Autophagy in Macrophages: Impacting Inflammation and Bacterial Infection

Abstract

Macrophages are on the front line of host defense. They possess an array of germline-encoded pattern recognition receptors/sensors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) and which activate downstream effectors/pathways to help mediate innate immune responses and host defense. Innate immune responses include the rapid induction of transcriptional networks that trigger the production of cytokines, chemokines, and cytotoxic molecules; the mobilization of cells including neutrophils and other leukocytes; the engulfment of pathogens by phagocytosis and their delivery to lysosome for degradation; and the induction of autophagy. Autophagy is a catabolic process that normally maintains cellular homeostasis in a lysosome-dependent manner, but it also functions as a cytoprotective response that intersects with a variety of general stress-response pathways. This review focuses on the intimately linked molecular mechanisms that help govern the autophagic pathway and macrophage innate immune responses.

Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

“…Currently, how autophagy deficiency may mechanistically affect NP pathogenesis is unknown. There is compelling evidence that autophagy plays a key role in eliminating the invading intracellular microorganisms . Thus, it is reasonably speculated that suppression of autophagy promotes infection on nasal and sinus mucosa, contributing to persistent inflammation in NPs.…”

Golgi-associated LC3 lipidation requires V-ATPase in noncanonical autophagy

“…However, the Golgi complex, mitochondria–ER contact sites and plasma membrane-derived endocytic organelles can also contribute to autophagosomes biogenesis. 34 The source of membranes on which LC3 lipidation occurs could be also diverse in NCA, which can give rise to either double- or single-membrane vesicles. 7 …”

Extracellular stimulation of VSIG4/complement receptor Ig suppresses intracellular bacterial infection by inducing autophagy

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