defensins as avian ß-defensins (AvBDs) from AvBD1 to AvBD14. In this study, we characterized chicken AvBD5 and demonstrated its immune modulatory functions in chicken macrophage cell line (HD11). Chicken AvBD5 is composed of a signal, pro, and mature peptides containing one α-helix, four ß-sheet, and three disulfide bonds. Here, we also showed that chicken AvBD5 induced Th1, Th2, and Th17 cytokines in chicken macrophage cell line and stimulated MAPK signaling pathways through ERK1/2 and p38 molecules. In addition, AvBD5 stimulated MyD88 and CD40 to regulate immune systems. Taken together, chicken AvBD5 can modulate host immune systems by inducing cytokines expression and stimulating MAPK signaling pathway.
Asunto(s)
Proteínas Aviares/genética , Pollos/inmunología , Factores Inmunológicos/genética , beta-Defensinas/genética , Secuencia de Aminoácidos , Animales , Proteínas Aviares/química , Proteínas Aviares/inmunología , Línea Celular , Pollos/genética , Factores Inmunológicos/química , Factores Inmunológicos/inmunología , Macrófagos , Proteínas Recombinantes/química , Proteínas Recombinantes/genética , Proteínas Recombinantes/inmunología , beta-Defensinas/química , beta-Defensinas/inmunologíaRESUMEN
BACKGROUND: Chicken erythrocytes are involved in immunity through binding of toll-like receptors (TLRs) with their ligands to activate downstream signaling and lead to cytokine production in erythrocytes. Some avian ß-defensins (AvBDs) are constitutively expressed in tissues and some others can be induced by various bacteria and viruses. However, the expression of AvBDs in erythrocytes has not yet been studied extensively. RESULTS: The transcripts of eight AvBDs (AvBD1 to AvBD7, and AvBD9) and liver-expressed antimicrobial peptide-2 (LEAP-2) were found in normal chicken erythrocytes. The expression levels of AvBD2, 4 and 7 were significantly increased (P < 0.01), whereas the levels of AvBD1, 6 and 9 were significantly decreased (P < 0.01) after Marek's disease virus (MDV) infection. The mRNA expression level of LEAP-2 was not significantly changed after MDV infection. Highest viral nucleic acid (VNA) of MDV in the feather tips among the tested time points was found at 14 days post-infection (d.p.i.). In addition, 35 MD5-related gene segments were detected in the erythrocytes at 14 d.p.i. by transcriptome sequencing. CONCLUSIONS: These results suggest that the AvBDs in chicken erythrocytes may participate in MDV-induced host immune responses.
Asunto(s)
Pollos/sangre , Eritrocitos/metabolismo , Enfermedad de Marek/sangre , Enfermedades de las Aves de Corral/sangre , beta-Defensinas/sangre , Animales , Péptidos Catiónicos Antimicrobianos/sangre , Péptidos Catiónicos Antimicrobianos/genética , Pollos/genética , Plumas/virología , Masculino , Enfermedad de Marek/genética , Enfermedades de las Aves de Corral/genética , Enfermedades de las Aves de Corral/virología , ARN Mensajero/sangre , Carga Viral/veterinaria , beta-Defensinas/genéticaRESUMEN
Avian pathogenic Escherichia coli (APEC) can cause severe disease in ducks, characterized by perihepatitis, pericarditis, and airsacculitis. Although the studies of bacteria isolation and methods of detection have been reported, host immune responses to APEC infection remain unclear. In response, we systemically examined the expression of immune-related genes and bacteria distribution in APEC-infected ducks. Results demonstrated that APEC can quickly replicate in the liver, spleen, and brain, with the highest bacteria content at 2 days post infection. The expression of toll-like receptors (TLRs), avian ß-defensins (AvBDs) and major histocompatibility complex (MHC) were tested in the liver, spleen, and brain of infected ducks. TLR2, TLR4, TLR5, and TLR15 showed different expression patterns, which indicated that they all responded to APEC infection. The expression of AvBD2 was upregulated in all tested tissues during the 3 days of testing, whereas the expression of AvBD4, AvBD5, AvBD7, and AvBD9 were downregulated, and though MHC-I was upregulated on all test days, MHC-II was dramatically downregulated. Overall, our results suggest that APEC can replicate in various tissues in a short time, and the activation of host immune responses begins at onset of infection. These findings thus clarify duck immune responses to APEC infection and offer insights into its pathogenesis.
RESUMEN
The immune response in the lower part of the hen oviduct is of crucial importance to protect the oviductal tissues from infection by microorganisms colonizing the cloaca. The aim of this study was to examine whether different TLRs can recognize their ligands to induce expression of proinflammatory cytokines and avian ß-defensins (AvBDs) in the uterus and vagina of laying hens. The mucosal tissues of the uterus and vagina were collected, cultured in TCM-199 medium and stimulated with or without different ligands of TLRs, namely Pam3CSK4 (TLR2), poly I:C (TLR3), flagellin (TLR5), R848 (TLR7), and CpG-ODN (TLR21) and incubated for 3h. The expression of IL1B in the uterus and vagina was upregulated by all TLR ligands tested. The expression of IL6 in the uterus and vagina was upregulated by poly I:C and CpG-ODN, and it was also upregulated by Pam3CSK4 in the uterus and by R848 in the vagina. The expression of AvBD10 was upregulated by poly I:C in the uterus and by flagellin in the vagina. On the other hand, the AvBD10 expression was downregulated by CpG-ODN in the uterus and by R848 in the vagina, whereas its expression was not affected by Pam3CSK4 in both tissues. The expression of AvBD12 in the uterus and vagina was not affected by any TLR ligands except for CpG-ODN, which downregulated its expression in the vagina. These results suggest that TLR2, 3, 5, 7, and 21 in the uterine and vaginal tissues are functionally active in inducing proinflammatory cytokines in response to their specific ligands, although the effect on the expression of AvBDs is limited. Proinflammatory cytokines induced by interaction of TLRs with their ligands may play roles in the defense against infectious microorganisms.