Title:Innate Immune Surveillance in the Central Nervous System Following Legionella pneumophila Infection
Volume: 16
Issue: 10
Author(s): Pasqualina Lagana*, Luca Soraci, Maria Elsa Gambuzza, Giuseppe Mancuso and Santi Antonino Delia
Affiliation:
- Regional Reference Laboratory of Clinical and Environmental Surveillance of Legionellosis, Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina,Italy
Keywords:
Central nervous system, inflammation, innate immunity, legionnaire’s disease, Legionella pneumophila, pattern
recognition receptors.
Abstract: Background & Objective: The innate immune response is a common occurrence in many
neuroinflammatory diseases. Central Nervous System (CNS) resident immune cells are able to detect
and react to infections and sterile trauma. Peripheral immune cell migration into CNS is regulated by
the blood-brain barrier, although peripheral immune cells can invade CNS through meninges, choroid
plexus, perivascular spaces, and cerebrospinal fluid. Consequently, in the brain, immune reactions can
be mediated by both resident and peripheral immune cells. Both in the periphery and within the CNS,
innate immune response is regulated by a wide array of pattern recognition receptors, including Tolllike,
scavenger, Retinoic Acid-inducible Gene-1 like, and nucleotide-binding oligomerization domainslike
responsible for inflammasome formation. Inflammasome pathway activation induces pyroptosis, a
highly inflammatory cell death pattern that occurs to remove intracellular pathogens. Legionella pneumophila
is an intracellular microorganism responsible for Legionnaires' disease, a lung infection always
associated to neurological dysfunctions. Recent studies have been shown that Toll-like receptors,
nucleotide-binding oligomerization domains-like receptors, and RIG-1 like, are activated by L. pneumophila.
This flagellated bacterium is able to replicate in phagocytic cells, including macrophages and
microglia, responding by activating inflammasome pathways that may be the cause of CNS dysfunction
detected in several infected patients.
Conclusion: The aim of this review is to bring together the latest findings concerning L. pneumophila
infection and innate immune host cell responses. A deeper knowledge of these processes could allow
the use of immunomodulatory compounds able to counteract CNS involvement following L. pneumophila
infection.
