Nucleotide-oligomerizing domain-1 (NOD1) receptor activation induces pro-inflammatory responses and autophagy in human alveolar macrophages View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-09-25

AUTHORS

Esmeralda Juárez, Claudia Carranza, Fernando Hernández-Sánchez, Elva Loyola, Dante Escobedo, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Martha Torres, Eduardo Sada

ABSTRACT

BACKGROUND: Nucleotide-binding oligomerizing domain-1 (NOD1) is a cytoplasmic receptor involved in recognizing bacterial peptidoglycan fragments that localize to the cytosol. NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells and murine macrophages. NOD1 mediates intracellular pathogen clearance in the lungs of mice; however, little is known about NOD1's role in human alveolar macrophages (AMs) or its involvement in Mycobacterium tuberculosis (Mtb) infection. METHODS: AMs, monocytes (MNs), and monocyte-derived macrophages (MDMs) from healthy subjects were assayed for NOD1 expression. Cells were stimulated with the NOD1 ligand Tri-DAP and cytokine production and autophagy were assessed. Cells were infected with Mtb and treated with Tri-DAP post-infection. CFUs counting determined growth control, and autophagy protein recruitment to pathogen localization sites was analyzed by immunoelectron microscopy. RESULTS: NOD1 was expressed in AMs, MDMs and to a lesser extent MNs. Tri-DAP stimulation induced NOD1 up-regulation and a significant production of IL1β, IL6, IL8, and TNFα in AMs and MDMs; however, the level of NOD1-dependent response in MNs was limited. Autophagy activity determined by expression of proteins Atg9, LC3, IRGM and p62 degradation was induced in a NOD1-dependent manner in AMs and MDMs but not in MNs. Infected AMs could be activated by stimulation with Tri-DAP to control the intracellular growth of Mtb. In addition, recruitment of NOD1 and the autophagy proteins IRGM and LC3 to the Mtb localization site was observed in infected AMs after treatment with Tri-DAP. CONCLUSIONS: NOD1 is involved in AM and MDM innate responses, which include proinflammatory cytokines and autophagy, with potential implications in the killing of Mtb in humans. More... »

PAGES

152

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2466-14-152

DOI

http://dx.doi.org/10.1186/1471-2466-14-152

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008855318

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25253572


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63 cells
64 clearance
65 control
66 cytokine production
67 cytokines
68 cytoplasmic receptors
69 cytosol
70 degradation
71 determined growth control
72 domain 1
73 domain-1 (NOD1) receptor activation
74 epithelial cells
75 expression
76 extent MNs
77 fragments
78 growth
79 growth control
80 healthy subjects
81 human alveolar macrophages
82 humans
83 immunoelectron microscopy
84 implications
85 infected alveolar macrophages
86 infection
87 inflammation
88 innate response
89 intracellular growth
90 intracellular pathogen clearance
91 involvement
92 killing
93 killing of Mtb
94 lesser extent MNs
95 levels
96 ligand Tri-DAP
97 localization sites
98 lung
99 lungs of mice
100 macrophages
101 manner
102 mechanism
103 mice
104 microscopy
105 monocyte-derived macrophages
106 monocytes
107 murine macrophages
108 oligomerizing domain-1
109 p62 degradation
110 pathogen clearance
111 pathogen localization sites
112 peptidoglycan fragments
113 potential implications
114 pro-inflammatory response
115 production
116 proinflammatory cytokines
117 protein Atg9
118 protein recruitment
119 receptor activation
120 receptors
121 recruitment
122 recruitment of NOD1
123 regulation
124 response
125 role
126 significant production
127 sites
128 stimulation
129 subjects
130 treatment
131 tuberculosis infection
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