α1-Acid glycoprotein production in rat dorsal air pouch in response to inflammatory stimuli, dexamethasone and honey bee venom

Abstract

This study shows the rapid and differential production of the 40–43 kDa and the 70–90 kDa α1-acid glycoprotein (AGP) fucosylated glycoforms after treatment of the dorsal air pouch with bacterial lipopolysaccharide (LPS), HgCl2 or Freund's complete adjuvant (FCA). The 40–43 kDa and the 70–90 kDa AGP production is peaked 1–3 h post-LPS treatment. We observed that the responses to LPS and FCA are similar in that both AGP isoforms are induced whereas they differ in that the FCA exhibits a 6 h lag period. The response to HgCl2, however, exhibits the specific biphasic induction only of the 40–43 kDa AGP. The serum 40–43 kDa AGP glycoform gradually increases in response to all of the above stimulants and peaks by 24 h post- treatment. The increase of the 70–90 kDa AGP levels in the air pouch occurs in association with the accumulation of polymorphonuclear (PMN) cells while dexamethasone (DEX) increases only the 40–43 kDa AGP production in the absence of PMN accumulation. Macrophage–monocyte lineage cells forming the air pouch lining tissue may potentially be the cells that secrete the 40–43 kDa AGP while polymorphonuclear cells that infiltrate the air pouch secrete the 70–90 kDa AGP. The 40–43 kDa and 70–90 kDa AGP production induced by LPS in the air pouch precedes that of interleukin-1 (IL-1) or interleukin-6 (IL-6) while the 40–43 kDa AGP glycoform potentially increases IL-6 production by air pouch PMN exudate cells. These significant differences suggest a local pro-inflammatory role of AGP. Honeybee venom suppressed arthritis development and exhibited differential local or systemic regulation of AGP in serum vs. air pouch exudate or synovial fluid. This study with the air pouch model of facsimile synovium tissue suggests that local α1-acid glycoprotein (AGP) production may contribute to pro-inflammatory and anti-inflammatory activities during the local acute phase response or during chronic inflammatory stress as in arthritis.

S-Methylcysteine (SMC) Ameliorates Intestinal, Hepatic, and Splenic Damage Induced by Cryptosporidium parvum Infection Via Targeting Inflammatory Modulators and Oxidative Stress in Swiss Albino Mice

“…Our results exhibited an increase in pro-inflammatory cytokines secretion (TNF-α, IL-6, IFN-γ) in infected non-treated mice compared to control ones, indicating the inflammatory responses attributed to Cryptosporidium infestation. Earlier investigations found that α1-globulin is significantly elevated in rats infected with C. parvum [ 53 ] through an increasing level of serum amyloid A and/or serum amyloid P that were previously confirmed to be increased during infection [ 62 ] and inflammation [ 63 ]. Interestingly, a landmark study has revealed a significant increase in the expression of TNF-α, IL-6 genes in leukocytes of C. parvum -infected mice [ 64 ].…”

Chemical characterization, antioxidant, anti-inflammatory and cytotoxic properties of bee venom collected in Northeast Portugal

“…BV has been used as a traditional medicine to treat chronic inflammatory (arthritis, rheumatism and back pain) (Chang and Bliven, 1979;Kwon et al, 2001;Kim et al, 2003;Son et al, 2007;Park et al, 2008;Vasileiadou et al, 2010) and skin (Escrig et al, 1997;Han et al, 2012) diseases. In fact, the anti-inflammatory properties of BV samples from different origins such as Egypt (Amin and Abdel-Raheem, 2014), Korea (Park et al, 2007;Park et al, 2008;Lee et al, 2009), USA (Chang and Bliven, 1979) and even commercial samples (Jang et al, 2005;Moon et al, 2007;Yoon et al, 2008) have been reported in apitherapy.…”

Προσδιορισμός Διαφόρων Ανοσοβιολογικών Παραμέτρων Σε Αρθριτικούς Επίμυς

“…In vitro, αναστέλλει την ενεργοποίηση των πολυμορφοπύρηνων ουδετερόφιλων κυττάρων (Vasson et al, 1994), τροποποιεί την επαγόμενη από LPS έκκριση κυτοκινών από μονοκύτταρα/μακροφάγα (Boutten et al, 1992) και αυξάνει την έκκριση του αναστολέα της IL-1 από τα μακροφάγα μυός, κυρίως του ανταγωνιστή του υποδοχέα της IL-1 (IL-1Ra) (Bories et al, 1990;Tilg et al, 1993). Επίσης, δρα συνεργιστικά με τον LPS και αυξάνει την έκκριση της IL-6 από τα μονοπύρηνα κύτταρα του αεροθύλακα επίμυων (Vasileiadou et al, 2010). In vivo, αποτρέπει την απόπτωση που επάγεται από τον TNFα σε κύτταρα ποντικού (Libert et al, 1994 (Crestani et al, 1998).…”

“…Παράλληλα, οδηγεί σε μείωση των επιπέδων της AGP στον ορό και την αύξησή της τοπικά στην άρθρωση στα αρχικά στάδια ανάπτυξης της νόσου (Vasileiadou et al, 2010). Το γεγονός αυτό δείχνει την πιθανή διαφορική δράση της AGP που εξαρτάται από την τοπική (άρθρωση) ή τη γενικευμένη (ορός) παραγωγή της στα αρχικά στάδια της νόσου.…”

“…Το γεγονός αυτό δείχνει την πιθανή διαφορική δράση της AGP που εξαρτάται από την τοπική (άρθρωση) ή τη γενικευμένη (ορός) παραγωγή της στα αρχικά στάδια της νόσου. Συγκεκριμένα, η αυξημένη παραγωγή και έκκρισή της στον ορό οδηγεί σε επιδείνωση της νόσου, ενώ αντίθετα η τοπική παραγωγή της στην άρθρωση οδηγεί σε καταστολή της ανάπτυξης της νόσου (Yiangou et al, 1993;Vasileiadou et al, 2010).…”