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Journal articles on the topic 'LC3 associated phagocytosis (LAP)'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Yuan, Jin, Qiuyu Zhang, Shihua Chen, Min Yan, and Lei Yue. "LC3-Associated Phagocytosis in Bacterial Infection." Pathogens 11, no. 8 (July 30, 2022): 863. http://dx.doi.org/10.3390/pathogens11080863.

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LC3-associated phagocytosis (LAP) is a noncanonical autophagy process reported in recent years and is one of the effective mechanisms of host defense against bacterial infection. During LAP, bacteria are recognized by pattern recognition receptors (PRRs), enter the body, and then recruit LC3 onto a single-membrane phagosome to form a LAPosome. LC3 conjugation can promote the fusion of the LAPosomes with lysosomes, resulting in their maturation into phagolysosomes, which can effectively kill the identified pathogens. However, to survive in host cells, bacteria have also evolved strategies to evade killing by LAP. In this review, we summarized the mechanism of LAP in resistance to bacterial infection and the ways in which bacteria escape LAP. We aim to provide new clues for developing novel therapeutic strategies for bacterial infectious diseases.

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2

Duan, Zhimin, Qing Chen, Leilei Du, Jianbo Tong, Song Xu, Rong Zeng, Yuting Ma, Xu Chen, and Min Li. "Phagocytosis of Candida albicans Inhibits Autophagic Flux in Macrophages." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/4938649.

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Autophagy machinery has roles in the defense against microorganisms such as Candida albicans. Lipidated LC3, the marker protein of autophagy, participates in the elimination of C. albicans by forming a single-membrane phagosome; this process is called LC3-associated phagocytosis (LAP). However, the influence of C. albicans on autophagic flux is not clear. In this study, we found that C. albicans inhibited LC3 turnover in macrophages. After the phagocytosis of C. albicans in macrophages, we observed fewer acridine orange-positive vacuoles and RFP-GFP-LC3 puncta without colocalization with phagocytized C. albicans. However, phagocytosis of C. albicans led to LC3 recruitment, but p62 and ATG9A did not colocalize with LC3 or C. albicans. These effects are due to an MTOR-independent pathway. Nevertheless, we found that the C. albicans pattern-associated molecular pattern β-glucan increased LC3 turnover. In addition, phagocytosis of C. albicans caused a decrease in BrdU incorporation. Blocking autophagic flux aggravated this effect. Our findings suggest that phagocytosis of C. albicans decreases autophagic flux but induces LAP in an MTOR-independent manner in macrophages. Occupation of LC3 by recruiting engulfed C. albicans might contribute to the inhibition of autophagic flux. Our study highlights the coordinated machinery between canonical autophagy and LAP that defends against C. albicans challenge.

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3

Galais, Mathilde, Baptiste Pradel, Isabelle Vergne, Véronique Robert-Hebmann, Lucile Espert, and Martine Biard-Piechaczyk. "La phagocytose associée à LC3 (LAP)." médecine/sciences 35, no. 8-9 (August 2019): 635–42. http://dx.doi.org/10.1051/medsci/2019129.

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Phagocytose et macroautophagie, appelée ici autophagie, sont deux mécanismes essentiels de dégradation lysosomale de divers cargos englobés dans des structures membranaires. Ils sont tous deux impliqués dans la régulation du système immunitaire et la survie cellulaire. Cependant, la phagocytose permet l’ingestion de matériel extracellulaire alors que l’autophagie dégrade des composants intra-cytoplasmiques, avec des mécanismes d’activation et de maturation différents. La LAP (LC3-associated phagocytosis) est une forme particulière de phagocytose qui utilise certains éléments de l’autophagie. Elle permet l’élimination de pathogènes, de complexes immuns, de cellules avoisinantes, mortes ou vivantes, constituant un danger pour l’organisme, et de débris cellulaires, tels que les segments externes des photorécepteurs (POS, photoreceptor outer segment), ou la pièce centrale du pont intercellulaire produit en fin de mitose. Les cellules ont ainsi « optimisé » leurs moyens d’éliminer les composés potentiellement dangereux en partageant certains éléments essentiels des deux voies de dégradation lysosomale.

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4

Lai, Shu-chin, and Rodney J. Devenish. "LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy." Cells 1, no. 3 (July 30, 2012): 396–408. http://dx.doi.org/10.3390/cells1030396.

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Morita, Maya, Mayu Kajiye, Chiye Sakurai, Shuichi Kubo, Miki Takahashi, Daiki Kinoshita, Naohiro Hori, and Kiyotaka Hatsuzawa. "Characterization of MORN2 stability and regulatory function in LC3-associated phagocytosis in macrophages." Biology Open 9, no. 6 (May 15, 2020): bio051029. http://dx.doi.org/10.1242/bio.051029.

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ABSTRACTMicrotubule-associated protein A1/B1-light chain 3 (LC3)-associated phagocytosis (LAP) is a type of non-canonical autophagy that regulates phagosome maturation in macrophages. However, the role and regulatory mechanism of LAP remain largely unknown. Recently, the membrane occupation and recognition nexus repeat-containing-2 (MORN2) was identified as a key component of LAP for the efficient formation of LC3-recruiting phagosomes. To characterize MORN2 and elucidate its function in LAP, we established a MORN2-overexpressing macrophage line. At a steady state, MORN2 was partially cleaved by the ubiquitin-proteasome system. MORN2 overexpression promoted not only LC3-II production but also LAP phagosome (LAPosome) acidification during Escherichia coli uptake. Furthermore, the formation of LAPosomes containing the yeast cell wall component zymosan was enhanced in MORN2-overexpressing cells and depended on reactive oxygen species (ROS). Finally, MORN2-mediated LAP was regulated by plasma membrane-localized soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) such as SNAP-23 and syntaxin 11. Taken together, these findings demonstrate that MORN2, whose expression is downregulated via proteasomal digestion, is a limiting factor for LAP, and that membrane trafficking by SNARE proteins is involved in MORN2-mediated LAP.

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6

Martinez, Jennifer, Andrew Oberst, Thirumala Devi-Kanneganti, and Douglas Green. "LC3-associated phagocytosis is a critical regulator of innate immunity. (P1261)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 56.13. http://dx.doi.org/10.4049/jimmunol.190.supp.56.13.

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Abstract The magnitude and quality of the innate immune response is shaped by many factors, both cell-intrinsic and -extrinsic. The process of autophagy is a cell-intrinsic pathway that has been implicated in the suppression of innate pro-inflammatory cytokines, and polymorphisms in autophagy genes (ATG16L) have been linked to inflammatory disease. A similar but distinct pathway, LC3-associated phagocytosis (LAP), is also important in shaping innate immune responses, largely by linking the sensing of PAMPS to the autophagic machinery, a process critical for the clearance of both pathogens and dead host cells. As autoimmunity may arise from a failure to engulf or degrade dying cells, we sought to determine if LAP might function to dampen inflammatory responses by halting otherwise constitutive signals from within the phagosome. Indeed, we show that mice with phagocytes deficient for LAP machinery (such as ATG7) exhibit increased pro-inflammatory cytokines levels in the serum when challenged with exogenous dead cells. Moreover, successful clearance of the pathogen Listeria monocytogenes requires LAP, rather than conventional autophagy. In order to fully understand this distinct and vital mechanism for effective host defense, it will be necessary to identify molecular events that are unique to LAP, which will allow us to further distinguish the physiological and pathological roles for LAP.

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Wen, Haitao, Tianliang Li, Xinghui Li, Yu Lei, and Douglas R. Green. "Mitochondrial Calcium Signaling Facilitates Bacterial Survival by Restraining LC3-associated Phagocytosis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 227.1. http://dx.doi.org/10.4049/jimmunol.204.supp.227.1.

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Abstract Mitochondria in eukaryotic cells are believed to have originated from proteobacteria through endosymbiosis 2.5 billion years ago. Accumulating evidence suggests essential roles of mitochondria in host defense response against invading pathogens. Whether intracellular bacteria can hijack mitochondria to promote their survival remains elusive. Here, we demonstrate a previously unappreciated pro-survival strategy employed by intracellular bacteria Listeria monocytogenesthat involves the suppression of LC3-associated phagocytosis (LAP) by mitochondrial Ca2+ signaling. Invasion of macrophages by L. monocytogenes caused a robust mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), leading to elevated acetyl-coenzyme A (acetyl-CoA) production via the pyruvate dehydrogenase (PDH). Acetylation of LAP effector Rubicon with the use of acetyl-CoA antagonized LAP formation. Genetic ablation of Mcuimproved bacterial killing due to elevated LAP formation. Our study indicates that modulation of mitochondrial Ca2+ signaling is a beneficial strategy for bacterial survival and highlights the importance of mitochondrial metabolism in host-microbial interaction.

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8

Inomata, Megumi, Shuying Xu, Pallavi Chandra, Simin N. Meydani, Genzou Takemura, Jennifer A. Philips, and John M. Leong. "Macrophage LC3-associated phagocytosis is an immune defense against Streptococcus pneumoniae that diminishes with host aging." Proceedings of the National Academy of Sciences 117, no. 52 (December 21, 2020): 33561–69. http://dx.doi.org/10.1073/pnas.2015368117.

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Streptococcus pneumoniae is a leading cause of pneumonia and invasive disease, particularly, in the elderly. S. pneumoniae lung infection of aged mice is associated with high bacterial burdens and detrimental inflammatory responses. Macrophages can clear microorganisms and modulate inflammation through two distinct lysosomal trafficking pathways that involve 1A/1B-light chain 3 (LC3)-marked organelles, canonical autophagy, and LC3-associated phagocytosis (LAP). The S. pneumoniae pore-forming toxin pneumolysin (PLY) triggers an autophagic response in nonphagocytic cells, but the role of LAP in macrophage defense against S. pneumoniae or in age-related susceptibility to infection is unexplored. We found that infection of murine bone-marrow-derived macrophages (BMDMs) by PLY-producing S. pneumoniae triggered Atg5- and Atg7-dependent recruitment of LC3 to S. pneumoniae-containing vesicles. The association of LC3 with S. pneumoniae-containing phagosomes required components specific for LAP, such as Rubicon and the NADPH oxidase, but not factors, such as Ulk1, FIP200, or Atg14, required specifically for canonical autophagy. In addition, S. pneumoniae was sequestered within single-membrane compartments indicative of LAP. Importantly, compared to BMDMs from young (2-mo-old) mice, BMDMs from aged (20- to 22-mo-old) mice infected with S. pneumoniae were not only deficient in LAP and bacterial killing, but also produced higher levels of proinflammatory cytokines. Inhibition of LAP enhanced S. pneumoniae survival and cytokine responses in BMDMs from young but not aged mice. Thus, LAP is an important innate immune defense employed by BMDMs to control S. pneumoniae infection and concomitant inflammation, one that diminishes with age and may contribute to age-related susceptibility to this important pathogen.

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9

Wan, JingHong, Emmanuel Weiss, Sanae Ben Mkaddem, Morgane Mabire, Pierre-Marie Choinier, Olivia Picq, Tristan Thibault-Sogorb, et al. "LC3-associated phagocytosis protects against inflammation and liver fibrosis via immunoreceptor inhibitory signaling." Science Translational Medicine 12, no. 539 (April 15, 2020): eaaw8523. http://dx.doi.org/10.1126/scitranslmed.aaw8523.

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Sustained hepatic and systemic inflammation, particularly originating from monocytes/macrophages, is a driving force for fibrosis progression to end-stage cirrhosis and underlies the development of multiorgan failure. Reprogramming monocyte/macrophage phenotype has emerged as a strategy to limit inflammation during chronic liver injury. Here, we report that LC3-associated phagocytosis (LAP), a noncanonical form of autophagy, protects against hepatic and systemic inflammation during chronic liver injury in rodents, with beneficial antifibrogenic effects. LAP is enhanced in blood and liver monocytes from patients with fibrosis and cirrhosis. Pharmacological inhibition of LAP components in human monocytes from patients with cirrhosis or genetic disruption of LAP in mice with chronic liver injury exacerbates both the inflammatory signature in isolated human monocytes and the hepatic inflammatory profile in mice, resulting in enhanced liver fibrosis. Mechanistically, patients with cirrhosis showed increased monocyte expression of Fc fragment of IgG receptor IIA (FcγRIIA) and enhanced engulfment of immunoglobulin G in LC3+ phagosomes that triggers an FcγRIIA/Src homology region 2 domain–containing phosphatase-1 (SHP-1) inhibitory immunoreceptor tyrosine-based activation motif (ITAMi) anti-inflammatory pathway. Mice overexpressing human FcγRIIA in myeloid cells show enhanced LAP in response to chronic liver injury and resistance to inflammation and liver fibrosis. Activation of LAP is lost in monocytes from patients with multiorgan failure and restored by specifically targeting ITAMi signaling with anti-FcγRIIA F(ab′)2 fragments, or with intravenous immunoglobulin (IVIg). These data suggest the existence of an ITAMi-mediated mechanism by which LAP might protect against inflammation. Sustaining LAP may open therapeutic perspectives for patients with chronic liver disease.

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10

Li, Xuelei, Mark Prescott, Ben Adler, John D. Boyce, and Rodney J. Devenish. "Beclin 1 Is Required for Starvation-Enhanced, but Not Rapamycin-Enhanced, LC3-Associated Phagocytosis of Burkholderia pseudomallei in RAW 264.7 Cells." Infection and Immunity 81, no. 1 (October 31, 2012): 271–77. http://dx.doi.org/10.1128/iai.00834-12.

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LC3-associated phagocytosis (LAP) ofBurkholderia pseudomalleiby murine macrophage (RAW 264.7) cells is an intracellular innate defense mechanism. Beclin 1, a protein with several roles in autophagic processes, is known to be recruited to phagosomal membranes as a very early event in LAP. We sought to determine whether knockdown of Beclin 1 by small interfering RNA (siRNA) would affect recruitment of LC3 and subsequent LAP of infectingB. pseudomallei. Both starvation and rapamycin treatment can induce Beclin 1-dependent autophagy. Therefore, we analyzed the consequences of Beclin 1 knockdown for LAP in infected cells that had been either starved or treated with rapamycin by determining the levels of bacterial colocalization with LC3 and intracellular survival. Concurrently, we confirmed the location of bacteria as either contained in phagosomes or free in the cytoplasm. We found that both rapamycin and starvation treatment enhanced LAP ofB. pseudomalleibut that the rapamycin response is Beclin 1 independent whereas the starvation response is Beclin 1 dependent.

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11

Asare, Patrick F., Hai B. Tran, Plinio R. Hurtado, Griffith B. Perkins, Phan Nguyen, Hubertus Jersmann, Eugene Roscioli, and Sandra Hodge. "Inhibition of LC3-associated phagocytosis in COPD and in response to cigarette smoke." Therapeutic Advances in Respiratory Disease 15 (January 2021): 175346662110397. http://dx.doi.org/10.1177/17534666211039769.

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Introduction/Rationale: In chronic obstructive pulmonary disease (COPD), defective macrophage phagocytic clearance of cells undergoing apoptosis by efferocytosis may lead to secondary necrosis of the uncleared cells and contribute to airway inflammation. The precise mechanisms for this phenomenon remain unknown. LC3-associated phagocytosis (LAP) is indispensable for effective efferocytosis. We hypothesized that cigarette smoke inhibits the regulators of LAP pathway, potentially contributing to the chronic airways inflammation associated with COPD. Methods: Bronchoalveolar (BAL)-derived alveolar macrophages, lung tissue macrophages obtained from lung resection surgery, and monocyte-derived macrophages (MDM) were prepared from COPD patients and control participants. Lung/airway samples from mice chronically exposed to cigarette smoke were also investigated. Differentiated THP-1 cells were exposed to cigarette smoke extract (CSE). The LAP pathway including Rubicon, as an essential regulator of LAP, efferocytosis and inflammation was examined using western blot, ELISA, flow cytometry, and/or immunofluorescence. Results: Rubicon was significantly depleted in COPD alveolar macrophages compared with non-COPD control macrophages. Rubicon protein in alveolar macrophages of cigarette smoke-exposed mice and cigarette smoke-exposed MDM and THP-1 was decreased with a concomitant impairment of efferocytosis. We also noted increased expression of LC3 which is critical for LAP pathway in COPD and THP-1 macrophages. Furthermore, THP-1 macrophages exposed to cigarette smoke extract exhibited higher levels of other key components of LAP pathway including Atg5 and TIM-4. There was a strong positive correlation between Rubicon protein expression and efferocytosis. Conclusion: LAP is a requisite for effective efferocytosis and an appropriate inflammatory response, which is impaired by Rubicon deficiency. Our findings suggest dysregulated LAP due to reduced Rubicon as a result of CSE exposure. This phenomenon could lead to a failure of macrophages to effectively process phagosomes containing apoptotic cells during efferocytosis. Restoring Rubicon protein expression has unrecognized therapeutic potential in the context of disease-related modifications caused by exposure to cigarette smoke.

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12

Muñoz-Sánchez, Salomé, Michiel van der Vaart, and Annemarie H. Meijer. "Autophagy and Lc3-Associated Phagocytosis in Zebrafish Models of Bacterial Infections." Cells 9, no. 11 (October 29, 2020): 2372. http://dx.doi.org/10.3390/cells9112372.

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Modeling human infectious diseases using the early life stages of zebrafish provides unprecedented opportunities for visualizing and studying the interaction between pathogens and phagocytic cells of the innate immune system. Intracellular pathogens use phagocytes or other host cells, like gut epithelial cells, as a replication niche. The intracellular growth of these pathogens can be counteracted by host defense mechanisms that rely on the autophagy machinery. In recent years, zebrafish embryo infection models have provided in vivo evidence for the significance of the autophagic defenses and these models are now being used to explore autophagy as a therapeutic target. In line with studies in mammalian models, research in zebrafish has shown that selective autophagy mediated by ubiquitin receptors, such as p62, is important for host resistance against several bacterial pathogens, including Shigella flexneri, Mycobacterium marinum, and Staphylococcus aureus. Furthermore, an autophagy related process, Lc3-associated phagocytosis (LAP), proved host beneficial in the case of Salmonella Typhimurium infection but host detrimental in the case of S. aureus infection, where LAP delivers the pathogen to a replication niche. These studies provide valuable information for developing novel therapeutic strategies aimed at directing the autophagy machinery towards bacterial degradation.

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13

Martinez, Jennifer. "LAP it up, fuzz ball: a short history of LC3-associated phagocytosis." Current Opinion in Immunology 55 (December 2018): 54–61. http://dx.doi.org/10.1016/j.coi.2018.09.011.

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14

Moore, Jamie A., Jayna J. Mistry, Charlotte Hellmich, Rebecca H. Horton, Edyta Wojtowicz, Aisha Jibril, Tom Wileman, et al. "LC3-Associated Phagocytosis in Bone Marrow Macrophages Suppresses AML Progression through Mitochondrial DAMP Induced Sting Activation." Blood 138, Supplement 1 (November 5, 2021): 3441. http://dx.doi.org/10.1182/blood-2021-152778.

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Abstract The bone marrow (BM) microenvironment regulates acute myeloid leukemia (AML) initiation, proliferation and chemotherapy resistance. Following cancer cell death, a growing body of evidence suggests an important role for uncleared apoptotic debris in regulating the immunologic response to, and growth of, solid tumors. LC3-associated phagocytosis (LAP) maintains tissue homeostasis by regulating immune responses, such as tumor immunity. Here we investigate the role of LAP in macrophage within the BM microenvironment of AML. We find that depletion of BM macrophages via clodronate liposomes increased AML growth in-vivo. We show that LAP is an important pathway in BM macrophage to process dead and dying cells in the AML microenvironment. We used two syngeneic leukemia models (HOXA9/Meis1 and MN1) to investigate the role of LAP on AML proliferation. AML cells were injected into LAP deficient (Atg16L1 E230-) and wild-type (Atg16L1 E230+) mice. Targeted inhibition of LAP leads to accumulation of apoptotic cells (AC) and apoptotic bodies (AB) in the tumor microenvironment resulting in accelerated leukemia growth and decreased animal survival. Mechanistically, we show, via cytokine arrays and gene analysis, that the phagocytosis of AML derived AB via LAP in BM macrophage resulted in STING pathway activation in the phagocytic cells. Furthermore, through inhibition of STING using H-151 STING inhibitor, we show that STING activation in vivo supressed leukemia growth. STING activation can lead to a type I IFN response and to recruitment of cytotoxic T-cells. We saw no increase in CD8 + T-cell numbers or activation, however, via ex vivo analysis found that STING activation is required for phagocytic functions in macrophages. Next, we found that leukemic AB can induce a STING response in BM derived macrophages and that leukemic AB have increased mitochondria content that are processed by macrophages. Moreover, we identify that mitochondrial damage associated molecular patterns (DAMPs) from leukemic AB are processed by BM macrophages via LAP. Additionally, the depletion of mitochondrial DNA (mtDNA) in AML derived AB identified that the mtDNA from leukemic AB is responsible for the induction of STING signalling in BM macrophages. In summary, we report that LAP in BM macrophage of apoptotic debris in the AML microenvironment suppresses leukemic growth, through mechanisms stimulated by AML apoptotic bodies which contain mtDNA in the BM microenvironment. This process is mediated by the activation of the STING pathway. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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15

Chamilos, Georgios, Tonia Akoumianaki, Irene Kyrmizi, Axel Brakhage, Anne Beauvais, and Jean-Paul Latge. "Melanin targets LC3-associated phagocytosis (LAP): A novel pathogenetic mechanism in fungal disease." Autophagy 12, no. 5 (March 30, 2016): 888–89. http://dx.doi.org/10.1080/15548627.2016.1157242.

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16

Mehta, Payal, Jill Henault, Jennifer Martinez, Jeffery Riggs, Jane Tian, Lorraine Clarke, Miwa Sasai, et al. "LC3-associated phagocytosis mediates IFN-alpha secretion in response to DNA-immune complexes. (BA3P.207)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 44.13. http://dx.doi.org/10.4049/jimmunol.192.supp.44.13.

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Abstract TLR9 compartmentalization is largely responsible for discriminating self from pathogenic DNA. However, association of host DNA with autoantibodies activates TLR9, inducing the secretion of large amounts of type I IFNs in plasmacytoid dendritic cells. Here, we show that TLR9-mediated production of IFN-α depends on the convergence of the phagocytic and autophagic pathways in response to DNA-containing immune complexes, a process called LC3-associated phagocytosis (LAP). LAP is required for TLR9 trafficking into a specialized IRF7-signaling compartment (ISC) by a mechanism that involves ATG7 but not the conventional autophagic pre-initiation complex. Progression to this compartment did not require AP-3, a protein that mediates TLR9 trafficking and IFN-α secretion in response to CpG oligonucleotides. Our findings unveil a new role for autophagy in inflammatory responses, and provide one of the mechanisms by which anti-DNA autoantibodies, such as those found in several autoimmune disorders, bypass the controls that normally restrict TLR9 activation to pathogenic DNA. Further, we have established phagosomal enrichment assays that will allow us to characterize precise nature ISC as well as the role of LAP in ISC regulation .

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Yefimova, Marina G., Celia Ravel, Antoine D. Rolland, Nicolas Bourmeyster, and Bernard Jégou. "MERTK-Mediated LC3-Associated Phagocytosis (LAP) of Apoptotic Substrates in Blood-Separated Tissues: Retina, Testis, Ovarian Follicles." Cells 10, no. 6 (June 9, 2021): 1443. http://dx.doi.org/10.3390/cells10061443.

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Timely and efficient elimination of apoptotic substrates, continuously produced during one’s lifespan, is a vital need for all tissues of the body. This task is achieved by cells endowed with phagocytic activity. In blood-separated tissues such as the retina, the testis and the ovaries, the resident cells of epithelial origin as retinal pigmented epithelial cells (RPE), testis Sertoli cells and ovarian granulosa cells (GC) provide phagocytic cleaning of apoptotic cells and cell membranes. Disruption of this process leads to functional ablation as blindness in the retina and compromised fertility in males and females. To ensure the efficient elimination of apoptotic substrates, RPE, Sertoli cells and GC combine various mechanisms allowing maintenance of tissue homeostasis and avoiding acute inflammation, tissue disorganization and functional ablation. In tight cooperation with other phagocytosis receptors, MERTK—a member of the TAM family of receptor tyrosine kinases (RTK)—plays a pivotal role in apoptotic substrate cleaning from the retina, the testis and the ovaries through unconventional autophagy-assisted phagocytosis process LAP (LC3-associated phagocytosis). In this review, we focus on the interplay between TAM RTKs, autophagy-related proteins, LAP, and Toll-like receptors (TLR), as well as the regulatory mechanisms allowing these components to sustain tissue homeostasis and prevent functional ablation of the retina, the testis and the ovaries.

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Oikonomou, Vasileios, Giorgia Renga, Antonella De Luca, Monica Borghi, Marilena Pariano, Matteo Puccetti, Giuseppe Paolicelli, et al. "Autophagy and LAP in the Fight against Fungal Infections: Regulation and Therapeutics." Mediators of Inflammation 2018 (2018): 1–7. http://dx.doi.org/10.1155/2018/6195958.

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Phagocytes fight fungi using canonical and noncanonical, also called LC3-associated phagocytosis (LAP), autophagy pathways. However, the outcomes of autophagy/LAP in shaping host immune responses appear to greatly vary depending on fungal species and cell types. By allowing efficient pathogen clearance and/or degradation of inflammatory mediators, autophagy proteins play a broad role in cellular and immune homeostasis during fungal infections. Indeed, defects in autophagic machinery have been linked with aberrant host defense and inflammatory states. Thus, understanding the molecular mechanisms underlying the relationship between the different forms of autophagy may offer a way to identify drugable molecular signatures discriminating between selective recognition of cargo and host protection. In this regard, IFN-γ and anakinra are teaching examples of successful antifungal agents that target the autophagy machinery. This article provides an overview of the role of autophagy/LAP in response to fungi and in their infections, regulation, and therapeutic exploitation.

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Gong, Lan, Shu-Chin Lai, Puthayalai Treerat, Mark Prescott, Ben Adler, John D. Boyce, and Rodney J. Devenish. "Burkholderia pseudomallei Type III Secretion System Cluster 3 ATPase BsaS, a Chemotherapeutic Target for Small-Molecule ATPase Inhibitors." Infection and Immunity 83, no. 4 (January 20, 2015): 1276–85. http://dx.doi.org/10.1128/iai.03070-14.

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Melioidosis is an infectious disease of high mortality for humans and other animal species; it is prevalent in tropical regions worldwide. The pathogenesis of melioidosis depends on the ability of its causative agent, the Gram-negative bacteriumBurkholderia pseudomallei, to enter and survive in host cells.B. pseudomalleican escape from the phagosome into the cytosol of phagocytic cells where it replicates and acquires actin-mediated motility, avoiding killing by the autophagy-dependent process, LC3 (microtubule-associated protein light chain 3)-associated phagocytosis (LAP). The type III secretion system cluster 3 (TTSS3) facilitates bacterial escape from phagosomes, although the mechanism has not been fully elucidated. Given the recent identification of small-molecule inhibitors of the TTSS ATPase, we sought to determine the potential of the predicted TTSS3 ATPase, encoded bybsaS, as a target for chemotherapeutic treatment of infection. AB. pseudomalleibsaSdeletion mutant was generated and used as a control against which to assess the effect of inhibitor treatment. Infection of RAW 264.7 cells with wild-type bacteria and subsequent treatment with the ATPase inhibitor compound 939 resulted in reduced intracellular bacterial survival, reduced escape from phagosomes, and increased colocalization with both LC3 and the lysosomal marker LAMP1 (lysosome-associated membrane protein 1). These changes were similar to those observed for infection of RAW 264.7 cells with thebsaSdeletion mutant. We propose that treatment with the ATPase inhibitor compound 939 decreased intracellular bacterial survival through a reduced ability of bacteria to escape from phagosomes and increased killing via LAP. Therefore, small-molecule inhibitors of the TTSS3 ATPase have potential as therapeutic treatments against melioidosis.

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Boonhok, Rachasak, Nattawan Rachaphaew, Apisak Duangmanee, Pornpimol Chobson, Sittiporn Pattaradilokrat, Pongsak Utaisincharoen, Jetsumon Sattabongkot, and Marisa Ponpuak. "LAP-like process as an immune mechanism downstream of IFN-γ in control of the human malaria Plasmodium vivax liver stage." Proceedings of the National Academy of Sciences 113, no. 25 (May 16, 2016): E3519—E3528. http://dx.doi.org/10.1073/pnas.1525606113.

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IFN-γ is a major regulator of immune functions and has been shown to induce liver-stage Plasmodium elimination both in vitro and in vivo. The molecular mechanism responsible for the restriction of liver-stage Plasmodium downstream of IFN-γ remains uncertain, however. Autophagy, a newly described immune defense mechanism, was recently identified as a downstream pathway activated in response to IFN-γ in the control of intracellular infections. We thus hypothesized that the killing of liver-stage malarial parasites by IFN-γ involves autophagy induction. Our results show that whereas IFN-γ treatment of human hepatocytes activates autophagy, the IFN-γ–mediated restriction of liver-stage Plasmodium vivax depends only on the downstream autophagy-related proteins Beclin 1, PI3K, and ATG5, but not on the upstream autophagy-initiating protein ULK1. In addition, IFN-γ enhanced the recruitment of LC3 onto the parasitophorous vacuole membrane (PVM) and increased the colocalization of lysosomal vesicles with P. vivax compartments. Taken together, these data indicate that IFN-γ mediates the control of liver-stage P. vivax by inducing a noncanonical autophagy pathway resembling that of LC3-associated phagocytosis, in which direct decoration of the PVM with LC3 promotes the fusion of P. vivax compartments with lysosomes and subsequent killing of the pathogen. Understanding the hepatocyte response to IFN-γ during Plasmodium infection and the roles of autophagy-related proteins may provide an urgently needed alternative strategy for the elimination of this human malaria.

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Martinez, Jennifer. "Non-canonical autophagy mediates immunosuppression during challenge." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 46.6. http://dx.doi.org/10.4049/jimmunol.200.supp.46.6.

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Abstract Autophagy is an evolutionarily conserved, catabolic pathway that lies at the intersection of homeostasis and host immune response. The autophagy machinery functions in a multitude of biological pathways, including the recycling of intracellular nutrients during starvation or stress (macroautophagy), the quality control removal of damaged proteins or organelles (aggrephagy, mitophagy), or the degradation of and host defense to extracellular threats, such as pathogens or dying cells. However, the non-canonical roles of the autophagy machinery are a critical node in the immune response to invasive pathogens, as well as prevention of autoimmunity. We have identified a form of non-canonical autophagy termed LC3-associated phagocytosis (LAP), a phenomenon in which phagosomes containing engulfed particles, including pathogens and dying cells, recruit certain elements of the autophagy pathway to facilitate phagosome maturation, digestion of cargo, and modulation of innate immunity. Importantly we have characterized Rubicon as a LAP-specific, autophagy-independent molecule, allowing the study of the unique role of LAP. We recently demonstrated that defects in LAP, but not canonical autophagy, result in a lupus-like disease with age. Using Rubicon−/− mice, we are now investigating the role of LAP in other autoimmune disease onset and progression. Our evidence clearly indicates that LAP is critical in the maintenance of immunotolerance in a variety of inflammatory diseases, including type 1 diabetes, allergic asthma, and atopic dermatitis. Mechanistically, we have begun to dissect the molecular pathways, such as metabolism, that LAP modulates in order to achieve immunosuppression. This research was supported by the NIEHS.

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Martinez, Jennifer, Thomas H. Oguin, Joseph P. Kolb, Gregory Whitehead, Seddon Y. Thomas, Ginger W. Muse, Laura Miller DeGraff, and Donald N. Cook. "The role of RUBCN in exacerbating allergic airway inflammation." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 234.7. http://dx.doi.org/10.4049/jimmunol.204.supp.234.7.

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Abstract Allergic airway inflammation (typified by atopic asthma) is a classic example of type 2 immunity, which can be triggered by non-microbial environmental stimuli, such as allergens. Importantly, type 2 immunity engages the entire affected tissue and can involve the activity of not only immune cells, like Th2 cells and eosinophils, but also non-hematopoietic cells, like epithelial cells. Often, type 2 immunity exists in competition with type 1 immunity, classically defined as the activity of phagocytic cells, such as classically activated “M1” macrophages, and IFNg-producing adaptive immune cells, like CD8+ T cells and Th1 cells. Our past studies have demonstrated that deficiency in LC3-associated phagocytosis (LAP), a non-canonical form of autophagy requiring Rubcn, results in increased type 1 inflammation across a variety of stimuli, suggesting that LAP represents an important mechanism to regulate the inflammatory response. How Rubcn deficiency affects the onset and severity of type 2 immunity, such as allergic airway inflammation, remains unknown. Here, we demonstrate that, in response to house dust extract (HDE)/OVA exposure, lungs from Rubcn−/− mice contain increased levels of Th1 and Tr17 cells (potent regulatory CD4+ T cells that co-express FOXP3 and RORg), decreased Th2 cells, and decreased neutrophils, resulting in overall protection from allergic airway pathology. Rubcn-deficiency was required in non-hematopoietic cells, presumably airway epithelial cells, to exert this protective effect. As approximately 50% of asthmatics suffer from corticosteroid-resistant, neutrophil-mediated inflammation, inhibition of RUBCN could represent a novel therapy for steroid-resistant asthmatics.

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Parekh, Vrajesh V., Sudheer K. Pabbisetty, Lan Wu, Eric Sebzda, Jennifer Martinez, Jianhua Zhang, and Luc Van Kaer. "Autophagy-related protein Vps34 controls the homeostasis and function of antigen cross-presenting CD8α+ dendritic cells." Proceedings of the National Academy of Sciences 114, no. 31 (July 17, 2017): E6371—E6380. http://dx.doi.org/10.1073/pnas.1706504114.

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The class III PI3K Vacuolar protein sorting 34 (Vps34) plays a role in both canonical and noncanonical autophagy, key processes that control the presentation of antigens by dendritic cells (DCs) to naive T lymphocytes. We generated DC-specific Vps34-deficient mice to assess the contribution of Vps34 to DC functions. We found that DCs from these animals have a partially activated phenotype, spontaneously produce cytokines, and exhibit enhanced activity of the classic MHC class I and class II antigen-presentation pathways. Surprisingly, these animals displayed a defect in the homeostatic maintenance of splenic CD8α+ DCs and in the capacity of these cells to cross-present cell corpse-associated antigens to MHC class I-restricted T cells, a property that was associated with defective expression of the T-cell Ig mucin (TIM)-4 receptor. Importantly, mice deficient in the Vps34-associated protein Rubicon, which is critical for a noncanonical form of autophagy called “Light-chain 3 (LC3)-associated phagocytosis” (LAP), lacked such defects. Finally, consistent with their defect in the cross-presentation of apoptotic cells, DC-specific Vps34-deficient animals developed increased metastases in response to challenge with B16 melanoma cells. Collectively, our studies have revealed a critical role of Vps34 in the regulation of CD8α+ DC homeostasis and in the capacity of these cells to process and present antigens associated with apoptotic cells to MHC class I-restricted T cells. Our findings also have important implications for the development of small-molecule inhibitors of Vps34 for therapeutic purposes.

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Romao, Susana, and Christian Münz. "LC3-associated phagocytosis." Autophagy 10, no. 3 (January 7, 2014): 526–28. http://dx.doi.org/10.4161/auto.27606.

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Heckmann, Bradlee L., Emilio Boada-Romero, Larissa D. Cunha, Joelle Magne, and Douglas R. Green. "LC3-Associated Phagocytosis and Inflammation." Journal of Molecular Biology 429, no. 23 (November 2017): 3561–76. http://dx.doi.org/10.1016/j.jmb.2017.08.012.

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Heckmann, Bradlee L., and Douglas R. Green. "LC3-associated phagocytosis at a glance." Journal of Cell Science 132, no. 5 (February 20, 2019): jcs222984. http://dx.doi.org/10.1242/jcs.222984.

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Schille, Stefan, Peter Crauwels, Rebecca Bohn, Katrin Bagola, Paul Walther, and Ger van Zandbergen. "LC3-associated phagocytosis in microbial pathogenesis." International Journal of Medical Microbiology 308, no. 1 (January 2018): 228–36. http://dx.doi.org/10.1016/j.ijmm.2017.10.014.

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Ligeon, Laure-Anne, Monica Loi, and Christian Münz. "LC3-Associated Phagocytosis and Antigen Presentation." Current Protocols in Immunology 123, no. 1 (September 25, 2018): e60. http://dx.doi.org/10.1002/cpim.60.

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Wakida, Nicole M., Alice L. Lau, Jessica Nguyen, Gladys Mae S. Cruz, Gianna M. Fote, Joan S. Steffan, Leslie M. Thompson, and Michael W. Berns. "Diminished LC3-Associated Phagocytosis by Huntington’s Disease Striatal Astrocytes." Journal of Huntington's Disease 11, no. 1 (March 1, 2022): 25–33. http://dx.doi.org/10.3233/jhd-210502.

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Background: In recent years the functions of astrocytes have shifted from conventional supportive roles to also include active roles in altering synapses and engulfment of cellular debris. Recent studies have implicated astrocytes in both protective and pathogenic roles impacting Huntington’s disease (HD) progression. Objective: The goal of this study is to determine if phagocytosis of cellular debris is compromised in HD striatal astrocytes. Methods: Primary adult astrocytes were derived from two HD mouse models; the fast-progressing R6/2 and slower progressing Q175. With the use of laser nanosurgery, a single astrocyte was lysed within an astrocyte network. The phagocytic response of astrocytes was observed with phase contrast and by fluorescence microscopy for GFP-LC3 transiently transfected cells. Results: Astrocyte phagocytosis was significantly diminished in primary astrocytes, consistent with the progression of HD in R6/2 and Q175 mouse models. This was defined by the number of astrocytes responding via phagocytosis and by the average number of vesicles formed per cell. GFP-LC3 was found to increasingly localize to phagocytic vesicles over a 20-min imaging period, but not in HD mice, suggesting the involvement of LC3 in astrocyte phagocytosis. Conclusion: We demonstrate a progressive decrease in LC3-associated phagocytosis in HD mouse striatal astrocytes.

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Upadhyay, Sandeep, and Jennifer A. Philips. "LC3-associated phagocytosis: host defense and microbial response." Current Opinion in Immunology 60 (October 2019): 81–90. http://dx.doi.org/10.1016/j.coi.2019.04.012.

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Fazeli, Gholamreza, and Ann Marie Wehman. "Safely removing cell debris with LC3-associated phagocytosis." Biology of the Cell 109, no. 10 (August 25, 2017): 355–63. http://dx.doi.org/10.1111/boc.201700028.

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Stempels, Femmy C., and Geert van den Bogaart. "LC3-associated phagocytosis: a sorting mechanism for ubiquitinated membrane proteins?" Autophagy Reports 1, no. 1 (March 22, 2022): 25–28. http://dx.doi.org/10.1080/27694127.2022.2040765.

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Herb, Marc, Alexander Gluschko, and Michael Schramm. "LC3-associated phagocytosis - The highway to hell for phagocytosed microbes." Seminars in Cell & Developmental Biology 101 (May 2020): 68–76. http://dx.doi.org/10.1016/j.semcdb.2019.04.016.

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Cunha, Larissa D., Mao Yang, Robert Carter, Clifford Guy, Lacie Harris, Jeremy C. Crawford, Giovanni Quarato, et al. "LC3-Associated Phagocytosis in Myeloid Cells Promotes Tumor Immune Tolerance." Cell 175, no. 2 (October 2018): 429–41. http://dx.doi.org/10.1016/j.cell.2018.08.061.

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Wang, Chin-Wei, Romain A. Colas, Jesmond Dalli, Hildur H. Arnardottir, Daniel Nguyen, Hatice Hasturk, Nan Chiang, Thomas E. Van Dyke, and Charles N. Serhan. "Maresin 1 Biosynthesis and Proresolving Anti-infective Functions with Human-Localized Aggressive Periodontitis Leukocytes." Infection and Immunity 84, no. 3 (December 14, 2015): 658–65. http://dx.doi.org/10.1128/iai.01131-15.

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Localized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis linked to periodontal infection with uncontrolled inflammation and leukocyte-mediated tissue destruction. The resolution of inflammation is an active process orchestrated by specialized proresolving lipid mediators (SPMs). Since the level of the Maresin pathway marker 14-hydroxy-docosahexaenoic acid (14-HDHA) was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosynthetic pathway in these subjects and its role in regulating phagocyte functions. Macrophages from LAP patients had a lower level of expression of 12-lipoxygenase (∼30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 ± 50 pg/106cells versus 239.1 ± 32 pg/106cells). Phagocytosis by LAP macrophages was reduced ∼40% compared to that of HC, and killing of periodontal pathogens, includingPorphyromonas gingivalisandAggregatibacter actinomycetemcomitans, were similarly reduced. LAP neutrophils also displayed slower kinetics (∼30%) and decreased maximal phagocytosis (∼20% lower) with these pathogens than those of HC. The administration of MaR1 at 1 nM enhanced phagocytosis (31 to 65% increase), intracellular antimicrobial reactive oxygen species production (26 to 71% increase), bacterial killing of these periodontal pathogens (22 to 38% reduction of bacterial titers), and restored impairment of LAP phagocytes. Together, these results suggest that therapeutics targeting the Maresin pathway have clinical utility in treating LAP and other oral diseases associated with infection, inflammation, and altered phagocyte functions.

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Heckmann, Bradlee L., and Douglas R. Green. "Correction: LC3-associated phagocytosis at a glance (doi:10.1242/jcs.222984)." Journal of Cell Science 132, no. 5 (March 1, 2019): jcs231472. http://dx.doi.org/10.1242/jcs.231472.

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Akoumianaki, Tonia, Irene Kyrmizi, Isabel Valsecchi, Mark S. Gresnigt, George Samonis, Elias Drakos, Dimitrios Boumpas, et al. "Aspergillus Cell Wall Melanin Blocks LC3-Associated Phagocytosis to Promote Pathogenicity." Cell Host & Microbe 19, no. 1 (January 2016): 79–90. http://dx.doi.org/10.1016/j.chom.2015.12.002.

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Fu, Qiang, Kang Chen, Qian Zhu, Weijia Wang, Fuda Huang, Lishao Miao, and Xinger Wu. "β-catenin promotes intracellular bacterial killing via suppression of Pseudomonas aeruginosa-triggered macrophage autophagy." Journal of International Medical Research 45, no. 2 (March 21, 2017): 556–69. http://dx.doi.org/10.1177/0300060517692147.

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Objective To investigate β-catenin-mediated bacterial elimination during Pseudomonas aeruginosa infection of macrophage-like RAW264.7 cells. Methods Cell viability and catenin beta 1 ( CTNNB1) expression in RAW264.7 cells following P. aeruginosa infection versus uninfected cells, were detected by cell counting kit-8 assay and β-catenin Western blots. RAW264.7 cells with CTNNB1 overexpression were established with β-catenin lentivirus using flow cytometry and clonogenic limiting dilution assays. Bacterial killing was measured by plate counts; phagocytosis and nitric oxide (NO) were measured by flow cytometry; and reactive oxygen species (ROS) were measured using Griess reaction. Autophagy was determined by microtubule-associated protein 1 light chain 3 alpha-phosphatidylethanolamine conjugate (LC3-II) protein levels and formation of LC3 puncta, using Western blot and immunofluorescence staining. Results Following P. aeruginosa infection, RAW264.7 cell β-catenin levels were reduced in a time- and multiplicity of infection-dependent manner. CTNNB1 overexpression was associated with increased P. aeruginosa elimination, but had no effect on RAW264.7 cell phagocytosis, ROS and NO. CTNNB1 overexpression reduced LC3-II levels and formation of LC3 puncta, suggesting autophagy inhibition. Rapamycin/starvation-induced autophagy resulted in reduced bacterial killing following P. aeruginosa infection. Conclusion β-catenin may promote bacterial killing via suppression of P. aeruginosa-induced macrophage autophagy.

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Cohen-Kedar, Sarit, Efrat Shaham Barda, Keren M. Rabinowitz, Danielle Keizer, Shoshana Schwartz, Kawsar Kaboub, Ian D. White, et al. "24: HUMAN INTESTINAL EPITHELIAL CELLS INTERNALIZE LUMINAL FUNGI VIA LC3-ASSOCIATED PHAGOCYTOSIS." Gastroenterology 162, no. 7 (May 2022): S—10. http://dx.doi.org/10.1016/s0016-5085(22)60024-6.

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Stempels, Femmy C., Maaike H. Janssens, Martin Beest, Rob J. Mesman, Natalia H. Revelo, Melina Ioannidis, and Geert den Bogaart. "Novel and conventional inhibitors of canonical autophagy differently affect LC3‐associated phagocytosis." FEBS Letters 596, no. 4 (January 21, 2022): 491–509. http://dx.doi.org/10.1002/1873-3468.14280.

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Masud, Samrah, Tomasz K. Prajsnar, Vincenzo Torraca, Gerda E. M. Lamers, Marianne Benning, Michiel Van Der Vaart, and Annemarie H. Meijer. "Macrophages target Salmonella by Lc3-associated phagocytosis in a systemic infection model." Autophagy 15, no. 5 (January 24, 2019): 796–812. http://dx.doi.org/10.1080/15548627.2019.1569297.

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Matte, Christine, Pierre-André Casgrain, Olivier Séguin, Neda Moradin, Wan Jin Hong, and Albert Descoteaux. "Leishmania major Promastigotes Evade LC3-Associated Phagocytosis through the Action of GP63." PLOS Pathogens 12, no. 6 (June 9, 2016): e1005690. http://dx.doi.org/10.1371/journal.ppat.1005690.

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Sprenkeler, Evelien G. G., Mark S. Gresnigt, and Frank L. van de Veerdonk. "LC3-associated phagocytosis: a crucial mechanism for antifungal host defence againstAspergillus fumigatus." Cellular Microbiology 18, no. 9 (July 6, 2016): 1208–16. http://dx.doi.org/10.1111/cmi.12616.

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Roychowdhury, Sanjoy, Anugraha Gandhirajan, and Vidula Vachharajani. "61: ETHANOL REPRESSES LC3-ASSOCIATED PHAGOCYTOSIS VIA SIRTUIN 2 IN HUMAN MACROPHAGES." Critical Care Medicine 51, no. 1 (December 15, 2022): 31. http://dx.doi.org/10.1097/01.ccm.0000906120.11167.6d.

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Roychowdhury, Sanjoy, Anugraha Gandhirajan, Rachel Scheraga, and Vidula Vachharajani. "1195: SIRT2 REPRESSES LC3-ASSOCIATED PHAGOCYTOSIS IN ETHANOL-EXPOSED MACROPHAGES VIA PFKP." Critical Care Medicine 51, no. 1 (December 15, 2022): 596. http://dx.doi.org/10.1097/01.ccm.0000910516.99934.f6.

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Deen, Nadia S., Lan Gong, Thomas Naderer, Rodney J. Devenish, and Terry Kwok. "Analysis of the Relative Contribution of Phagocytosis, LC3-Associated Phagocytosis, and Canonical Autophagy DuringHelicobacter pyloriInfection of Macrophages." Helicobacter 20, no. 6 (April 10, 2015): 449–59. http://dx.doi.org/10.1111/hel.12223.

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Gresnigt, Mark S., Katharina L. Becker, Floris Leenders, M. Fernanda Alonso, Xiaowen Wang, Jacques F. Meis, Judith M. Bain, Lars P. Erwig, and Frank L. van de Veerdonk. "Differential Kinetics of Aspergillus nidulans and Aspergillus fumigatus Phagocytosis." Journal of Innate Immunity 10, no. 2 (December 16, 2017): 145–60. http://dx.doi.org/10.1159/000484562.

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Invasive aspergillosis mainly occurs in immunocompromised patients and is commonly caused by Aspergillus fumigatus, while A.nidulans is rarely the causative agent. However, in chronic granulomatous disease (CGD) patients, A. nidulans is a frequent cause of invasive aspergillosis and is associated with higher mortality. Immune recognition of A. nidulans was compared to A. fumigatus to offer an insight into why A. nidulans infections are prevalent in CGD. Live cell imaging with J774A.1 macrophage-like cells and LC3-GFP-mCherry bone marrow-derived macrophages (BMDMs) revealed that phagocytosis of A. nidulans was slower compared to A. fumigatus. This difference could be attributed to slower migration of J774A.1 cells and a lower percentage of migrating BMDMs. In addition, delayed phagosome acidification and LC3-associated phagocytosis was observed with A. nidulans. Cytokine and oxidative burst measurements in human peripheral blood mononuclear cells revealed a lower oxidative burst upon challenge with A. nidulans. In contrast, A. nidulans induced significantly higher concentrations of cytokines. Collectively, our data demonstrate that A. nidulans is phagocytosed and processed at a slower rate compared to A. fumigatus, resulting in reduced fungal killing and increased germination of conidia. This slower rate of A. nidulans clearance may be permissive for overgrowth within certain immune settings.

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Akoumianaki, Tonia, Katerina Vaporidi, Eleni Diamantaki, Frédéric Pène, Remi Beau, Mark S. Gresnigt, Marina Gkountzinopulou, et al. "Uncoupling of IL-6 signaling and LC3-associated phagocytosis drives immunoparalysis during sepsis." Cell Host & Microbe 29, no. 8 (August 2021): 1277–93. http://dx.doi.org/10.1016/j.chom.2021.06.002.

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49

Gluschko, Alexander, Marc Herb, Katja Wiegmann, Oleg Krut, Wolfram F. Neiss, Olaf Utermöhlen, Martin Krönke, and Michael Schramm. "The β2 Integrin Mac-1 Induces Protective LC3-Associated Phagocytosis of Listeria monocytogenes." Cell Host & Microbe 23, no. 3 (March 2018): 324–37. http://dx.doi.org/10.1016/j.chom.2018.01.018.

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Ambrosi, Cecilia, Daniela Scribano, Meysam Sarshar, Carlo Zagaglia, Bernhard B. Singer, and Anna Teresa Palamara. "Acinetobacter baumannii Targets Human Carcinoembryonic Antigen-Related Cell Adhesion Molecules (CEACAMs) for Invasion of Pneumocytes." mSystems 5, no. 6 (December 22, 2020): e00604-20. http://dx.doi.org/10.1128/msystems.00604-20.

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ABSTRACTMultidrug-resistant Acinetobacter baumannii is regarded as a life-threatening pathogen mainly associated with nosocomial and community-acquired pneumonia. Here, we show that A. baumannii can bind the human carcinoembryonic antigen-related cell adhesion molecule (CEACAM) receptors CEACAM1, CEACAM5, and CEACAM6. This specific interaction enhances A. baumannii internalization in membrane-bound vacuoles, promptly decorated with Rab5, Rab7, and lipidated microtubule-associated protein light chain 3 (LC3). Dissecting intracellular signaling pathways revealed that infected pneumocytes trigger interleukin-8 (IL-8) secretion via the extracellular signal-regulated kinase (ERK)1/2 and nuclear factor-kappa B (NF-κB) signaling pathways for A. baumannii clearance. However, in CEACAM1-L-expressing cells, IL-8 secretion lasts only 24 h, possibly due to an A. baumannii-dependent effect on the CEACAM1-L intracellular domain. Conversely, the glycosylphosphatidylinositol-anchored CEACAM5 and CEACAM6 activate the c-Jun NH2-terminal kinase (JNK)1/2-Rubicon-NOX2 pathway, suggestive of LC3-associated phagocytosis. Overall, our data show for the first time novel mechanisms of adhesion to and invasion of pneumocytes by A. baumannii via CEACAM-dependent signaling pathways that eventually lead to bacterial killing. These findings suggest that CEACAM upregulation could put patients at increased risk of lower respiratory tract infection by A. baumannii.IMPORTANCE This work shows for the first time that Acinetobacter baumannii binds to carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), CEACAM5, and CEACAM6. This binding significantly enhances A. baumannii internalization within alveolar host cell epithelia. Intracellular trafficking involves typical Rab5 and Rab7 vacuolar proteins as well as light chain 3 (LC3) and slowly progresses to bacterial killing by endosome acidification. CEACAM engagement by A. baumannii leads to distinct and specific downstream signaling pathways. The CEACAM1 pathway finely tunes interleukin-8 (IL-8) secretion, whereas CEACAM5 and CEACAM6 mediate LC3-associated phagocytosis. The present study provides new insights into A. baumannii-host interactions and could represent a promising therapeutic strategy to reduce pulmonary infections caused by this pathogen.

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