Pro-Inflammatory and Anti-Inflammatory Interleukins in Infectious Diseases: A Comprehensive Review

Abstract

Interleukins (ILs) are signaling molecules that are crucial in regulating immune responses during infectious diseases. Pro-inflammatory ILs contribute to the activation and recruitment of immune cells, whereas anti-inflammatory ILs help to suppress excessive inflammation and promote tissue repair. Here, we provide a comprehensive overview of the role of pro-inflammatory and anti-inflammatory ILs in infectious diseases, with a focus on the mechanisms underlying their effects, their diagnostic and therapeutic potential, and emerging trends in IL-based therapies.

Keywords: anti-inflammatory; diagnosis; immune response; infectious diseases; interleukins; pro-inflammatory; therapy.

Figure 1

Pro-inflammatory cytokine production and immune consequences. This activation triggers the recruitment of adaptor molecules, such as MyD88 which induces the activation of NF-κB. Nuclear translocation of NF-κB causes the expression of pro-inflammatory genes like pro-IL-1β and NLRP3 mRNA. Simultaneously, the activation of TLRs also triggers the assembly of NLRP3 inflammasome. This multiprotein complex, comprising NLRP3, ASC, and procaspase-1, is responsible for the processing and activation of inflammatory cytokines, like IL-1β and IL-18. Furthermore, the release of ATP from damaged cells or bacteria acts as a danger signal. ATP binds to the P2X7R, leading to its activation. P2X7R activation induces the formation of a pore, allowing the influx of ions, such as calcium, and the efflux of potassium. These events trigger the assembly and activation of the NLRP3 inflammasome, subsequently leading to the maturation and secretion of IL-1β and IL-18. Secretion of these cytokines results in immune cell recruitment and differentiation for a specialized immune response, such as TH17 response secreting IL-17 or IL-22 from dendritic cells or IL4 and IL10 from M2 polarized macrophages.