Azithromycin suppresses proliferation, interleukin production and mitogen-activated protein kinases in human peripheral-blood mononuclear cells stimulated with bacterial superantigen

Abstract

Azithromycin suppresses mitogen- or superantigen-induced proliferation of PBMCs by possibly inhibiting both cellular JNK and ERK activity.

Lactobacillus reuteri CRL1098 soluble factors modulate tumor necrosis factor alpha production in peripheral blood mononuclear cells: Involvement of lipid rafts

“…Bacterial superantigens and viral proteins are able to improve TNF-α production by PBMC through the activation of ERK MAPK pathway [31][32][33]. Moreover, active compounds from plants are able to downregulate TNF-α expression in PBMC and this effect has been associated to an inhibitory effect on ERK phosphorylation [33].…”

Fidaxomicin Inhibits Clostridium difficile Toxin A-Mediated Enteritis in the Mouse Ileum

“…ERK phosphorylation is required to elicit the secretion of proinflammatory cytokines in response to C. difficile toxins in vivo and in vitro (21,22, 38). Interestingly, another macrolide, azithromycin, suppresses IL-1␤ production and ERK phosphorylation in human peripheral blood mononuclear cells (39), while azithromycin and clarithromycin modulate proinflammatory cytokine secretion in human bronchial epithelial cells, in part through ERK activation (40). Thus, inhibition of proinflammatory cytokine transcription and MAP kinase activation may represent common anti-inflammatory responses of several macrolides (41), including fidaxomicin.…”

Azithromycin Synergistically Enhances Anti-Proliferative Activity of Vincristine in Cervical and Gastric Cancer Cells

“…The potential apoptotic effect of AZM has been examined in neutrophils, peripheral blood mononuclear cells and tracheal smooth muscle cells [8,10,11]. In agreement with these findings, AZM displayed the ability to induce apoptosis of Hela, SGC-7901 and BHK-21 cells at a comparable degree in vitro , as determined by an annexin V-FITC binding assay (Figure 3B), although it showed a preferential anti-proliferative activity to cancer over transformed cells (Figure 1A).…”

“…Like other macrolides, apart from its antimicrobial properties, AZM also exhibits anti-inflammation, immunomodulation, and anti-proliferation effects, as well as an autophagic effect by leading to apoptotic cell death [8,9]. AZM has shown an ability to induce neutrophil apoptosis, as well as inhibit proliferation of peripheral blood mononuclear cells [10]; these have been suggested to contribute the anti-inflammatory activity induced by AZM [11,12,13]. Additionally, AZM has shown an ability to suppress the proliferation of tracheal smooth muscle cells (SMCs) through a mechanism of induction of apoptotic cell death [8], and reverse resistance of P-glycoprotein-dependent anticancer drugs in vitro [14].…”