Abstract
It is well established that by modulating various immune functions, host infection may alter the course of concomitant inflammatory diseases, of both infectious and autoimmune etiologies. Beyond the major impact of commensal microbiota on the immune status, host exposure to viral, bacterial, and/or parasitic microorganisms also dramatically influences inflammatory diseases in the host, in a beneficial or harmful manner. Moreover, by modifying pathogen control and host tolerance to tissue damage, a coinfection can profoundly affect the development of a concomitant infectious disease. Here, we review the diverse mechanisms that underlie the impact of (co)infections on inflammatory disorders. We discuss epidemiological studies in the context of the hygiene hypothesis and shed light on the sometimes dual impact of germ exposure on human susceptibility to inflammatory disease. We then summarize the immunomodulatory mechanisms at play, which can involve pleiotropic effects of immune players and discuss the possibility to harness pathogen-derived compounds to the host benefit.
Highlights
The main functions of our immune system are to provide defenses against invasion by pathogens and tumor cells and to promote tissue homeostasis and repair
Through the process of immune tolerance, the immune system can distinguish self and nonself so that an immune response develops against nonself elements, while no harm is inflicted upon self
The disruption of tolerance may lead to the development of autoimmune diseases, which manifest by an attack on self-tissues as if they were foreign
Summary
The main functions of our immune system are to provide defenses against invasion by pathogens and tumor cells and to promote tissue homeostasis and repair. The disruption of tolerance may lead to the development of autoimmune diseases, which manifest by an attack on self-tissues as if they were foreign. The efficiency of the immune system to defend against pathogens, and the severity of its attacks against self after tolerance breakdown, are largely affected by intrinsic (for example, genetics) and extrinsic factors (for example, environmental cues or exposome), including exposure to pathogenic and/or commensal microorganisms. It is well established that by modulating various immune functions, host infection may alter the course of concomitant inflammatory diseases, of both infectious and autoimmune etiologies. Infections can either ameliorate or aggravate the clinical outcome of an inflammatory disorder. Numerous studies have contributed to identify the variety of mechanisms that govern the immune
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