The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection

Abstract

Proinflammatory cytokines are produced by macrophages and dendritic cells (DCs) after infection to stimulate T helper (Th) cells, linking innate and adaptive immunity. Virus infections can deregulate the proinflammatory cytokine response like tumor necrosis factor-α and interleukin (IL)-2, making the host more susceptible to secondary bacterial infections. Studies using various viruses such as lymphocytic choriomeningitis virus, influenza A virus, and human immunodeficiency virus have revealed several intriguing mechanisms that account for the increased susceptibility to several prevalent bacterial infections. In particular, type I interferons induced during a virus infection have been observed to play a role in suppressing the production of some key antibacterial proinflammatory cytokines such as IL-23 and IL-17. Other suppressive mechanisms as a result of cytokine deregulation by viral infections include reduced function of immune cells such as DC, macrophage, natural killer, CD4(+), and CD8(+) T cells leading to impaired clearance of secondary bacterial infections. In this study, we highlight some of the immune mechanisms that become deregulated by viral infections, and can thus become defective during secondary bacterial infections.

Innate and Adaptive Immune Memory: an Evolutionary Continuum in the Host’s Response to Pathogens

“…Moreover, earlier studies in the lung suggest that innate immune cells in the lung are indeed able to remember their inflammatory history. Studies investigating the effect of two unrelated subsequent viral infections, LCMV and influenza A virus, clearly showed that a first infection exerts the ability to alter a secondary innate immune response indicating a degree of innate immune training in these models of viral infections (Mehta et al, 2015). Beyond host defense, the consequences of topical innate immune training or inflammatory memory for the development of autoimmune and auto-inflammatory disorders remain to be investigated.…”

Will children reveal their secret? The coronavirus dilemma

“…Lung ILC2 were shown to be able to remember their activation status if stimulated by inhaled allergens [32]. Cytomegalovirus and influenza A can trigger a stronger NK mediated secondary innate immune response on reinfection [33]. It is demonstrated that common epigenetic mechanisms determine memory cell development, both in the adaptive and innate immune system [34].…”

Virus-Bacteria Interactions: An Emerging Topic in Human Infection

“…Furthermore, the virus alters the Toll-like receptor pathways, resulting in decreased neutrophil attraction, which in turn increases the attachment of bacterial cells onto host epithelium [7]. Additionally, infection with influenza can deregulate cytokine production through inducing type I interferon, which can down-regulate cytokine production [56]. MicroRNA-based mechanisms resulting from influenza infection can also down-regulate cytokine production.…”