The inappropriate or excessive use of antimicrobial agents caused an emerging public health problem due to the resulting resistance developed by microbes. Therefore, there is an urgent need to develop effective antimicrobial strategies relying on natural agents with different mechanisms of action. Nature has been known to offer many bioactive compounds, in the form of animal venoms, algae, and plant extracts that were used for decades in traditional medicine. Animal venoms and secretions have been deeply studied for their wealth in pharmaceutically promising molecules. As such, they were reported to exhibit many biological activities of interest, such as antibacterial, antiviral, anticancer, and anti-inflammatory activities. In this review, we summarize recent findings on the antimicrobial activities of crude animal venoms/secretions, and describe the peptides that are responsible of these activities.

Beside their toxicity, snake venom components possess several pharmacological effects and have been used to design many drugs. Recently, the cytotoxic, antibacterial, vasorelaxant, pro- and anti-coagulant as well as inflammatory activities of Montivipera bornmuelleri venom have been described in vitro. However, the in vivo effects of this Lebanese snake venom on the immune system has not been established yet. Here, we investigate the immunomodulatory effects of M. bornmuelleri venom on the murine splenic levels of TNF-α, IFN-γ, IL-4, IL-10, IL-1ß and IL-17 at 6 and 24 h post treatment. Different doses of the venom (1 mg/kg, 2 mg/kg, 4 mg/kg and 6 mg/kg) were injected intraperitoneally in BALB/c mice. Using the logit method, LD50 of M. bornmuelleri was proved to be 1.92 mg/kg in our experimental conditions. This study also shows that 1 mg/kg and 2 mg/kg of M. bornmuelleri venom are able to modulate the levels of cytokines in the spleen of mice, as assessed by ELISA. In fact, this snake's venom up-regulates TNF-α, IFN-γ, IL-1ß and IL-17 with a trend in decreasing IL-4 and IL-10. Therefore, by favoring Th1 and Th17 over Th2 and Treg responses, M. bornmuelleri venom might have important clinical implication especially in the field of cancer immunotherapy.

Snake venom serves as a tool of defense against threat and helps in prey digestion. It consists of a mixture of enzymes, such as phospholipase A2, metalloproteases, and l-amino acid oxidase, and toxins, including neurotoxins and cytotoxins. Beside their toxicity, venom components possess many pharmacological effects and have been used to design drugs and as biomarkers of diseases. Viperidae is one family of venomous snakes that is found nearly worldwide. However, three main vipers exist in the Middle Eastern region: Montivipera bornmuelleri, Macrovipera lebetina, and Vipera (Daboia) palaestinae. The venoms of these vipers have been the subject of many studies and are considered as a promising source of bioactive molecules. In this review, we present an overview of these three vipers, with a special focus on their venom composition as well as their biological activities, and we discuss further frameworks for the exploration of each venom.

C‑reactive protein (CRP) and oxidized low density lipoprotein (oxLDL) serve major roles at both early and advanced stages of atherosclerosis. CRP exists in two isoforms, monomeric (m) and pentameric (p), that bring about pro‑ or anti‑inflammatory effects in macrophages. In addition, CRP may form a complex with oxidized low‑density lipoprotein (oxLDL) via phosphatidylcholine, thus decreasing its pro‑inflammatory effects within macrophages. The aim of the present study was to investigate the single and the combined effects of mCRP, pCRP and oxLDL on U937‑derived macrophages. In the current study, U937‑derived macrophages were treated in vitro with different combinations of CRP isoforms with or without oxLDL. The levels of major inflammatory cytokines [interleukin (IL)‑1β, IL‑6, IL‑8 and tumor necrosis factor (TNF)‑α] along with the production of reactive oxygen species (ROS) were determined. TNF‑α and IL‑6 levels were significantly decreased (P<0.05) by the effect of mCRP and pCRP combined with oxLDL. No significant changes were observed in IL‑1β, IL‑8 or ROS levels.

Infection with a high dose of the intracellular parasitic protozoan L. major induces a sustained hyperalgesia in susceptible BALB/c mice accompanied by up-regulation of the pro-inflammatory cytokines IL-1β and IL-6. Interleukin-13 (IL-13) has been shown to reduce this hyperalgesia (despite increased levels of IL-6) and the levels of IL-1β during and after the treatment period. These findings favor the cytokine cascade leading to the production of sympathetic amines (involving TNF-α and KC) over prostaglandins (involving IL-1β and IL-6) as the final mediators of hyperalgesia. The aim of this study was to investigate the effect of daily treatment with the β-blockers atenolol on L. major-induced inflammation in mice with respect to hyperalgesia as well as the levels of TNF-α and KC (the analogue of IL-8 in mice). Our data demonstrates that atenolol is able to reduce the L. major induced sustained peripheral hyperalgesia, which does not seem to involve a direct role for neither IL-1β nor KC. Moreover, our results show that TNF-α may play a pivotal and direct role in sensitizing the peripheral nerve endings (nociceptors) since its level was reduced during the period of atenolol treatment, which correlates well with the reduction of the observed peripheral, but not central, hyperalgesia. These findings contribute to a better understanding of the cytokine cascade leading to hyperalgesia and may lead to the development of new and more efficient medications for many types of pain.